小檗碱对培养大鼠神经细胞“缺血”性损伤的保护作用

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。

Protective effects of berberine on ischemic injury in cultured rat cortical neurons

AIM To investigate protective effects of berberine(Ber) on ischemic injury in cultured rat cortical neurons. METHODS Cortical neurons of fe tal of rat were cultured in vitro . The protective effects of Ber on ischemic injury by treating cells with sodium dithionite in glucose free medium were observed. RESULTS Ber 5, 25 μmol·L -1 reduced the number of cell death and lowered LDH content in extra cellular bathing media in oxygen/glucose deprived cortical cultures. When cultures were incubated for 24 h with hypoxic/hypoglycemic medium, level of Ca 2+ ] i and content of MDA increase while the content of GSH and the activity of SOD decreased. Ber 5 and 25 μmol·L -1 prevented the elevation of Ca 2+ ] i and MDA and increased the content of GSH and the activity of SOD. CONCLUSION Ber protects cerebral cortical neurons from ischemic injury by preventing the rise of Ca 2+ ] i, suppressing the generation of lipid peroxide and increasing the content of GSH and the activity of SOD.