小檗碱对氧化应激损伤中枢神经细胞的保护作用

 目的:研究小檗碱(berberine,Ber)对培养大鼠神经细胞氧化应激损伤的保护作用?方法:体外培养大鼠胎鼠大脑皮质神经细胞,观察谷氨酸、“缺血"或“缺血/再灌注"及血红素对细胞的毒性及Ber的保护作用?结果:在培养的大鼠胎鼠大脑皮质神经细胞中,加入谷氨酸、血红素及“缺血"或“缺血/再灌注"损伤,细胞出现明显损伤性变化,死亡率明显升高,培养上清液中乳酸脱氢酶(LDH)释放增加,而细胞匀浆中谷胱甘肽(GSH)含量明显减少,丙二醛(MDA)生成显著增多?Ber 1～25μmol·L^-1能不同程度地抑制谷氨酸、血红素或“缺血/再灌注"引起的损伤性改变,培养上清液中LDH释放减少,而细胞匀浆中GSH含量明显增加,MDA生成显著降低?结论:Ber对氧化应激损伤中枢神经细胞具有保护作用,其作用机制可能与其提高抗氧化物质谷胱甘肽含量,减少脂质过氧化物生成有关?

Protective effects of berberine on cultured central neuronal injuries induced by oxidative stress

OBJECTIVE: To study the neuroprotective effects of berberine (Ber) on cultured central neuronal injuries induced by oxidative stress. METHODS: Cytotoxicities of glutamate (Glu 500molL-1,15min),hemoglobin (Hb 100molL-1,24h) or "ischemia (6h)/reperfusion(24h)" and protective effects of Ber on cultured rat cortical neurons were observed. RESULTS: Exposure of rat fetus cerebral cells to Glu,Hb or hypoxic/hypoglycemic medium developed a neurotoxicity expressed in the increase of LDH leakage and MDA content and the decrease of GSH content,as well as the development of morphological injury.Ber (125molL-1) significantly protected neurons against above damages. CONCLUSION: Ber protected cerebral cells from the injuries induced by oxidative stress via increasing the content of GSH and inhibiting lipid peroxidation.