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 h...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.展开更多
Objective: To study the correlation of electrophysiological characteristics Tp-ec and Tp-e/QT with myocardial injury and oxygen free radical generation in patients with acute myocardial infarction. Methods: Patients w...Objective: To study the correlation of electrophysiological characteristics Tp-ec and Tp-e/QT with myocardial injury and oxygen free radical generation in patients with acute myocardial infarction. Methods: Patients who were diagnosed with acute myocardial infarction in our hospital between March 2014 and March 2017 were selected as the AMI group, and healthy subjects who received physical examination were selected as the control group, electrocardiography was done to determine Tp-ec and Tp-e/QT, serum was collected to determine the levels of myocardial injury markers, oxygen free radical generation indexes and apoptosis indexes, and peripheral blood was collected to determine the expression of oxygen free radical generation indexes. Results: Tp-ec and Tp-e/QT of AMI group were significantly higher than those of control group, and serum CK-MB, cTnI, H-FABP, MDA, sTWEAK, sFas and sTRAIL contents as well as peripheral blood Nrf-2, NRE and HO-1 mRNA expression were significantly higher than those of control group and positively correlated with Tp-ec and Tp-e/QT. Conclusion: Electrophysiological characteristics Tp-ec and Tp-e/QT increase, and the transseptal dispersion of repolarization increases in patients with acute myocardial infarction, and they are closely related to myocardial injury and oxygen free radical generation.展开更多
The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by ...The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe 2+ were tested by differential spectrum. Superoxide anion (O 2)from xanthine xanthine oxidase (Xan XO) system and hydroxyl radical (·OH) from FeSO 4 H 2O 2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan XO and FeSO 4 H 2O 2 system. The IC 50 of Bre were 93 01 μmol·L -1 for Xan XO system and 62 18 μmol·L -1 for FeSO 4 H 2O 2 system. Bre also scavenged O 2 and ·OH produced by Xan XO and FeSO 4 H 2O 2 systems. The IC 50 of Bre were 32 63 μmol·L -1 for O - 2 and 20 22 μmol·L -1 for ·OH. Furthermore, the chelating Fe 2+ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe 2+ and scavenging O 2 as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.展开更多
Objective: To investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits. Methods: 30 healthy white rabbits were randomly divided into th...Objective: To investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits. Methods: 30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH ( 8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured. Results: The contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P< 0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly. Conclusions: TRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.展开更多
文摘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.
文摘Objective: To study the correlation of electrophysiological characteristics Tp-ec and Tp-e/QT with myocardial injury and oxygen free radical generation in patients with acute myocardial infarction. Methods: Patients who were diagnosed with acute myocardial infarction in our hospital between March 2014 and March 2017 were selected as the AMI group, and healthy subjects who received physical examination were selected as the control group, electrocardiography was done to determine Tp-ec and Tp-e/QT, serum was collected to determine the levels of myocardial injury markers, oxygen free radical generation indexes and apoptosis indexes, and peripheral blood was collected to determine the expression of oxygen free radical generation indexes. Results: Tp-ec and Tp-e/QT of AMI group were significantly higher than those of control group, and serum CK-MB, cTnI, H-FABP, MDA, sTWEAK, sFas and sTRAIL contents as well as peripheral blood Nrf-2, NRE and HO-1 mRNA expression were significantly higher than those of control group and positively correlated with Tp-ec and Tp-e/QT. Conclusion: Electrophysiological characteristics Tp-ec and Tp-e/QT increase, and the transseptal dispersion of repolarization increases in patients with acute myocardial infarction, and they are closely related to myocardial injury and oxygen free radical generation.
文摘The mechanisms by which breviscapine (Bre) inhibits the lipid preoxidation in rat brain mitochondria were investigated. The mitochondrial lipid peroxidation of rat brain induced by oxygen free radical was measured by thiobarbituric acid spectrophotometry. The chelating activities of Bre for Fe 2+ were tested by differential spectrum. Superoxide anion (O 2)from xanthine xanthine oxidase (Xan XO) system and hydroxyl radical (·OH) from FeSO 4 H 2O 2 system were determined with spectrophotometry. It was found that Bre could effectively inhibit the lipid peroxidation of brain mitochondria induced by free radicals driven from Xan XO and FeSO 4 H 2O 2 system. The IC 50 of Bre were 93 01 μmol·L -1 for Xan XO system and 62 18 μmol·L -1 for FeSO 4 H 2O 2 system. Bre also scavenged O 2 and ·OH produced by Xan XO and FeSO 4 H 2O 2 systems. The IC 50 of Bre were 32 63 μmol·L -1 for O - 2 and 20 22 μmol·L -1 for ·OH. Furthermore, the chelating Fe 2+ activity of Bre was shown. It may be concluded that Bre inhibited lipid peroxidation at different stages of the reaction of oxygen free redial with the mitochondria membrane: (1) the formation of ·OH; (2) the initiation of the lipid peroxidation, by chelating Fe 2+ and scavenging O 2 as well as ·OH. The scavenging oxygen free radicals and chelating iron are the mechanisms of inhibitory effect of Bre on lipid peroxidation.
文摘Objective: To investigate the early effect of thyrotropin-releasing hormone (TRH) on cerebral free radical reactions after acute brain injury in rabbits. Methods: 30 healthy white rabbits were randomly divided into three groups: Group A (n=10), Group B (n=12) and Group C (n=8). The rabbits in Group A and Group B were injured by direct hit. At 0.5-4 hours after injury, the rabbits in Group A were injected with TRH ( 8 mg/kg body weight) through a vein and the rabbits in Group B were injected with normal saline of equal volume. The rabbits in Group C served as the normal control. Then all the rabbits were killed and brain tissues were obtained. The content of lipoperoxide (LPO), the activity of superoxide dismutase (SOD) and the water content of the brain tissues were measured. Results: The contents of LPO and water in brain tissues in Group A were lower and the activity of SOD was higher than those of Group B (P< 0.05). After injury, intracranial pressure (ICP) rose rapidly and continuously with time passing by. When TRH was given to the animals in Group A, the rising speed of ICP slowed down significantly. Conclusions: TRH can decrease the cerebral free radical reactions and cerebral edema after acute brain injury in rats.
