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目的:探讨表没食子儿茶素没食子酸酯(EGCG)对蛛网膜下腔出血(SAH)脑损伤的影响及其可能机制。方法:选取健康雄性Sprague-Dawley(SD)大鼠80只,按照随机数字表法分为假手术组(Sham组)、SAH组、SAH+EGCG组、蛛网膜下出血+生理盐水组(SAH+NS组),每组各20只。SAH造模成功后1d、3d,检测大鼠神经功能评分及脑组织含水量;造模成功3d后,脑组织石蜡切片HE染色观察脑细胞形态,并采用超敏C-反应蛋白(hs CRP)试剂盒检测血清hs CRP水平,通过Western blotting检测脑组织脑源性神经生长因子(brain derived neurotrophic factor,BDNF)及与其高度亲和的酪氨酸激酶受体B(tropomyosin-related kinase B,TrkB)的表达。结果:(1)SAH+EGCG组神经功能评分较Sham组明显降低,但较同期SAH组增高明显(P<0.05);(2)与Sham组比较,SAH+EGCG组脑组织含水量明显增加,但与同期SAH组比较,SAH+EGCG组脑组织含水量明显降低(P<0.05);(3)与SAH组比较,SAH+EGCG组血清hs CRP水平明显降低(P<0.05);(4)与SAH组比较,SAH+EGCG组脑组织石蜡切片HE染色神经细胞水肿明显减轻,且坏死神经元减少,细胞核固缩明显减轻;(5)与SAH组比较,SAH+EGCG组脑组织BDNF、TrkB的表达量明显升高(P<0.05)。结论:EGCG能够有效的保护大鼠SAH后的脑损伤,促进神经功能修复,减轻预后神经功能障碍,可能与其促进脑组织BDNF、TrkB的表达有关。
Objective: To investigate the effect of epigallocatechin gallate (EGCG) on brain injury induced by subarachnoid hemorrhage (SAH) and its possible mechanism. Methods: Eighty healthy male Sprague-Dawley (SD) rats were randomly divided into Sham group, SAH group, SAH + EGCG group, subarachnoid hemorrhage + saline group (SAH + NS group), 20 in each group. Neurological function scores and water content of brain tissue were detected on the 1st day and the 3rd day after SAH model was established successfully. After successful 3d modeling, the morphological changes of brain cells were observed by HE staining, and the hsCRP The serum hs CRP levels were detected by Western blotting. The brain derived neurotrophic factor (BDNF) and its highly -related Trophoblastomycin-related kinase B (TrkB) expression. Results: (1) Compared with Sham group, SAH + EGCG group showed significantly lower scores of neurological function than those of Sham group (P <0.05); (2) Compared with Sham group, SAH + EGCG group increased brain water content obviously, (3) Compared with SAH group, the level of hsCRP in SAH + EGCG group was significantly lower (P <0.05); (4) Compared with SAH group, SAH + EGCG group had significantly decreased brain water content Compared with SAH group, SAH + EGCG group of brain tissue paraffin sections of HE staining neuronal edema was significantly reduced, and necrotic neurons decreased significantly reduced nuclear pyknosis; (5) Compared with the SAH group, SAH EGCG group of brain tissue BDNF, TrkB The expression was significantly increased (P <0.05). CONCLUSION: EGCG can effectively protect the brain from injury after SAH in rats, promote the repair of neurological function and alleviate the neurological dysfunction in prognosis, which may be related to the promotion of BDNF and TrkB in brain tissue.