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目的探讨对氨基水杨酸钠(PAS-Na)对亚急性染锰大鼠学习记忆能力、海马细胞凋亡、线粒体功能和神经胶质细胞生长分化基因表达的影响。方法雄性大鼠每日腹腔注射(ip)MnCl2.4H2O,15 mg/kg,每周5 d,连续4周。然后,每日背部皮下注射PAS-Na 100(低-PAS)或200(高-PAS)mg/kg,连续3周或6周。采用Morris水迷宫检测大鼠学习记忆能力,Real-Time PCR(RT-PCR)方法检测海马Bax、CoxⅡ、CoxⅣ、GFAP基因的mRNA原始表达量。结果观察期7周时,测试第5天染锰组逃避潜伏期、游泳路程比对照组长,低-PAS组逃避潜伏期、游泳路程较染锰组短(P<0.05)。染锰组Bax、CoxⅡ、GFAP基因表达比对照组增强,CoxⅣ基因表达比对照组减弱(P<0.05);低、高-PAS组CoxⅡ基因表达比染锰组降低(P<0.01)。观察期10周时,测试第4天染锰组逃避潜伏期、游泳路程比对照组长,低、高-PAS组逃避潜伏期、游泳路程较染锰组短(P<0.05)。染锰组Bax、CoxⅡ、GFAP基因表达比对照组增强,CoxⅣ基因表达比对照组减弱;低、高-PAS组Bax、CoxⅡ和高-PAS组GFAP基因表达均明显比染锰组降低(P<0.05);低、高-PAS组CoxⅣ基因表达比染锰组增强(P<0.05)。结论 PAS-Na对锰致大鼠学习记忆能力降低、海马细胞凋亡、线粒体功能紊乱和神经胶质细胞生长分化增多的基因表达异常有拮抗作用。
Objective To investigate the effect of sodium salicylate (PAS-Na) on learning and memory abilities, hippocampal apoptosis, mitochondrial function and glial growth and differentiation gene expression in sub-acutely infected rats. Methods Male rats were intraperitoneally injected with MnCl2.4H2O (ip) 15 mg / kg ip for 5 days per week for 4 weeks. Then, PAS-Na100 (low-PAS) or 200 (high-PAS) mg / kg were injected subcutaneously daily for 3 or 6 weeks. The learning and memory abilities of rats were detected by Morris water maze and the mRNA expression of Bax, CoxⅡ, CoxⅣ and GFAP in hippocampus was detected by Real-Time PCR (RT-PCR). Results During the observation period of 7 weeks, the escape latency of the manganese-treated group on the fifth day of the test was longer than that of the control group and the latency of swimming in the low-PAS group (P <0.05). Compared with the control group, the expression of Bax, CoxⅡand GFAP in Mn-Zn group was significantly increased (P <0.05), while the expression of CoxⅣ gene was lower than that in the control group (P <0.01). During the observation period of 10 weeks, on the 4th day of the test, the escape latency of the manganese-treated group was longer than that of the control group, and the swimming distance was shorter than that of the control group (P <0.05). Compared with the control group, the expression of Bax, CoxⅡ and GFAP in Mn-Zn group was enhanced and the expression of CoxⅣ gene was weaker than that in the control group. The GFAP gene expression in Bax, CoxⅡ and Hyp-PAS group was significantly lower than that in Mn-Mn group in low and high-PAS groups (P < 0.05). The mRNA expression of CoxⅣ in low and high-PAS groups was significantly higher than that in manganese group (P <0.05). CONCLUSION: PAS-Na can inhibit the learning and memory ability of rats induced by manganese and antagonize the abnormal gene expression of hippocampal apoptosis, mitochondrial dysfunction and increased glial cell growth and differentiation.