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目的:研究胶球藻多糖对线栓法大鼠脑缺血再灌注损伤的保护作用。方法:100只SD大鼠随机分为假手术组、模型组、尼莫地平(1 mg/kg)组、胶球藻多糖(50 mg/kg)剂量组、胶球藻多糖(100 mg/kg)剂量组。采用线栓法建立大鼠脑缺血再灌注模型,用Longa’s法、TTC染色法评价大鼠的神经功能评分和脑梗死体积;检测脑组织中一氧化氮合酶(NOS)、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸脱氢酶(LDH)的含量,ELISA法检测对脑组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β水平的影响。结果:与假手术组相比,模型组大鼠神经功能症状、梗死范围明显增高,降低SOD活力,提高MDA,NO,NOS,LDH水平,促进TNF-α和IL-1β的表达。与模型组相比,胶球藻多糖(50 mg/kg)剂量组、(100 mg/kg)剂量组及尼莫地平(1 mg/kg)组可显著降低脑缺血再灌注大鼠的神经功能评分,减轻脑组织损伤程度,减少脑梗死范围,提高SOD活力,降低MDA,NO,NOS,LDH水平,抑制TNF-α和IL-1β的表达。结论:胶球藻多糖对大鼠缺血再灌注损伤具有明显的保护作用,其机制可能与改善神经功能、减少自由基损伤和抑制炎症因子表达有关。
Objective: To study the protective effect of polysaccharides from Gloasnella on cerebral ischemia-reperfusion injury induced by thread-plugging in rats. Methods: 100 SD rats were randomly divided into sham operation group, model group, nimodipine (1 mg / kg) group, Cationic polysaccharide (50 mg / kg) ) Dose group. The rat model of cerebral ischemia-reperfusion was established by the method of thread embolism. The neurological function scores and cerebral infarction volume of rats were evaluated by Longa’s method and TTC staining. The levels of nitric oxide synthase (NOS), nitric oxide (NO), superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH) were determined by enzyme-linked immunosorbent assay. The levels of tumor necrosis factor-α (TNF-α), interleukin 1β (IL-1β) .Results: Compared with the sham operation group, the neurological function and infarct size in the model group were significantly increased, the activity of SOD was decreased, the levels of MDA, NO, NOS and LDH were increased and the levels of TNF-α And IL-1β were significantly decreased compared with the model group (P <0.05) .Compared with the model group, the dose of polysaccharides (50 mg / kg), the dose of 100 mg / kg and the group of nimodipine After reperfusion, the neurological function score, the degree of brain injury, the range of cerebral infarction, the activity of SOD and the levels of MDA, NO, NOS and LDH in the blood were decreased, and the expressions of TNF-α and IL-1β were inhibited.Conclusion: Algal polysaccharide has a significant protective effect on ischemia-reperfusion injury in rats, and its mechanism may be related to improving neurological function, reducing free radical damage and inhibiting the expression of inflammatory cytokines turn off.