洛伐他汀对PC12神经细胞中α7尼古丁受体的上调作用及其神经保护作用

Upregulation of α7 nicotinic receptor and neuroprotective effect induced by Lovastatin in PC12 cells

目的研究洛伐他汀(Lovastatin)对PC12神经细胞中α7尼古丁受体的调节作用。方法体外培养用PC12神经细胞,加入不同浓度的洛伐他汀培养48h,或与β淀粉样蛋白、自由基诱导剂同时处理,然后测定细胞MTT水平、α7尼古丁受体密度及mRNA水平、细胞脂质过氧化水平。结果适量浓度的洛伐他汀(100nmol/L以下)使细胞中〔125I〕标记α金蛇环毒素配体与α7尼古丁受体结合密度升高,并使α7尼古丁受体mRNA表达水平增强;洛伐他汀可对抗β淀粉样蛋白或自由基诱导剂引起的脂质过氧化。结论洛伐他汀可增强α7尼古丁受体与配体的结合和上调该受体的基因表水平达,并有一定的神经保护作用。

Objective To investigate the regulation role of lovastatin on expression of α7 nicotinic acetylcholine receptor （nAChR） in PC12 ceils. Methods PC12 ceils in vitro were incubated by different concentrations of lovastatin or by lovastatin with α-amyloid （AI3） or with free radical inducer for 48 h to determine MTF level, number of α7 nAChR binding sites and its mRNA expression, and lipid peroxidation level. Results Certain concentrations of lovastain （ 〈 100 nmol/L） increased the binding sites of [^125 Ⅰ α-bungarotoxin to α7 nAChR, and upregulated the expression of α7 nAChR mRNA; lovastatin opposed the increase of lipid peroxidation induced by Aβ or free radical inducer. Conclusions Lovastatin could increase the biding sites ofα 7 nAChR to its ligand and upregulate the gene expression of the receptor, playing a neuroprotective effect.