Pterostilbene Ameliorates Glycemic Control,Dyslipidemia and Liver Injury in Type 2 Diabetes Rats

Type 2 diabetes mellitus(T2DM)is typified by the increment of chronic blood glucose levels that is caused by an absolute and/or a relative deficiency of insulin,accounts for 90%of diabetes and causes a range of complications[1].

The Mechanism of Acute Lung Injury Induced by Nickel Carbonyl in Rats

Nickel carbonyl is a highly toxic metal compound produced from the reaction that occurs between nickel and carbon monoxide under pressure. As previously reported, nickel carbonyl can cause acute aspiration pneumonia, and animal experiments showed it was toxic to animal lung, liver, brain, and other vital organs[1]. However, few studies have investigated nickel carbonyl poisoning in humans.

A comprehensive study of long-term skeletal changes after spinal cord injury in adult rats

Spinal cord injury（SCI）-induced bone loss represents the most severe osteoporosis with no effective treatment.Past animal studies have focused primarily on long bones at the acute stage using adolescent rodents. To mimic chronic SCI in human patients, we performed a comprehensive analysis of long-term structural and mechanical changes in axial and appendicular bones in adult rats after SCI. In this experiment, 4-month-old Fischer 344 male rats received a clinically relevant T13 contusion injury. Sixteen weeks later, sublesional femurs, tibiae,and L4 vertebrae, supralesional humeri, and blood were collected from these rats and additional non-surgery rats for micro-computed tomography（m CT）, micro-finite element, histology, and serum biochemical analyses.At trabecular sites, extreme losses of bone structure and mechanical competence were detected in the metaphysis of sublesional long bones after SCI, while the subchondral part of the same bones showed much milder damage. Marked reductions in bone mass and strength were also observed in sublesional L4 vertebrae but not in supralesional humeri. At cortical sites, SCI induced structural and strength damage in both sub- and supralesional long bones. These changes were accompanied by diminished osteoblast number and activity and increased osteoclast number and activity. Taken together, our study revealed site-specific effects of SCI on bone and demonstrated sustained inhibition of bone formation and elevation of bone resorption at the chronic stage of SCI.

Effects of Chuanxiongqin hydrochloride on increasing the fluidity of brain cell membrane and scavenging free radicals in model rats with ischemia/reperfusion injury

BACKGROUND: The fluidity of cell membrane can be affected by various factors. Many experiments have confirmed that the ischemia/reperfusion of organic tissue can increase the contents of free radicals, which lead to high rigidity and low fluidity of cell membrane, and the conditions can be changed by Chuanxiongqin. OBJECTIVE: To observe the effect and mechanism of Chuanxiongqin hydrochloride on the fluidity of brain cell membrane in rat models of ischemia/reperfusion. DESIGN: A completely randomized controlled animal trial. SETTINGS: Institute of Brain Sciences; Department of Physiology, Medical College, Datong University. MATERIALS: Twenty male grade Ⅰ Wistar rats of 170-220 g were randomly divided into model group (n =10) and control group (n =10). Chuanxiongqin hydrochloride (molecular mass was 172.2) was purchased from the National Institute for the Control of Pharmaceutical and Biological Products (batch number: 0817-9803); Spin labelers: 5-doxyl-stearlic acid methylester (5DS), 16-doxyl-stearlic acid methylester (16DS), xanthine, xanthine oxidase (XOD) and 5,5-dimeth-1-pyrroline- N-oxide (DMPO) from Sigma Company; Bruker ESP 300 electron paramagnetic resonance (EPR) spectrometer by Bruker Company (Germany). METHODS: The experiments were carried out in the State Key Laboratory of Natural and Biomimetic Drugs, Peking University from June 2001 to July 2002. In the model group, rats were made into models of cerebral ischemia by 30-minute ligation and 2-hour reperfusion of common carotid arteries; The rats in the control group were not made into models. The order parameter (S) and rotational correlation time (τc) were detected with the ESR spectrometer by means of spin labeling. The greater the S and τc, the smaller the fluidity. Meanwhile, the clearance rate of free radicals was detected with ESR spin trapping. The measurement data were compared using the t test. MAIN OUTCOME MEASURES: The S, τc and clearance rates of O2 · and OH· free radicals were compared between the model group and control group. RESULTS: The S and τc in the model group [0.738 4±0.003 5; (8.472±0.027)×10-10 s/circle] were obviously different from those in the control group [0.683 9±0.008 3; (7.945±0.082)×10-10 s/circle, t =5.731, 5.918, P < 0.05], which suggested that ischemia/reperfusion injury decreased the fluidity of brain cell membrane. After adding Chuanxiongqin hydrochloride, there were no obvious differences between the model group [0.688 5±0.030 5; (7.886±0.341)×10-10 s/circle] and control group (P > 0.05), indicating that Chuanxiongqin hydrochloride could recover the fluidity of brain cell membrane after ischemia/reperfusion injury close to the level in the normal control group. Chuanxiongqin hydrochloride could directly scavenge the O2 · and OH· free radicals, and the maximal clearance rates were 83.92% and 44.99% respectively. CONCLUSION: Chuanxiongqin hydrochloride increases the fluidity of membrane of ischemia-injured brain cell by scavenging both O2 ·and OH· free radicals.

Effects of NG-nitro-L-arginine on focal cerebral ischemic injury in rats

BACKGROUND： Previous researches have proved that aminoguanidin can cure cerebral ischemic injury remarkably as a selective induced nitricoxide synthase （iNOS） inhibitor. However, whether nonselective NOS inhibitor could protect cerebral ischemic injury or not is unclear. OBJECTIVE： To investigate the effects of NG-nitro-L-arginine （L-NA）, a nonselective nitricoxide synthase （NOS） inhibitor, on cerebral ischemic injury of rats and the possible mechanism.DESIGN： Randomized controlled study.SETTING ： Pharmacological Department of Medical Academy of Science of Hebei Province.MATERIALS： A total of 56 male healthy SD rats, of grade Ⅱ, weighting 250-290 g, were provided by the Experimental Animal Center of Hebei Province （certification： 04036）. METHODS： The experiment was completed in the Pharmacological Department of Medical Academy of Science of Hebei Province from March 2005 to January 2006.① Grouping： Rats were randomly divided into 3 groups： sham operation group （n=8）, model group （n=24） and L-NA group （n=24）.② Modeling： Middle cerebral artery （MCA） was established on rats in model group and L-NA group with intreluminal line occlusion methods, and rats in sham operation group were separated their external carotid arteries without occlusion of internal carotid artery. ③ Intervention study： Rats in model group and L-NA group were injected intreperitoneally with 10 mL/kg and 20 mg/kg L-NA at 2, 6 and 12 hours respectively after ischemia twice a day for 3 consecutive days. ④ Rats were sacrificed on the third day for measuring volume of cerebral infarction with image analysis and swelling degrees and activities of mitochondria with electron microscope. Effect of L-NA on ultrastructural changes of neurons in cortex was observed after ischemia. MAIN OUTCOME MEASURES：① Volume of cerebral infarction; ②Swelling degrees, contents of nitric oxide （NO） and malondialdehyde （MDA） and activities of adenosine triphosphatase （ATPase）, superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） in mitochondria;③ Ultrastructural changes of mitochondria in brain tissue after cerebral ischemia. RESULTS： ① At 12 hour after ischemia, volume of cerebral infarction in L-NA group was lower than that in model group （P 〈 0.01）. ② Content of NO in mitochondria in L-NA group was decreased as compared with that in model group at 2, 6 and 12 hours after ischemia （P 〈 0.05）; swelling degree of mitochondria in brain tissue was relieved in L-NA group at 12 hour after ischemia, and content of MDA was decreased （P 〈 0.05）; mitochondrial activity in L-NA group was increased at 12 hour after ischemia, and activities of ATPase, SOD and GSH-Px in mitochondria were increased （P 〈 0.05）.③ Degrees of mitochondrial injury in brain tissue were relieved in L-NA group at 12 hour after ischemia as compared with those in model group and L-NA group at 2 and 6 hours after ischemia. CONCLUSION ： ①L-NA can beneficially inhibit NO production, but not protect brain against damage in ischemia acute stage. ②L-NA might have protective effects on cerebral injury through inhibiting the production of oxygen free radical, increasing antioxidation, ameliorating energy metabolism, beneficially improving the integrity of form and function of mitochondria in brain tissue during postischemia in rats.

Influence of rotating magnetic field on cerebral infarction volume, cerebral edema and free radicals metabolism after cerebral ischemia/reperfusion injury in rats

BACKGROUND: It has shown that magnetic field can improve blood circulation, decrease blood viscosity, inhibit free radicals, affect Ca2+ flow in nerve cells, control inflammatory and immunological reaction, and accelerate nerve cell regeneration. In addition, protective effect of magnetic field, which acts as an iatrophysics, on ischemic brain tissues has been understood gradually. OBJECTIVE: To investigate the effects of rotating magnetic field (RMF) on volume of cerebral infarction, cerebral edema and metabolism of free radicals in rats after cerebral ischemia/reperfusion injury. DESIGN: Randomized controlled animal study. SETTING: Rehabilitation Center of disabled children, Liaoniang; Department of Rehabilitation, the Second Affiliated Hospital, China Medical University; Department of Rehabilitation Physiotherapy, the First Affiliated Hospital, China Medical University. MATERIALS: A total of 70 healthy Wistar rats aged 18-20 weeks of both genders were selected and randomly divided into 3 groups: sham operation group with 12 rats, control group with 20 rats and treatment group with 38 rats. The treatment group included 4 time points: immediate reperfusion with 6 ones, 6-hour reperfusion with 20 ones, 12-hour reperfusion with 6 ones and 18-hour reperfusion with 6 rats. Main instruments were detailed as follows: magnetic head of rotating magnetic device was 6 cm in diameter; magnetic induction intensity at the surface of magnetic head was 0.25 T in silence; the maximal magnetic induction intensity was 0.09 T at the phase of rotation; the average rotating speed was 2500 r per minute. METHODS: The experiment was carried out in the China Medical University in March 2003. Focal cerebral ischemic animal models were established with modified Longa’s method. Operation was the same in the sham operation, but the thread was inserted as 10 mm. Neurologic impairment was assessed with 5-rating method to screen out cases. Those survivals with grade 1 and grade 2 after ischemia for 2 hours and reperfusion for 24 hours were included in the control group and treatment group. Those in the sham operation group and control group were not treated with RMF. Magnetic head was directed towards the head of rats of the treatment group, and the magnetic head was about 7 mm from skin, treated for 15 minutes. The rats were decapitated to take out brains at 24 hours after reperfusion in each group. Water content of brain and volume of cerebral infarction were assessed with wet-dry weight method and TTC staining, respectively. Activity of superoxide dismutase (SOD), content of malondialdehyde (MDA) and change of brain histomorphology in brain tissue of ischemic side were analyzed. MAIN OUTCOME MEASURES: ① Volume of cerebral infarction and changes of water content in brain; ② measurements of SOD and MDA contents in brain tissue of rats in all groups. RESULTS: A total of 70 qualified animals were involved in the final analysis after rejecting the death and unqualified animal models. ① Water content of brain: Water content of brain in the treatment was less than that in the control group at any time point except the immediate time point, and cerebral edema was relieved [(2.48±0.22)%, (2.32±0.19)%, (2.23±0.36)%, (2.91±0.44)%, P < 0.05]. In addition, there were no significant differences among 6-hour, 12-hour and 18-hour reperfusion groups (P > 0.05). ② Volume of cerebral infarction: The absolute volume of cerebral infarction in the treatment group was smaller than that in the control group [(128.21±15.05), (171.22±40.50) mm3, t =2.438, P < 0.05], and the relative volume of cerebral infarction was smaller than that in the control group [(20.22±1.44)%, (25.17±3.85)%, t =2.95, P < 0.05]. ③ Contents of SOD and MDA in brain tissues: Compared with the control group, the SOD content in the brain tissue in the treatment group increased [(54.54±3.85), (69.52±5.88) kNU/g, t =5.568, P < 0.05], while the MDA content decreased [(0.85±0.06), (1.03±0.09) μmol/g, t =4.076, P < 0.05]. ④ General morphological observation: General morphology manifested that the edema was distinct in the right cerebral hemisphere in the control group, showing fat-like white, shallow anfractuosity, flat gyria, brittle tissue and easy to break up. The edema of right cerebral hemisphere was light and surface was hyperaemia in the treatment group. CONCLUSION: RMF may improve anti-oxidative ability of brain tissue of rats with acute focal cerebral ischemia/reperfusion injury and reduce volume of cerebral infarction and degrees of cerebral edema.

Protective effect of sodium valproate on motor neurons in the spinal cord following sciatic nerve injury in rats

BACKGROUND: Sodium valproate (VPA) is used to be an effective anti-epileptic drug. VPA possesses the characteristics of penetrating rapidly through the blood-brain barrier (BBB) and increasing levels of Bcl-2 and growth cone-associated protein (GAP) 43 in spinal cord. OBJECTIVE: To observe the effect of VPA on Bcl-2 expression and motor neuronal apoptosis in spinal cord of rats following sciatic nerve transection. DESIGN: Randomized controlled experiment. SETTING: Department of Hand Surgery and Microsurgery, Wuhan Puai Hospital. MATERIALS: A total of 30 male healthy SD rats of clean grade and with the body mass of 180-220 g were provided by Experimental Animal Center of Medical College of Wuhan University. Sodium Valproate Tablets were purchases from Hengrui Pharmaceutical Factory, Jiangsu. METHODS: The experiment was performed in the Central Laboratory of Wuhan Puai Hospital and Medical College of Wuhan University from February to May 2006. Totally 30 rats were randomly divided into two groups: treatment group (n =15) and model group (n =15). Longitudinal incision along backside of right hind limbs of rats was made to expose sciatic nerves, which were sharply transected 1 cm distal to the inferior margin of piriform muscle after nerve liberation under operation microscope to establish sciatic nerve injury rat models. Sodium Valproate Tablets were pulverized and diluted into 50 g/L suspension with saline. On the day of operation, the rats in the treatment group received 6 mL/kg VPA suspension by gastric perfusion, once a day, whereas model group received 10 mL/kg saline by gastric perfusion, once a day. L4-6 spinal cords were obtained at days 1, 4, 7, 14 and 28 after operation, respectively. Terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) technique and immunohistochemical method (SP method) were used to detect absorbance (A) of neurons with positive Bcl-2 expression. Apoptotic rate of cells (number of apoptotic cells/total number of cells×100%) was calculated. MAIN OUTCOME MEASURES: A value of neurons with positive Bcl-2 expression and apoptotic rate in spinal cord of rats in the two groups. RESULTS: A total of 30 SD rats were involved in the result analysis. ①expression of positive Bcl-2 neurons: A value of positive Bcl-2 neurons were 0.71±0.02, 0.86±0.04, 1.02±0.06 at days 4, 7 and 14, respectively after operation in the treatment group, which were obviously higher than those in the model group (0.62±0.03, 0.71±0.05, 0.89±0.04, t = 3.10-4.50, P < 0.05). ②apoptotic result of motor neurons: Apoptotic rate of motor neurons in spinal cord was (6.91±0.89)% and (15.12±2.34)% at days 7 and 14 in the treatment group, which was significantly lower than those in the model group [(9.45±1.61)%, (19.35±0.92)%, t = 2.39, 3.03. P < 0.05]. CONCLUSION: VPA can increase expression of Bcl-2 in spinal cord and reduce neuronal apoptosis in rats following sciatic nerve injury, and has protective effect on motor neuron in spinal cord of rats.

Changes of norepinephrine and tumor necrosis factor in submandibular gland of rats with sympathetic nerve injury and the protective effect of 17 beta-estradiol

BACKGROUND： Recent researches have indicated that estrogen has extensive neuroprotective effects. So some studies designed ovariectomized animal models and administrated with estrogen, so as to verify its neuroprotective effects. OBJECTIVE： To observe the effect of 17 beta-estradiol on the content of norepinephrine （NE） and level of tumor necrosis factor （TNF） in submandibular glands of rats with sympathetic nerve injury, and analyze the dose-dependence and pathway of action. DESIGN： A randomized control animal study SETTINGS： Department of Hand Surgery, the 252 Hospital of Chinese PLA; Department of Hand Surgery Union Hospital affiliated to Tongji Medical College, Huazhong University of Science and Technology. MATERIALS： Fifty healthy female Wistar rats were randomly divided into 5 groups with 10 rats in each group： sham-operated group, ovariectomy＋6-OHDA＋saline group, ovariectomy＋6-OHDA＋17β-estradiol 50, 200 and 500 μg/kg groups. METHODS： The experiments were carried out in Tongji Medical College, Huazhong University of Science and Technology between October 2005 and March 2006. Bilateral ovaries were only exposed but not resected for the rats in the sham-operated group, but bilateral ovaries were resected in all the other groups. In the ovariectomy＋6-OHDA＋176-estradiol 50, 200 and 500 μg/kg groups, the rats were administrated with intraperitoneal injection of 6-OHDA （8 mg/kg）, and then immediately given 176-estradiol of corresponding dosages respectively, once a day for 10 days continuously. Rats in the sham-operated group and ovariectomy＋6-OHDA＋saline group were administrated with saline of the same volume. After administration, 5 rats in each group were killed to determine the NE contents in bilateral submandibular glands with high performance liquid chromatography-electrochemical detector （HPLC-ECD）, and the other 5 rats were used to determine the TNF levels in submandibular glands with enzyme-linked immunosorbant assay. MAIN OUTCOME MEASURES： The NE contents and TNF levels in submandibular glands of rats in each group were observed. RESULTS： All the 50 rats were involved in the analysis of results. （1） The NE content was obviously lower in the ovariectomy＋6-OHDA＋saline group than in the sham-operated group [（1 035±196）, （1 823±314） ng/g, P 〈 0.05], there were no significant differences between the ovariectomy＋6-OHDA＋17β-estradiol 50 μg/kg group and ovariectomy＋6-OHDA＋saline group [（1 004±253）, （1 035±196） ng/g, P 〉 0.05], but obviously higher in the ovariectomy＋6-OHDA＋17β-estradiol 200 and 500 μg/kg groups than in the ovariectomy＋6-OHDA＋saline group [（1 487±268）, （1 939±274）, （1 035±196） ng/g, P 〈 0.05]. （2） The TNF level was obviously higher in the ovariectomy＋6-OHDA＋saline group than in the sham-operated group [（3.498±0.792）, （1.893±0.533） ng/g, P 〈 0.05], there were no significant differences between the ovariectomy＋ 6-OHDA＋17β-estradiol 50 μg/kg group and ovariectomy＋6-OHDA＋saline group [（3.328 ±0.712）, （3.498±0,792） ng/g, P 〉 0.05], but obviously lower in the ovariectomy＋6-OHDA＋17β-estradiol 200 and 500 μg/kg groups than in the ovariectomy＋6-OHDA＋saline group [（2.639±0.438）, （2.016±0.619）, （3.498＋0.792） ng/g, P 〈 0.05]. CONCLUSION： Estrogen has obvious protective effect dose-dependently on 6-OHDA induced chemical sympathetic nerve terminal injury in rats, and it may play its protective role by reducing TNF level and ameliorating inflammatory reaction.

Protective effect of ultrashortwave versus radix salviae miltiorrhizae on brains of rats with cerebral ischemia-reperfusion injury

BACKGROUND： HOW to control the effect of oxygen-derived free radicals on development of cerebral injury and cerebral edema is a key factor for treating cerebral ischemia-reperfusion injury. OBJECTIVE： To observe and compare the protective effects, synergistic action and mechanisms of ultrashortwave （USW） and radix salviae miltiorrhizae （RSM） on the focal cerebral ischemia-reperfusion injuries in rats. DESIGN： Randomized controlled animal study SEI-FING： Department of Rehabilitation Medicine, First Hospital affiliated to China Medical University MATERIALS： A total of 160 healthy Wistar rats of both genders and aged 18-20 weeks weighing 250-300 g of clean grade were selected in this study. 5 mL/ampoule RSM injection fluid was produced by the First Pharmaceutical Corporation of Shanghai （batch number： 011019, 0.01 mug）. The USW therapeutic device was produced by Shanghai Electronic Device Factory with the frequency of 40.68 MHz and the maximal export power of 40 W. The first channel of power after modulation was 11 W. METHODS： The experiment was carried out in the Rehabilitation Medicine Department of the First Hospital affiliated to China Medical University from May 2002 to January 2003. Focal ischemia-reperfusion model was established in rats by reversible right middle cerebral artery occlusion with filament. Right cerebral ischemia was for 2 hours and then with 24 hours reperfusion. The scores of neurological deficits were evaluated by 0 to 4 scales. After surgery, 64 successful rats models were divided into four groups according to digital table： control group, USW group, RSM group and RSM ＋ USW group with 16 cases in each group. Rats in control group were intraperitoneally injected with the same volume of saline （0.1 mL/g）; rats in USW group were given small dosage of USW on head for 10 minutes at 6 hours after reperfusion; rats in RSM group were intraperitoneally injected with 0.01 mL/g RSM solution at 30 minutes before reperfusion; rats in RSM ＋ USW group were intraperitoneally injected with 0.01 mL/g RSM parenteral solution at 30 minutes before reperfusion and given small dosage of USW on head for 10 minutes once at 6 hours after reperfusion; sixteen rats in sham operation group did not receive any treatment. All 80 rats were taken brains at 24 hours after reperfusion to measure wet and dry weights to calculate water content： Cerebral water content （%） = （1-dry/wet weight） × 100%. Superoxide dismutase （SOD） activity was measured by hydroxylamine method and malondialdehyde （MDA） content was measured by TBA photometric method. MAIN OUTCOME MEASURES ： Cerebral water content, SOD activity and MDA content RESULTS： All 160 rats except 80 failing in modeling were involved in the final analysis. （① The cerebral water content of left hemisphere made no significant difference （P 〉 0.05）. The cerebral water content of right hemisphere in the control group and the three treatment groups was obviously higher than that of the sham operation group [（81.26±0.77）%, （79.74±0.68）%, （79.76±0.81）%, （79.61±0.79）%, （77.43±0.61）%, P 〈 0.05]. The cerebral water content of right hemisphere in the three treatment groups was obviously lower than that of the control group （P〈 0.05）. There was no significant difference among the three treatment groups （P 〉 0.05）. ② Compared with the control group, SOD activity （right） of the control group decreased obviously （P 〈 0.05）, while MDA content increased obviously （P 〈 0.05）. SOD activity in the three therapeutic groups increased obviously, while MDA content decreased obviously （P 〈 0.05）; there was no significant difference among the three treatment groups （P 〉 0.05）. CONCLUSION： ① USW and RSM therapy have neuroprotective effects against focal cerebral ischemia-reperfusion injuries by means of decreasing cerebral water content and MDA and increasing the activity of SOD. ② Synergistic action was not observed between these two therapeutic methods.

Effect of ketamine on aquaporin-4 expression and neuronal apoptosis in brain tissues following brain injury in rats

BACKGROUND： Aquaporin-4 （AQP-4） is closely related to the formation of brain edema. Neuronal apoptosis plays an important part in the conversion of swelled neuron following traumatic brain injury. At present, the studies on the protective effect of ketamine on brain have involved in its effect on aquaporin-4 expression and neuronal apoptosis in the brain tissues following brain injury in rats. OBJECTIVE： To observe the effect of ketamine on AQP-4 expression and neuronal apoptosis in the brain tissue following rat brain injury, and analyze the time-dependence of ketamine in the treatment of brain injury.DESIGN： Randomized grouping design, controlled animal tria SETTING ： Department of Anesthesiology, the Medical School Hospital of Qingdao University MATERIALS： Totally 150 rats of clean grade, aged 3 months, were involved and randomized into control group and ketamine-treated group, with 75 rats in each. Each group was divided into 5 subgroups separately at 6,12, 24, 48 and 72 hours after injury, with 15 rats at each time point. Main instruments and reagents： homemade beat machine, ketamine hydrochloride （Hengrui Pharmaceutical Factory, Jiangsu）, rabbit anti-rat AQP-4 polyclonal antibody, SABC immunohistochemical reagent kit and TUNEL reagent kit （Boster Co.,Ltd., Wuhan）. METHODS： This trial was carried out in the Institute of Cerebrovascular Disease, Medical College of Qingdao University during March 2005 to February 2006. A weight-dropping rat model of brain injury was created with Feeney method. The rats in the ketamine-treated group were intraperitoneally administered with 50 g/L ketamine （120 mg/kg） one hour after injury, but ketamine was replaced by normal saline in the control group. In each subgroup, the water content of cerebral hemisphere was measured in 5 rats chosen randomly. The left 10 rats in each subgroup were transcardiacally perfused with ketamine, then the brain tissue was made into paraffin sections and stained by haematoxylin and eosin. Neuronal morphology was observed. AQP-4 expression and neuronal apoptosis were measured with immunohistochemical method and TUNEL method respectively. MAIN OUTCOME MEASURES： Water content in brain tissue, neuronal morphology, the number of AQP-4 positive neurons and TUNEL positive neurons in rats of two groups at each time point after injury. RESULTS： Totally 150 rats entered the stage of result analysis. （1） Water content of brain tissue： The water content of brain tissue at each time point after injury in the ketamine-treated group was lower than that in the control group. There were very significant differences in water content at 12 and 24 hours after injury respectively between ketamine-treated group and control group [（77.34±2.35）% vs. （82.31 ±1.48）%; （78.01 ±2.21 ）% vs. （83.86±2.37）%, t=-4.001 6,4.036 7, both P 〈 0.01]. （2） Neuronal morphology： Pathological changes in traumatic region and peripheral region of injury in the ketamine-treated group were significantly lessened, and necrotic and apoptotic cells in the ketamine-treated group were also significantly reduced as compared with control group. （3） AQP-4 expression： AQP-4 positive neurons at each time point in the ketamine-treated group were significantly less than those in the control group. There were very significant differences in AQP-4 expression at 12 and 24 hours after injury between ketamine-treated group and control group [（34.17±4.74） /visual field vs. （43.42±5.65） /visual field;（40.83±3.17） /visual field vs. （58.88±6.23） /visual field,t=3.966 3,8.165 7, both P〈 0.01]. （4） Neuronal apoptosis： TUNEL positive neurons at each time point in the ketamine-treated group were less than those in the control group. There were very significant differences in the neuronal apoptosis at 12 and 24 hours after injury between ketamine-treated group and control group [（26.25±3.04） /visual field vs. （32.75±4.39） /visual field; （29.33± 4.02） /visual field vs. （39.83±5.61） /visual field,t=-3.849 3,5.169 2,both P 〈 0.01]. CONCLUSION： Ketamine can reduce brain edema, AQP-4 expression and neuronal apoptosis following brain injury in rats, and has obvious therapeutic effect on brain injury, especially at 12 and 24 hours after injury.

Comparison of the severity of injury of hippocampal neuron in rats induced by simulated push-pull maneuver at various degrees

BACKGROUND： Push-pull effect is often caused during maneuver, and the changes of unconsciousness induced can affect or damage cerebral neurons at various degrees. OBJECTIVE： To observe the effect of simulated push-pull maneuver at various degrees on injury of hippocampal neurons in rats and analyze its phase effect. DESIGN： Randomized control study.SETTING ： Physiological Department of Jilin Medical College.MATERIALS： A total of 40 healthy male Wistar rats, of clean grade, weighting 205-300 g, aged 3-4 months, were randomly divided into control group （n=4） and three push-pull experimental groups, including ＋2 Gz group （intensity： -2 Gz to ＋2 Gz, n=12）, ＋6 Gz group （-6 Gz to ＋6 Gz, n=12） and ＋8 Gz group （-8 Gz to ＋8 Gz, n=12）.METHODS： The experiment was completed in the Physiological Department of Jilin Military Medical College from March 2002 to May 2003. ① Rats in the experimental groups were put at the specially rolling arm of animal centrifugal machine. Then, they were pushed and pulled with ±2 Gz, ±6 Gz and ±8 Gz, respectively. The jolt was 1 Gz/s. However, rats in control group were not treated with any ways. ② Stroke index and neurological evaluation were performed on rats in the experimental groups at 0.5, 6 and 24 hours after push-pull. Stroke index was 25 points in total. The higher the scores were, the severer the cerebral injury was. Neurological evaluation was 10 points in total. The higher the scores were, the severer the nerve injury was. ③ Hippocampal tissue in brain of rats were selected to cut into sections at each time points, and form and distribution of neurons were observed in hippocampal areas with HE staining. Degrees of neuronal injury in hippocampal CA1 area were assayed after push-pull at various degrees with electron microscope. ④ Measurement data were compared with t test.MAIN OUTCOME MEASURES：① Stroke index and neurological evaluation; ② form and distribution of neurons in hippocampal areas;③ degrees of neuronal injury in hippocampal CA1 area.RESULTS： A total of 40 rats were involved in the final analysis. ① Stroke index and neurological evaluation of rats in experimental groups： At 30 minutes and 6 hours after push-pull exposure, stroke index and neurological evaluation were higher in ±6Gz group and ±8 Gz group than those in control group （P 〈 0.01）, especially at 6 hours after push-pull exposure, those in ±8 Gz group were the highest at each time points [（11.00±2.16）, （5.75±1.70） points]. At 24 hours after exposure, those were decreased as compared with those within the former two time points, but the values were still higher than those in control group （P 〈 0.05-0.01）. ② Results of HE staining： At 6 and 24 hours after exposure, partially neuronal degeneration was observed in pyramidal layer in ±6 Gz group and ±8 Gz group, including crenation of neurons, tdangle or polygon, and karyopycnosis, especially the injury in ±8 Gz group was the most obvious at 6 hours after exposure. ③ Results of ultrastructure with electron microscope： Partially neuronal degeneration at various degrees was observed in hippocampal CA1 area in ±2 Gz group at 6 hours after exposure and in ±6 Gz group and ±8 Gz group at 6 and 24 hours after exposure. At 6 hours after exposure, nucleus of hippocampal neurons in ±8 Gz group was irregular and umbilication. Caryotin was aggregated, nuclear matrix was swelled and disorder, and vacuolation was also observed. Rough endoplasmic reticulum was expanded, mitochondrium was swelled, and crista was disappeared.CONCLUSION： ① Push-pull cannot damage hippocampal neurons of rats in ±2 Gz group. ② Exposure can cause injury of hippocampal neurons of rats in ±6Gz group and ±8 Gz group, especially the injury is the severest at 6 hours after exposure in ±8 Gz group and relieves gradually 24 hours later.

Evaluation of the effect of hydrogen sulfide postconditioning by p-v loop against myocardial i/r injury in rats

Objectives To evaluate the effect of hydrogen sulfide(H2S) postconditioning on myocardial ischemia-reperfusion (I/R) by pressure-volume loop(P-V loop). Methods The I/R model of rat in vivo was established by ligating the left anterior descending coronary artery for 30min and reperfusing for 120 min.Wistar rats(n=32) were ran- domly divided into 4 groups;Sham operation,ischemia-reperfusion (I/R),Ischemic postconditioning(IPO) and H2S postconditioning.In sham operation,there was no ligation.In IPO,at the start of reperfusion,three cycles of 30s reperfusion and 30s LAD reocclusion preceded the 3h of reperfusion. In H2S postconditioning,NaHS(15μmol/kg,Sodium hydrosulfide)was administrated before coronary artery reperfusion. The heart rate(HR),I/R arrhythmia,the left ventricular end-systolic pressure(LVESP),left ventricular enddiastolic pressure(LVEDP),the slope of the end- systolic P-V relation(ESPVR) and the slope of the end-diastolic P-V relation(EDPVR) were detected.Infarct size was determined by scanning the images of the rat heart ventricular sections stained with Evans blue and TTC.Results Compared with I/R group,the I/R arrhythmia and the infarct size were decreased significantly(PPP2S postconditioning group.Conclusions Myocardial I/R injury was decreased by H2S post-conditioning, and it was sensitive and accurate to evaluate the heart function by P-V loop.

Effect of FTY720 on RhoA expression after acute spinal cord injury in rats

Objective To investigate the effect of fingolimod (FTY720)on RhoA expression after spinal cord injury (SCI)in rats,and explore the possible mechanism of FTY720in the treatment of SCI.Methods A rat model of acute SCI was established with a

Brain-derived neurotrophical factor after olfactory ensheathing cells transplantation in spinal cord injury of rats

Objective To observe the expression of brain - derived neurotrophical factor ( BDNF) in injury spinal cord after transplantation olfactory ensheathing cells ( OECs) , and to investigate the mechanism of OECs repairing spinal cord injury. Methods OECs from GFP transgenic rats were separated and cultured for transplantation. Spinal cord injury rats were separated two groups by

Expression of bradykinin as a substrate of CD26 /DPP IV in rats ischemia/reperfusion injury following lung transplantation

Objective To investigate the expression of bradykinin as a substrate of CD26 /DPP IV in rats with ischemia/reperfusion injury following lung transplantation ( LTx) . Methods Thirty - six syngeneic male SD rats were randomly allocated into control group and experimental group ( n = 18 each) ,and 36 rats served as do-

Improvement of neurological function in rats with spinal cord injury after the transplantation of neural stem cells directly differentiated from bone marrow mesenchymal stem cells

Objective To study the effect and mechanism of neurological function recovery in rats with spinal cord injury ( SCI) rats after transplantation of neural stem cells which are directly differentiated from bone marrow mesenchymal stem cells ( BMSC ) ,and to investigate the suitable engraftment time. Methods BMSC at 3rd passage were differentiated into neural stem cells ( NSC) , and immunofluorescence staining was used to

Effects of low dose Glibenclamide on secondary damage after acute spinal cord injury in rats

Objective To investigate the effects of Glibenclamide on reduction of secondary damage after acute spinal cord injury in rats.Methods Ninety rats were randomly divided into control group(laminectomy alone),spinal cord injury group(injury group),and treatment group(treated

Effect and mechanism of adrenomedullin on apoptosis of renal tubular epithelial cell in rats induced by renal ischemia reperfusion injury

Objective To investigate the effect and mechanism of adrenomedullin ( AM ) on apoptosis of renal tubular epithelial cell in rats induced by renal ischemia reperfusion injury. Methods Thirty-two Wistar rats were randomly divided into 4 groups: control group,IRI group, empty plasmid group and AM group. One week after re-

Expression of transforming growth factor-β in local bony callus in traumatic brain injury combined with extremity fracture in rats

Objective To investigate gene expression of transforming growth factor-β(TGF-β)in local bony callus in tracumatic brain in jury combined with extremity long bone fracture in rats.Methods Eighty male SD rats were randomized into 2 even

Biological characteristics of dynamic expression of nerve regeneration related growth factors in dorsal root ganglia after peripheral nerve injury

The regenerative capacity of peripheral nerves is limited after nerve injury.A number of growth factors modulate many cellular behaviors,such as proliferation and migration,and may contribute to nerve repair and regeneration.Our previous study observed the dynamic changes of genes in L4–6 dorsal root ganglion after rat sciatic nerve crush using transcriptome sequencing.Our current study focused on upstream growth factors and found that a total of 19 upstream growth factors were dysregulated in dorsal root ganglions at 3,9 hours,1,4,or 7 days after nerve crush,compared with the 0 hour control.Thirty-six rat models of sciatic nerve crush injury were prepared as described previously.Then,they were divided into six groups to measure the expression changes of representative genes at 0,3,9 hours,1,4 or 7 days post crush.Our current study measured the expression levels of representative upstream growth factors,including nerve growth factor,brain-derived neurotrophic factor,fibroblast growth factor 2 and amphiregulin genes,and explored critical signaling pathways and biological process through bioinformatic analysis.Our data revealed that many of these dysregulated upstream growth factors,including nerve growth factor,brain-derived neurotrophic factor,fibroblast growth factor 2 and amphiregulin,participated in tissue remodeling and axon growth-related biological processes Therefore,the experiment described the expression pattern of upstream growth factors in the dorsal root ganglia after peripheral nerve injury.Bioinformatic analysis revealed growth factors that may promote repair and regeneration of damaged peripheral nerves.All animal surgery procedures were performed in accordance with Institutional Animal Care Guidelines of Nantong University and ethically approved by the Administration Committee of Experimental Animals,China(approval No.20170302-017)on March 2,2017.