论文部分内容阅读
目的观察小檗碱(Ber)对缺氧/缺糖培养引起的大鼠脑皮层神经元“缺血”性损伤的保护作用,并初步探讨其作用机制。方法体外培养大鼠胎鼠脑皮层神经元,以缺氧加缺糖培养作为细胞“缺血”性损伤模型,观察Ber对神经元“缺血”性损伤的保护作用。结果Ber5,25μmol·L-1能显著降低神经细胞“缺血”性损伤时的细胞死亡率,减少乳酸脱氢酶(LDH)的漏出,改善细胞形态,对缺氧/缺糖诱导的神经细胞内游离钙浓度([Ca2+]i)的升高有明显的抑制作用,并能减少脂质过氧化物生成,提高谷胱甘肽(GSH)含量及超氧化物歧化酶(SOD)活性。结论Ber对培养大鼠脑皮层神经元“缺血”性损伤具有保护作用,其机制可能与Ber抑制“缺血”性损伤诱导的[Ca2+]i异常升高,减少脂质过氧化物生成,增加抗氧化物质的含量有关。
Objective To observe the protective effect of berberine on ischemia-induced injury of rat cortical neurons induced by hypoxia/glucose deprivation, and to explore its mechanism. Methods The rat cortical neurons were cultured in vitro. Hypoxia plus glucose deprivation culture was used as a cell “ischemia” injury model to observe the protective effect of Ber on neuronal ischemic injury. Results Ber5 and 25μmol·L-1 could significantly reduce the cell death rate of ischemic injury, decrease the leakage of lactate dehydrogenase (LDH), and improve the cell morphology. The cells induced by hypoxia/glucose deprivation could be reduced. The increase of intracellular free calcium concentration ([Ca2+]i) significantly inhibited the production of lipid peroxides, increased the content of glutathione (GSH) and the activity of superoxide dismutase (SOD). Conclusion Ber has a protective effect on ischemic injury of cultured rat cortical neurons, and its mechanism may be that Ber inhibits the abnormal increase of [Ca2+]i induced by “ischemic” injury and reduces lipid peroxide production. Increase the content of antioxidant substances.