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作 者:刘秋芳[1] 杨敬华[1] 巫生文[1] 蔡原[1]
机构地区:[1]中国医科大学公共卫生学院卫生毒理学教研室,辽宁沈阳110001
出 处:《环境与健康杂志》2012年第5期397-399,共3页Journal of Environment and Health
基 金:国家自然科学基金(30800925)
摘 要:目的研究氯化镧对小鼠大脑皮质星形胶质细胞凋亡相关基因表达的影响。方法原代培养的小鼠大脑皮质星形胶质细胞分别于终浓度为0(对照)、0.25、0.5、1.0 mmol/L氯化镧无血清培养基处理24 h后,采用RT-PCR法检测星形胶质细胞B细胞淋巴瘤2(B-cell lymphoma 2,Bcl-2)、B细胞淋巴瘤2相关X基因(Bcl-2-associated Xgene,Bax)、半胱氨酸天冬氨酸蛋白酶-3(caspase-3)、caspase-8和caspase-9 mRNA的表达水平。结果与对照组比较,0.25、0.5和1.0 mmol/L氯化镧染毒小鼠星形胶质细胞Bax、caspase-3和caspase-9 mRNA的表达水平均显著升高,0.5和1.0 mmol/L氯化镧染毒小鼠星形胶质细胞Bcl-2 mRNA的表达水平均显著降低,差异有统计学意义(P<0.05);且随着氯化镧染毒剂量的升高,小鼠星形胶质细胞Bax、caspase-3和caspase-9 mRNA的表达水平均呈上升趋势,Bcl-2 mRNA的表达水平呈下降趋势。而各组小鼠星形胶质细胞caspase-8 mRNA的表达水平间比较,差异无统计学意义。结论氯化镧对星形胶质细胞产生毒作用的机制可能与氯化镧致促凋亡基因Bax和caspase-3、caspase-9表达升高以及抑凋亡基因Bcl-2表达下降有关。Objective To study the effects of lanthanum chloride(LaCl3) on apoptosis-related genes expression in astrocytes of cerebral cortex in mice. Methods Primary cultured astrocytes of cerebral cortex in mice were treated with 0 (control), 0.25,0.5 and 1.0 mmol/L LaCl3 in free-serum medium for 24 h. Bcl-2, Bax, caspase-3, caspase-8 and caspase-9 mRNA expression levels were detected by RT-PCR. Results Compared with control group, astrocytic Bax ,caspase-3 and caspase-9 mRNA expression levels of cerebral cortex in mice administrated with 0.25,0.5 and 1.0 mmol/L LaC13 increased significantly, and Bc1-2 mRNA expression levels of cerebral cortex in mice administrated with 0.5 and 1.0 mmol/L LaCI3 decreased significantly (P〈0.05). Besides ,with increasing dose of LaC13, there were increasing tendency in the astrocytic Bax, caspase-3 and caspase-9 mRNA expression levels of cerebral cortex in mice, and there was decrease tendency in the astrocytic Bcl-2 mRNA expression levels of cerebral cortex in mice. However,there was no significant statistical difference in the astrocytic caspase-8 mRNA expression levels of cerebral cortex in mice of all groups. Conclusion The toxic effect of LaCl3 on astrocytes is related with up-regnlation of proapototic Bax, caspase-3 and caspase-9 expression and down-regulation of anti-apoptotic Bcl-2 expression caused by LaCl3 in astrocytes.
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