论文部分内容阅读
目的研究白藜芦醇(Res)对脑缺血再灌注损伤的保护作用及可能的机制。方法线栓法制作大鼠大脑中动脉栓塞(middle cerebral artery occlusion,MCAO)模型,缺血2 h再灌注。将76只大鼠分成假手术组(S组)、缺血再灌注组(I/R组)、Res低剂量组(15 mg/kg,I/R+R1组)和Res高剂量组(30 mg/kg,I/R+R2组),每组19只。再灌注24 h,采用TTC法测量脑梗死体积,化学比色法测定血清及脑组织中MDA含量,RT-PCR及Western blot检测Nrf2、HO-1基因和蛋白表达,HE染色观察脑组织的病理改变。结果与I/R组比较,Res能明显缩小脑梗死体积[I/R组(42.67±2.51)%vsI/R+R1组(30.53±1.45)%、I/R+R2组(20.27±2.11)%,P<0.01],降低血清中MDA的含量[I/R组(9.29±0.42)nmol/mlvsI/R+R1组(4.03±0.08)nmol/ml、I/R+R2组(2.68±0.27)nmol/ml,P<0.01],及脑组织中MAD含量[I/R组(1.40±0.02)nmol/mgvsIR+R1组(1.19±0.07)nmol/mg、IR+R2组(0.85±0.03)nmol/mg,P<0.01]。显著上调Nrf2、HO-1基因和蛋白的表达(P<0.05),改善脑组织的病理变化。结论 Res对局灶性脑缺血再灌注损伤有良好的保护作用,其机制可能是通过激活Nrf2/ARE信号通路进而增强抗氧化蛋白HO-1表达实现的。
Objective To study the protective effect and possible mechanism of resveratrol (Res) on cerebral ischemia reperfusion injury. METHODS: The middle cerebral artery occlusion (MCAO) model was established by thread embolization, and ischemia was reperfusioned for 2 hours. Seventy-six rats were divided into sham group (S group), ischemia reperfusion group (I/R group), low dose of Res group (15 mg/kg, I/R+R1 group) and high dose of Res group (30 Mg/kg, I/R+R2 group), 19 mice in each group. After 24 hours of reperfusion, the volume of cerebral infarction was measured by TTC method. The content of MDA in serum and brain tissue was determined by chemical colorimetry. The expression of Nrf2 and HO-1 gene and protein were detected by RT-PCR and Western blot. The pathological changes of brain tissue were observed by HE staining. change. Results Compared with the I/R group, Res significantly reduced the volume of cerebral infarction [I/R group (42.67±2.51)% vsI/R+R1 group (30.53±1.45)%, I/R+R2 group (20.27±2.11)] %,P<0.01],reduced MDA content in serum [I/R group (9.29±0.42) nmol/ml vs I/R+R1 group (4.03±0.08) nmol/ml, I/R+R2 group (2.68±0.27 Nmol/ml, P<0.01], and MAD content in brain tissue [I/R group (1.40±0.02) nmol/mgvs IR+R1 group (1.19±0.07) nmol/mg, IR+R2 group (0.85±0.03) Nmol/mg, P<0.01]. Significantly up-regulated the expression of Nrf2, HO-1 gene and protein (P<0.05), and improved the pathological changes of brain tissue. Conclusion Res has a good protective effect against focal cerebral ischemia-reperfusion injury. The mechanism may be that the activation of Nrf2/ARE signaling pathway enhances the expression of anti-oxidation protein HO-1.