香菇多糖对大鼠脑缺血再灌注损伤的保护作用及机制研究

Protective effect and mechanism of Lentinan on cerebral ischemia-reperfusion injury in rats

目的探讨香菇多糖(LNT)对大鼠脑缺血再灌注损伤的保护作用及可能机制。方法 30只健康雄性SD大鼠随机分成假手术组(Sham)、大脑中动脉闭塞组(MCAO)和香菇多糖处理组(MCAO+LNT)。采用线栓法建立大鼠MCAO,术后给予LNT干预,每日一次,连续1周。HE染色观察脑组织病理学改变;ELISA检测血清内炎症因子改变;Western blot技术检测脑损伤标志物、炎症相关蛋白及Akt/FOXO1信号通路蛋白表达。结果与MCAO组相比,LNT处理显著减轻大鼠脑内病理改变;降低血清内促炎症因子TNF-α及IL-6的表达,增加抗炎因子IL-10的表达;降低S100β、NF-κB和COX-2的蛋白表达,上调p-Akt与p-FoxO1表达。结论 LNT处理对大鼠脑缺血再灌注损伤有保护作用,其潜在机制可能与激活Akt/FoxO1信号通路相关。

Objective To investigate the protective effect of lentinan(LNT) on cerebral ischemia-reperfusion injury in rats and its possible mechanism. Methods 30 healthy male SD rats were randomly divided into sham operation group(sham), middle cerebral artery occlusion group(MCAO) and Lentinan treatment group(MCAO+LNT). MCAO was established by suture method, and LNT intervention was given after operation, once a day for 1 week. HE staining was used to observe the pathological changes of brain tissue. Serum inflammatory factors were detected by ELISA. Western blot was used to detect the expression of brain injury markers, inflammation related proteins and Akt/FoxO1 signaling pathway proteins. Results Compared with MCAO group, LNT significantly reduced the pathological changes in brain, decreased the expression of pro-inflammatory factors TNF-α and IL-6, and increased the expression of anti-inflammatory factor IL-10. The expression of S100 β, NF-κ B and COX-2 was decreased, and the expression of p-Akt and p-FoxO1 was increased. Conclusion LNT treatment has protective effect on cerebral ischemia-reperfusion injury in rats, and its potential mechanism may be related to activation of Akt/FoxO1 signaling pathway.