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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.