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SIRT1/NF-κB通路参与白藜芦醇改善大鼠脑缺血再灌注损伤炎性反应 被引量:26

SIRT1/NF-κB pathway participates in resveratrol improve inflammatory response of cerebral ischemia-reperfusion injury in rats
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摘要 目的研究大鼠脑缺血再灌注损伤后沉默信息调节因子1(SIRT1)对缺血脑组织周边炎性反应的影响及其与核转录因子-κB(NF-κB)通路的关系。方法选择健康雄性SD大鼠40只,随机均分为4组:假手术组、模型组、白藜芦醇组、EX527组。采用逆转录-聚合酶链反应(RT-PCR)法和Western blot法检测各组大鼠脑组织匀浆中白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、SIRT1及NF-κB mRNA含量及蛋白表达变化。于1、3、7、14 d对大鼠进行神经功能缺损评分。结果白藜芦醇组3、7、14 d神经功能缺损评分明显低于模型组和EX527组(P<0.01)。白藜芦醇组NF-κB、IL-1β、IL-6、TNF-αmRNA及蛋白表达量明显低于模型组和EX527组(P<0.01);SIRT1明显高于模型组和EX527组(P<0.01)。结论 SIRT1的激活可促进脑缺血再灌注大鼠的神经功能缺损恢复,减轻炎性反应,其机制可能与NF-κB通路有关。 Objective To investigate the role of silent information regulator protein 1 ( SIRT1 ) in inflammatory reaction in peri-ischemic brain tissue after ischemia reperfusion injury in rats and its relationship with nuclear factor- K-gene binding (NF-KB) pathway. Methods Forty healthy male SD rats were randomly divided into sham group, I/R group, Res + I/R group and EX527 + L/R group ( 10 in each group). The expression levels of interleukin (IL) -1β, IL-6, tumor necrosis factor-α ( TNF-α), SIRT1 and NF-KB in peri-ischemic brain tissues were detected using Western blot and RT-PCR respectively. Neurological severity score(NSS) were measured 1 d, 3 d,7 d and 14 d after reperfusion. Results NSS in Res + I/R group in 3,7, 14 day after reperfusion was significantly lower than those of I/R group and EX527 + I/R group (P 〈0.01 ) ; Compared with I/R and EX527 + I/R group,the peri-ischemic brain tissue mRNA expression and the protein expression of NF-KB, IL-1β, IL-6 and TNF-α were signifi- cantly decreased in Res + I/R group. SIRT1 was significantly increased (P 〈 0.01 ). Conclusion The activation of SIRT1 can improve cerebral ischemic damage and reduce inflammatory reaction in rats. Its mechanism may be related to the NF-KB pathways.
出处 《安徽医科大学学报》 CAS 北大核心 2018年第1期6-9,共4页 Acta Universitatis Medicinalis Anhui
基金 国家自然科学基金(编号:81171108) 全军医药卫生科研基金(编号:15MS172 14MS039)
关键词 缺血再灌注 SIRT1 白藜芦醇 NF-ΚB ischemia/reperfusion SIRT1 resveratrol NF-KB
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