小檗碱对培养大鼠神经细胞“缺血”性损伤的保护作用  

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

作　　者：吴俊芳[1,2] 刘少林[1,2] 潘鑫鑫[1,2] 刘天培 

机构地区：[1]南京医科大学药理学教研室 [2]中国协和医科大学中国医学科学院药物研究所

出　　处：《中国药理学通报》1999年第3期243-246,共4页Chinese Pharmacological Bulletin

基　　金：江苏省科委资助

摘　　要：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。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.

关 键 词：小檗碱 大脑皮层神经元 脑缺血 细胞培养 钙 

分 类 号：R282.71[医药卫生—中药学] R277.733.1[医药卫生—中医学]