小檗碱对氧化应激损伤中枢神经细胞的保护作用

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

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。Ｂｅｒ１～２５μｍｏｌ·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。

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.