摘要
目的 探讨人参皂苷Rg1对大鼠脑缺血再灌注(I/R)损伤的保护作用及机制。方法 将SD大鼠分成假手术组、脑I/R损伤模型组、低剂量给药组(人参皂苷Rg1 30mg/kg)、高剂量给药组(人参皂苷Rg1 60mg/kg)。假手术组、脑I/R损伤模型组大鼠腹腔内注射生理盐水,低剂量给药组与高剂量给药组大鼠腹腔内注射人参皂苷Rg1。对各组大鼠行大脑中动脉闭塞手术后进行运动神经功能缺损评分的比较;酶联免疫吸附测定法(ELISA)检测各组大鼠血浆中肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)及白细胞介素1β(IL-1β)的含量;实时荧光定量PCR(qRT-PCR)检测各组大鼠皮层脑组织中TLR4 mRNA的表达;蛋白免疫印迹(Western blot)检测各组大鼠皮层脑组织中TLR4蛋白及介导的通路蛋白My D88、NF-κB的表达。结果 与假手术组比较,脑I/R损伤模型组大鼠运动神经功能缺损评分、血浆中TNF-α、IL-6及IL-1β炎症因子的含量、大鼠皮层脑组织中TLR4 mRNA及蛋白的表达明显升高;与脑I/R损伤模型组比较,人参皂苷Rg1预处理的大鼠运动神经功能缺损评分、大鼠血浆中TNF-α、IL-6以及IL-1β炎症因子的含量、大鼠皮层脑组织中TLR4 mRNA及蛋白的表达随着剂量的增加而逐渐降低。同时,脑I/R损伤模型组大鼠皮层脑组织中MyD88及NF-κB蛋白的表达增加,而应用人参皂苷Rg1预处理的大鼠随着给药剂量的增加,MyD88及NF-κB蛋白的表达逐渐减少,呈剂量相关。结论 人参皂苷Rg1通过减轻大鼠脑I/R损伤后的炎症反应发挥抗脑I/R损伤的作用,其机制可能与抑制TLR4介导的MyD88/NF-κB通路有关。
Objective To investigate the protective effect and mechanism of ginsenoside Rg1 on cerebral ischemia/reperfusion(I/R) injury in rats. Methods SD rats were divided into sham operation group, brain I/R injury group, ginsenoside Rg1 low-dose and high-dose groups(30mg/kg,60mg/kg). Rats in sham operation group and brain I/R injury group were injected intraperitoneally with normal saline, and rats in low and high dose groups were injected intraperitoneally with ginsenoside Rg1. After middle cerebral artery occlusion operation, the neurological deficit scores was compared among all groups. Plasma levels of tumor necrosis factor α(TNF-α), interleukin 6(IL-6) and interleukin 1β(IL-1β) were determined by enzyme-linked immunosorbent assay(ELISA). Real-time fluorescence quantitative PCR(qRT-PCR) was used to detect the expression of TLR4 mRNA in cortical brain tissues of rats in each group. The expression of TLR4 protein and the mediated pathway proteins My D88 and NF-κB were detected by Western blot. Results Compared with sham operation group, brain I/R injury significantly increased neurological deficit scores, contents of TNF-α, IL-6 and IL-1β inflammatory factors in plasma, and expression of TLR4mRNA and protein in cortical brain tissues of rats. Compared with the brain I/R injury group, ginsenoside Rg1-pretreated rats’ neurological deficit scores, the contents of TNF-α,IL-6 and IL-1β inflammatory factors in plasma,the expression of TLR4 mRNA and protein in cortical brain tissues of rats decreased gradually with the increase of ginsenoside Rg1 dose, showing a dose-dependent manner. Meanwhile, brain I/R injury increased the expression of My D88and NF-κB protein in cortical brain tissues of rats, while the expression of MyD88 and NF-κB protein in rats pretreated with ginsenoside Rg1 decreased with the increase of ginsenoside Rg1 dose, presenting a dose-dependent manner. Conclusion Ginsenoside Rg1 plays an anti-brain I/R injury by reducing the inflammatory response after brain I/R injury in rats, and the mechanism may be related to the inhibition of TLR4-mediated My D88/NF-κB pathway.
作者
马雪飞
冯冬军
于文霞
谭明
刘跃
翟凤国
Ma Xuefei;Feng Dongjun;Yu Wenxia(Department of Pharmacology,Mudanjiang Medical University,Mudanjiang 157011)
出处
《中国现代医药杂志》
2022年第3期1-6,共6页
Modern Medicine Journal of China
基金
黑龙江省省属高校基本科研业务攀登计划项目(编号:2018-KYYWFMY-0005)
牡丹江医学院研究生创新科研项目(编号:YJSCX-MY11)。
关键词
脑缺血
人参皂苷RG1
炎症
作用机制
Cerebral ischemia
Ginsenoside Rg1
Inflammation
Mechanism
