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目的观察氯化镧(LaCl3)对大鼠大脑皮质星形胶质细胞(Ast)中葡糖调节蛋白-94(GRP-94)、蛋白激酶R样内质网激酶(PERK)、生长阻滞和DNA损伤诱导蛋白153(GADD153)、半胱天冬蛋白酶-12(caspase-12)表达的影响。方法分别用0、0.25、0.5、1.0 mmol/L LaCl3作用Ast细胞24 h,再以四甲基偶氮唑盐法检测Ast细胞活力,以流式细胞仪检测Ast细胞凋亡,以Western blotting法检测Ast细胞GRP-94、PERK、磷酸化PERK(pPERK)、GADD153和caspase-12的水平。结果 0.25、0.5、1.0 mmol/L LaCl3染毒后,Ast细胞活力降低,Ast细胞凋亡升高,均呈剂量-效应关系,差异均有统计学意义(P<0.05)。0.25、0.5、1.0 mmol/L LaCl3染毒组Ast细胞的GRP-94、pPERK、GADD153、caspase-12水平均高于对照组,其中1.0 mmol/L LaCl3染毒组上述指标分别为对照组的3.10、5.25、2.73、3.14倍,差异均有统计学意义(P<0.05)。结论 GRP-94、pPERK、GADD153和caspase-12表达上调使凋亡异常增多,其可能是LaCl3对Ast细胞产生毒作用的机制之一。
Objective To investigate the effect of LaCl3 on the expression of GRP-94, PERK, growth arrest and the expression of GRK in rat cerebral cortex astrocytes (Ast) DNA damage-induced protein 153 (GADD153), caspase-12 expression. Methods Ast Astocytes were treated with 0, 0.25, 0.5 and 1.0 mmol / L LaCl 3 for 24 h, respectively. The viability of Ast cells was detected by MTT method. The apoptosis of Ast cells was detected by flow cytometry. Western blotting The levels of GRP-94, PERK, phosphorylated PERK (pPERK), GADD153 and caspase-12 in Ast cells were determined. Results After treated with 0.25, 0.5 and 1.0 mmol / L LaCl3, the viability of Ast cells decreased and the apoptosis of Ast cells increased. All of them showed dose - effect relationship with statistical significance (P <0.05). 0.25,0.5,1.0 mmol / L LaCl3 Ast cells treated groups GRP-94, pPERK, GADD153, caspase-12 levels were higher, wherein 1.0 mmol / L LaCl3 exposed groups the index of the control group were 3.10 , 5.25, 2.73 and 3.14 times respectively, the difference was statistically significant (P <0.05). Conclusion The up-regulation of GRP-94, pPERK, GADD153 and caspase-12 leads to abnormal apoptosis, which may be one of the mechanisms of LaCl3 toxic effect on Ast cells.