论文部分内容阅读
目的观察茶色素对大鼠脑缺血再灌注损伤的作用,并探讨其可能的保护机制。方法采用线栓法闭塞大鼠大脑中动脉建立脑缺血再灌注模型。雄性SD大鼠60只,随机分为缺血再灌注组、假手术组、银杏液组和茶色素组(50、100和200 mg/kg)。结果大鼠脑缺血再灌注后,梗死范围达23.5%±4.6%,神经症状评分增高为(2.8±0.4)分。中、高浓度茶色素可明显缩小脑缺血再灌注大鼠脑梗死范围(18.5%±3.6%和14.2%±2.9%)(P<0.01),高浓度茶色素可改善大鼠神经症状评分(1.9±0.3)分(P<0.05)。与假手术大鼠比较,大鼠脑缺血再灌注后,脑组织MDA含量显著增加,SOD和GSH-Px活性明显降低。中、高浓度茶色素可降低脑缺血再灌注大鼠脑组织MDA含量,增加SOD和GSH-Px活性。大鼠脑缺血再灌注后,脑组织一氧化氮(NO)含量和诱导型一氧化氮合酶(iNOS)活性分别为(16.98±0.95)μmol/mg·prot和(3.89±0.23)U/mg.prot,明显高于假手术组的(6.12±0.39)μmol/mg·prot和(1.89±0.21)U/mg·prot(P<0.01),中、高浓度茶色素处理后可明显抑制NO含量和iNOS活性增高,NO分别为(14.26±1.21)和(11.25±1.07)μmol/mg·prot,iNOS分别为(3.45±0.22)和(2.85±0.25)U/mg·prot。结论茶色素可浓度依赖性地对抗缺血再灌注引起的脑损伤,其机制可能与抑制iNOS诱导的NO产生增加有关。
Objective To observe the effect of tea pigment on cerebral ischemia-reperfusion injury in rats and to explore its possible protective mechanism. Methods The rat middle cerebral artery was occluded by thread occlusion to establish a model of cerebral ischemia-reperfusion. Sixty male SD rats were randomly divided into ischemia reperfusion group, sham operation group, ginkgo liquid group and tea pigment group (50, 100 and 200 mg / kg). Results After cerebral ischemia-reperfusion in rats, infarct size reached 23.5% ± 4.6% and neurological symptom scores increased by (2.8 ± 0.4) points. Medium and high concentration of tea pigments could obviously reduce the range of cerebral infarction (18.5% ± 3.6% and 14.2% ± 2.9%) in rats with cerebral ischemia and reperfusion (P <0.01). High concentration of tea pigments could improve the neurological symptom score 1.9 ± 0.3) points (P <0.05). Compared with the sham-operated rats, the content of MDA and the activities of SOD and GSH-Px in the brain tissue decreased significantly after cerebral ischemia-reperfusion in rats. Medium and high concentration of tea pigment can reduce the content of MDA in cerebral tissue of rats with cerebral ischemia-reperfusion and increase the activity of SOD and GSH-Px. The levels of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) in brain tissue after cerebral ischemia / reperfusion in rats were (16.98 ± 0.95) μmol / mg · prot and (3.89 ± 0.23) U / (6.12 ± 0.39) μmol / mg · prot and (1.89 ± 0.21) U / mg · prot (P <0.01) in sham-operation group. The medium- and high-concentration tea pigments could significantly inhibit NO (14.26 ± 1.21) and (11.25 ± 1.07) μmol / mg · prot, and iNOS were (3.45 ± 0.22) and (2.85 ± 0.25) U / mg · prot, respectively. Conclusion Tea pigment can protect brain against ischemia-reperfusion injury in a concentration-dependent manner, which may be related to the inhibition of iNOS-induced NO production.