Effects of Vitamin E and Selenium on Free Radicals Metabolism of Broilers

To study effects of vitamin E （VE） and selenium （Se） on dynamic variation rules, functions and metabolisms of different free radicals, 2 weeks age chicks were reared using four kinds of dietaries that differed in their VE and Se content. Free radicals in blood and tissues of broiler chicks were detected directly or indirectly using electron spin resonance （ESR） testing and biology chemistry methods. Results showed that NO free radical contents were decreasing due to the increasing of VE supplement in dietary and VE level was negatively correlated with NO free radicals. High Se supplement dietaries had the trend to induce the produce of NO free radicals. High VE and Se level dietaries significantly enhanced activities of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） in serum and liver. Depending on time, SOD and GSH-Px activities were declining and increasing respectively, which indicated that being short of VE and/or Se in dietaries could link to the produce of O-2, H2O2 free radicals. With the deficiency lasting, organism would continuously produce large amounts of O-2 free radicals but H2O2 free radicals were just produced explosively at the beginning of deficiency and than tended to be steady. Low VE and/or Se levels in dietaries could remarkably enhance malondialdehyde（MDA）contents in tissues and the effect of low Se was stronger. VE and Se in dietary had synergic effect on metabolisms of NO, O-2 and H2O2 free radicals.

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.

Correlation of OPG/RANKL expression in gingival crevicular fluid with inflammatory factors, free radical generation and bone metabolism in patients with diabetes mellitus complicated by periodontitis

Objective:To study the correlation of OPG/RANKL expression in gingival crevicular fluid with inflammatory factors, free radical generation and bone metabolism in patients with diabetes mellitus complicated by periodontitis.Methods:Patients with diabetes mellitus complicated by periodontitis who were treated in Xi'an No. 4 Hospital between March 2015 and May 2017 were selected as the periodontitis group for the research, and healthy volunteers who underwent periodontal examination during the same period were selected as the control group. The gingival crevicular fluid was collected to determine the expression of OPG/RANKL, the contents of inflammatory factors and bone metabolism molecules as well as the generation of free radicals.Results: OPG protein expression, OPG/RANKL expression ratio as well as ICTP and Runx2 contents in gingival crevicular fluid of periodontitis group were significantly lower than those of control group whereas RANKL protein expression, TNF-α, IL-1β, IL-17, HMGB1, DKK1 and MMP1 contents as well as ROS, MDA and 8-OHdG generation were significantly higher than those of control group;OPG/RANKL expression ratio in gingival crevicular fluid of periodontitis group was negatively correlated with TNF- , IL-1β, IL-17, HMGB1, DKK1 and MMP1 contents as well as ROS, MDA and 8-OHdG generation, and positively correlated with ICTP and Runx2 contents.Conclusion: The excessive activation of inflammation and oxidative stress in periodontal tissue of patients with diabetes mellitus complicated by periodontitis can cause OPG/RANKL expression disorder and then lead to bone metabolism disorder.

Studies on the Free Radicals and Thyroid Hormone Metabolism in Cattle with Iodine and Selenium Deficicncy

In order to interpret pathologic mechanism of free radicals and thyroid hormone metabolism in cattle iodine and selenium deficiency, 20 heads of yellow cattle were selected from NiuJia town, Wu Chang City, Heilongjiang Province, China, and were randomly devided into 4 groups with 5 for each. ① supplemented with 0.7 mg·kg -1 iodine(potassium iodine), ② supplemented with 0.2 mg·kg -1 selenium (sodium selenite), ③ supplemented with 0.7 mg·kg -1 iodine(potassium Iodine) plus 0.2 mg·kg -1 selenium (sodium selenite) per day for 30 days, respectively. ④control group. The whole blood glutathione peroxidase (GSH-px) and catalase (CAT) activities, free radicals (FR) concentration, erythrocyte superoxide dismutase (SOD) activity and molonaldehyde (MDA) concentration, the serum triiodothyronine (T 3)、thyroxine (T 4) and thyrotropin (TSH) were determined on the day of supplementation day-0 and day-30, respectively. It was showed that average iodine concentration in drinking water and diet were 3.82 μg·L -1 and 0.285mg·kg -1 , respectively, Diet selenium was 0.0498mg·kg -1 , Serum protein bound iodine(PBI) was 7.02 μg·100 mL, Blood selenium was 0.14 mg·L -1 , the schoolchildren′s goiter was 21.8%. It indicated that iodine and selenium were deficient in the investigated area. Whole blood GSH-px and CAT activities and serum T 3 concentration were significantly higher (P< 0.01 ), FR concentration and serum TSH were significantly lower(P<0.01) in the first three groups than that of the control, T 4 content in the first group was higher(P<0.05), T 4 was also higher (P>0.05) in the second group. and lower in the third group. The SOD and MDA in erythrocyte were not changed during the experimental period, The results also showed that GSH-px and CAT activities were increased, and FR decreased oberviously in the third group more than the other two groups, In addition, Thyroid hormone metabolism was more coincided with the physiologic status in the third group. the iodine and the selenium played an important role in the pathologic process of free radical metabolic disorder. selenium not only had the function of antioxidation by derectly scavenging free radicals, but also affected through GSH-px and CAT activities. iodine deficiency results in the Goiter, selenium deficiency aggravated iodine deficiency, Iodine and the selenium were dependent and restrained each other in the course of free radicals and thyroid hormone metabolism with a synergistic state.

Lipophilic Enhance of Vitamin C Protective Activity Against Free-radical-induced Damage in vivo

A group of experimental rats under free radical damage are given various amounts of a lipophilic vitamin C(ascorbyl-6-laurate, VC-12), and its parent compound, vitamin C, respectively. It has been found that the effects of 1 12 mmol/kg VC-12 on decreasing triglyceride(TG), total cholesterol(TC), low density lipoprotein cholesterol (LDL-c) and lipid peroxide(LPO), and increasing high density lipoprotein cholesterol(HDL-c) and superoxide dismutase(SOD) are similar to those of 2 27 mmol/kg vitamin C. In addition, VC-12(1 12 mmol/kg) can increase the prostacycline(PGI 2) and decrease the thromboxane(TXA 2) even better than vitamin C(2 27 mmol/kg). The above facts demonstrate that the antioxidative activity of VC-12 is higher than twice that of vitamin C. So, ascorbyl-6-laurate may be a novel antioxidant drug against free radical damage.

Free radicals in development of experimental gastric carcinoma and precan cerous lesions in ducedby N-methyl-N'-nitro-N-nitrosoguanidine in rats

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Oxidative stress disturbs energy metabolism of mitochondria in ethanol-induced gastric mucosa injury

AIM: To study the role of mitochondrial energy disorder in the pathogenesis of ethanol-induced gastric mucosa injury. METHODS: Wistar rats were used in this study. A gastric mucosal injury model was established by giving the rats alcohol. Gross and microscopic appearance of gastric mucosa and ultrastructure of mitochondria were evaluated. Malondiadehyde (MDA) in gastric mucosa was measured with thiobarbituric acid. Expression of ATP synthase (ATPase) subunits 6 and 8 in mitochondrial DNA (mtDNA) was determined by reverse transcription polymerase chain reaction (RT- PCR). RESULTS:The gastric mucosal lesion index was correlated with the MDA content in gastric mucosa. As the concentration of ethanol was elevated and theexposure time to ethanol was extended, the content of MDA in gastric mucosa increased and the extent of damage aggravated. The ultrastructure of mitochondria was positively related to the ethanol concentration and exposure time. The expression of mtDNA ATPase subunits 6 and 8 mRNA declined with the increasing MDA content in gastric mucosa after gavage with ethanol. CONCLUSION: Ethanol-induced gastric mucosa injury is related to oxidative stress, which disturbs energy metabolism of mitochondria and plays a critical role in the pathogenesis of ethanol-induced gastric mucosa injury.

西洋参叶20s-原人参二醇组皂苷抗实验性心肌缺血作用及其机制

目的 研究西洋参叶 2 0s 原人参二醇组皂苷 (Panaxquinquefolium12 0s protopanaxdiolsaponins,PQDS)的抗实验性心肌缺血作用及其机制。方法 通过大鼠结扎左冠状动脉前降支 (LAD)产生急性心肌梗死模型 ,观察PQDS对实验性心肌梗死的影响 ,并从生化学角度探讨其作用机制。结果 ivPQDS 12 .5～ 5 0mg·kg-1,对急性心肌梗死 2 4h大鼠可明显缩小心肌梗死面积 ,降低血清CK ,LDH活性及LPO含量 ,提高SOD ,CAT及GSH Px活性 ,并能使血浆TXA2 水平明显下降 ,PGI2 /TXA2比值明显增高 ;2 5 ,5 0mg·kg-1亦可使心肌梗死及非梗死区FFA及LA含量明显降低。结论 PQDS对急性心肌缺血具有保护作用 ,可能与其增强抗氧化酶活性 ,减少自由基对心肌的氧化损伤 ,纠正心肌缺血时FFA代谢紊乱和LA堆积及PGI2 /TXA2

20S-原人参二醇皂苷对高脂血症大鼠血脂代谢的影响及其抗氧化作用(英文)

目的 观察 2 0 S-原人参二醇皂苷 (PPDS)对实验性高脂血症大鼠血清总胆固醇 (TC)、脂蛋白 -胆固醇代谢的影响及其抗氧化作用。方法 PPDS按 2 5 ,5 0 ,10 0 mg/ (kg· d)给大鼠连续 ip12 d,测血清 TC、脂蛋白 -胆固醇及脂质过氧化物 (L PO)含量 ,血浆前列腺素 I2 (PGI2 ) ,血栓素 A2 (TXA2 )水平 ,血清和肝脏超氧化物歧化酶(SOD)活性及全血黏度 ,并观察肝脏脂肪沉积情况。结果 PPDS 5 0 ,10 0 mg/ kg能明显降低甘油三酯 (TG) ,TC,低密度脂蛋白胆固醇 (L DL- c) ,TXA2 ,L PO含量及全血黏度 ,并能明显提高实验性高脂血症大鼠高密度脂蛋白胆固醇 (HDL - c) ,PGI2 含量及 SOD活性 ,亦能使 TC/ HDL - c及 L DL - c/ HDL - c比值明显降低 ,PGI2 / TXA2 比值明显升高。病理检查可见肝脏脂肪沉积明显减轻。结论 PPDS可能通过调节体内血脂代谢、提高 PGI2 / TXA2 比值及纠正自由基代谢紊乱发挥抗动脉硬化作用。

20(S)-人参皂苷Rg_3对脑缺血大鼠脑线粒体损伤的保护作用

目的研究20(S)-人参皂苷Rg3对脑缺血所致大鼠脑线粒体损伤的保护作用,探讨20(S)-人参皂苷Rg3抗缺血性脑中风的机制。方法用栓线法制作大鼠大脑中动脉缺血(MCAO)模型,测定线粒体肿胀度、膜流动性、膜磷脂含量、呼吸功能、线粒体呼吸酶、超氧化物歧化酶(SOD)、丙二醛(MDA)、Ca2+等。结果大鼠MCAO后24 h,脑线粒体损伤明显,表现为肿胀、膜流动性降低,膜磷脂降解、呼吸功能衰减,呼吸酶、SOD活性降低,Ca2+、MDA含量升高;静脉注射20(S)-人参皂苷Rg3(5,10 mg.kg-1)能明显抑制缺血脑线粒体膜流动性的降低,膜磷脂降解,减少脑缺血引起的线粒体肿胀,抑制NADH脱氢酶、琥珀酸脱氢酶和细胞色素C氧化酶活性的降低,改善线粒体呼吸功能;同时20(S)-人参皂苷Rg3能明显降低脑缺血大鼠脑神经细胞线粒体MDA含量、升高SOD活性、抑制Ca2+过多摄入。结论20(S)-人参皂苷Rg3对缺血脑神经细胞线粒体的损伤有明显的保护作用,该作用可能与清除氧自由基、抑制脂质过氧化、拮抗Ca2+有关。

非1B/1R类型小麦雄性不育系KTSP3314A败育的生化机制

为了揭示K型非1B/1R类型小麦不育系雄性败育的生化机制。利用K型非1B/1R类型小麦雄性不育系KTSP3314A,其同型保持系TSP3314B,以K型1B/1R类型小麦雄性不育系K3314A、其同型保持系3314B为对照,分别对其叶片和穗子在不同发育时期的超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、过氧化物酶(POD)的活性和丙二醛(MDA)含量的变化进行测定。结果表明,K型非1B/1R类型小麦不育系中SOD,POD及CAT活性变化与K型1B/1R类型小麦雄性不育系酶活性变化一致,K型非1B/1R类型雄性不育小麦叶片和穗子的超氧化物歧化酶(SOD)后期则较低,过氧化氢酶(CAT)、过氧化物酶(POD)的活性后期较高,丙二醛(MDA)含量后期较高。说明二者的雄性败育生化机制基本一致,但前者比后者败育的时期较晚。且超氧化物歧化酶(SOD)活性与雄性育性有关。

S863天然果蔬饮料对力竭运动小鼠骨骼肌自由基代谢及超微结构的影响

为研究S863天然果蔬饮料对小鼠骨胳自由基代谢及耐力运动能力的影响,本实验采用小鼠力竭游泳为运动疲劳模型。将100只成年健康雄性小鼠随机分为对照组、实验组、对照游泳组和实验游泳组。观察各组小鼠骨骼肌超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量及骨骼肌超微结构的变化。实验结果表明:实验游泳组小鼠的游泳时间比对照游泳组小鼠的游泳时间显著延长(P<0.001)。实验组小鼠骨骼肌超氧化物歧化酶(SOD)活性显著高于对照组(P<0.01),丙二醛(MDA)含量则明显低于对照组(P<0.05)。实验游泳组与对照游泳组小鼠超氧化物歧化酶(SOD)活性无显著性差异(P>0.05),丙二醛(MDA)含量则显著低于对照组游泳组(P<0.01),骨骼肌超微结构的变化也表现出同样的规律。这些结果说明,S863天然果蔬饮料对超氧阴离子自由基具有极强的清除能力,能有效抑制脂质过氧化反应,具有极佳的抗氧化性能。

Wilson患者驱铜及抗氧化治疗前后血清中氧化物和抗氧化物水平的研究

目的 研究Wilson病 (WD)患者经驱铜及抗氧化剂治疗前后血清氧化物和抗氧化物水平的变化。方法 应用反相高效液相色谱法 (RP HPLC)和化学比色法测定 2 9例WD患者治疗前及两种不同治疗后血清中氧化物和抗氧化物浓度 ,并把患者组和正常对照组比较以及不同治疗前后比较。结果 与正常对照组比较 ,WD患者血清氧化物增高 ,抗氧化物下降 ,而驱铜及驱铜联合抗氧化剂治疗后 ,血清氧化物水平下降 ,抗氧化物水平上升 ,且后者改变更明显。结论 驱铜治疗能显著改善WD患者血清中自由基的代谢紊乱 ,而联合应用抗氧化剂后改善更明显。

针刺对大鼠痛阈及血清SOD、MDA影响的实验研究

目的观察针刺对大鼠痛阈及血清超氧化物歧化酶(SOD)、丙二醛(MDA)的影响,探讨针刺镇痛效应及其氧代谢机理。方法将30只大鼠随机分为正常对照组、电针穴位组、电针非经非穴组。于电针前后分别检测大鼠痛阈及血清SOD、MDA等指标。结果电针后,电针穴位组大鼠痛阈、SOD含量明显高于正常对照组(P<0.01),MDA含量明显低于正常对照组(P<0.01);电针非经非穴位组SOD含量高于正常对照组(P<0.05),而痛阈、MDA含量较正常对照组无显著性差异(P>0.05);电针穴位组痛阈、SOD含量明显高于电针非经非穴组(P<0.05),MDA含量明显低于电针非经非穴组(P<0.05)。结论电针穴位有明显的镇痛效应。电针镇痛情况下血清SOD含量明显升高,血清MDA含量明显降低,提示针刺调整氧代谢,减少或消除氧自由基可能是电针镇痛的机理之一。

大鼠骨质疏松症模型MDA、SOD的变化

为探讨骨质疏松症的发生与自由基的关系。对去势雌性大鼠绝经后骨质疏松症模型血清丙二醛 ( MDA)、超氧化物歧化酶( SOD)含量进行测定 ,并与正常假手术组比较。结果显示去势模型组血清 MDA明显高于对照组 ,SO D低于正常对照组 ,差异分别有非常显著意义 ( P<0 .0 1)和显著意义 ( P<0 .0 5 )。表明氧自由基代谢异常参与了绝经后骨质疏松症的病理进程。

S863天然果蔬饮料对力竭运动小鼠肝脏自由基代谢及超微结构的影响

为研究S86 3天然果蔬饮料对小鼠肝脏自由基代谢及耐力运动能力的影响 ,本实验采用小鼠力竭游泳为运动疲劳模型 ,将 10 0只成年健康雄性小鼠随机分为对照组、实验组、对照游泳组和实验游泳组。观察各组小鼠肝脏超氧化物歧化酶 (SOD)活性和丙二醛 (MDA)含量及肝脏超微结构的变化。实验结果表明 :实验游泳组小鼠的游泳时间比对照游泳组小鼠的游泳时间显著延长 (P <0 0 0 1)。实验组小鼠肝脏超氧化物歧化酶 (SOD)活性明显高于对照组 (P <0 0 5 ) ,丙二醛 (MDA)含量则显著低于对照组 (P <0 0 1)。实验游泳组与对照游泳组小鼠肝脏超氧化物歧化酶 (SOD)活性无显著性差异 (P >0 0 5 ) ,而丙二醛 (MDA)含量则与对照游泳组有非常显著的差异 (P <0 0 0 1) ,肝脏超微结构的变化也表现出同样的规律。这些结果表明 :S86 3天然果蔬饮料对超氧阴离子自由基具有极强的清除能力 ,能有效抑制脂质过氧化反应 。

中远红外线对荷瘤鼠S-180肝脏MDA、SOD和GSH-Px的影响

目的：通过体内实验，探讨中远红外线对荷瘤鼠S-180抗氧化作用。方法：采用黄嘌呤氧化法测定SOD活性，用改良巴比妥酸微量法测定MDA含量和GSH－Px的活力。结果：日光照射荷瘤鼠S-180肝脏SOD、MDA和GSH－Px未见明显改变；而应用中远红外线治疗，肝脏SOD、GSH-Px活性明显升高，MDA含量明显降低（P<0．01）．结论：在本实验条件下，中远红外线影响肝脏组织SOD、GSH－Px和MDA的产生和代谢。

谷胱甘肽S-转移酶P1基因多态性与胃癌发展的相关性研究

目的分析谷胱甘肽S-转移酶(glutathione-S-transferase GSTs)P1基因多态性与胃癌发展的相关性,探讨高风险GSTP1-Val等位基因在氧自由基致胃癌中的作用。方法以血液样本、胃癌细胞和相应正常胃黏膜细胞样本为实验材料,采用放射免疫分析法(RIA)测定血浆谷胱甘肽S-转移酶P(GSTP)的含量和活性改变;多聚酶链反应-限制性片段长度多态性(PCR-RFLP)技术检测外周血DNA GSTP1的多态性。结果胃癌、肠上皮化生和不典型增生两种癌前病变组织中GSTP染色的阳性率分别为78.00%(39/50)、48.00%(24/50)和74.00%(37/50),与正常胃黏膜比较差异有统计学意义(P<0.05);GSTP在胃癌时升高[(27.5±24.5)μg/L],明显高于正常人组[(7.1±2.3)μg/L],两组比较差异有高度统计学意义(P<0.01);GSTP在癌前病变组[(16.8±12.3)μg/L]高于正常人组(P<0.01);GSTP含量与肿瘤的分化程度呈正相关(r=0.914,P<0.01);高分化及中分化管状腺癌的阳性率分别为72.73%(8/11)和100.00%(21/21),高于低分化管状腺癌(58.33%),分化程度与GSTP表达呈正相关(r=0.732,P<0.01)。Val 105的酶代替具有Lle 105的酶对多环芳烃二醇环氧化作用的效力高7倍,说明携带Val等位基因的个体患胃癌危险性明显高于非携带Val等位基因个体。结论 GSTP是机体损伤解毒的酶,它与肿瘤的发生、发展有关,是肿瘤早期诊断有价值的标志酶;GSTP1基因多态性与胃癌发展相关。携带GSTP1 Val等位基因的个体胃癌发病风险增高。

S-布洛芬印迹复合膜的吸附及拆分性能

以聚偏氟乙烯(PVDF)微孔滤膜为基膜,S-布洛芬为模板分子,丙烯酰胺为功能单体,乙二醇二甲基丙烯酸酯为交联剂,采用热引发表面自由基聚合的方式制备了S-布洛芬印迹复合膜,并研究了其对布洛芬外消旋体的吸附及拆分性能。结果表明,该印迹膜对S-布洛芬具有一定的特异性吸附能力,当布洛芬异构体浓度在0.1～0.5mmol/L范围内逐渐增大时,吸附量也逐渐增大,吸附选择性因子则由1.68降至1.14;该膜对布洛芬异构体具有一定的拆分能力,渗透实验进行7 h,膜对R-布洛芬及S-布洛芬的渗透量分别为0.378和0.313μmol/(cm2.h),分离因子可达到1.21。

Superoxide dismutase prevents development of adenocarcinoma in a rat model of Barrett's esophagus

AIM： To test whether antioxidant treatment could prevent the progression of Barrett＇s esophagus to adenocarcinoma. METHODS： In a rat model of gastroduodenoesophageal reflux by esophagojejunal anastomosis with gastric preservation, groups of 6-10 rats were randomized to receive treatment with superoxide dismutase （SOD） or vehicle and followed up for 4 too. Rat＇s esophagus was assessed by histological analysis, superoxide anion and peroxinitrite generation, SOD levels and DNA oxidative damage. RESULTS： All rats undergoing esophagojejunostomy developed extensive esophageal mucosal ulceration and inflammation by mo 4. The process was associated with a progressive presence of intestinal metaplasia beyond the anastomotic area （9% 1st mo and 50% 4th too） （94% at the anastomotic level） and adenocarcinoma （11% 1^ST mo and 60% 4th too）. These changes were associated with superoxide anion and peroxinitrite mucosal generation, an early and significant increase of DNA oxidative damage and a significant decrease in SOD levels （P〈0.05）. Exogenous administration of SOD decreased mucosal superoxide levels, increased mucosal SOD levels and reduced the risk of developing intestinal metaplasia beyond the anastomotic area （odds ratio = 0.326; 95%CI： 0.108-0.981; P = 0.046）, and esophageal adenocarcinoma （odds ratio = 0.243; 95%CI： 0.073-0.804; P = 0.021）. CONCLUSION： Superoxide dismutase prevents the progression of esophagitis to Barrett＇s esophagus and adenocarcinoma in this rat model of gastrointestinal reflux, supporting a role of antioxidants in the chemoprevention of esophageal adenocarcinoma.