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目的探讨镍冶炼烟尘对大鼠肺组织细胞凋亡相关蛋白p-JNK、Bax、Caspase-9和Caspase-3表达水平的影响。方法健康Wistar雄性大鼠40只,随机分为5组:对照组及镍冶炼烟尘0.50、1.00、2.00、4.00 mg/kg组,第1天及第16天非暴露式气管内滴注受试尘,30 d处死。Hoechst33258法观察肺内细胞形态学改变;分光光度法测定肺组织匀浆中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)的含量;免疫印迹(Western blot)法检测肺细胞p-JNK、Bax、Caspase-9和Caspase-3蛋白表达水平。结果与对照组比较,各染毒组大鼠肺组织细胞凋亡率均增高,差异有统计学意义(P<0.05);4.00 mg/kg染毒组细胞出现胞核固缩碎裂等凋亡早期形态学特征;各染毒组大鼠肺组织中SOD、GSH-Px活力较对照组显著降低,MDA含量显著升高,差异有统计学意义(P<0.05);染毒组大鼠肺组织Bax蛋白表达均高于对照组(P<0.05),肺组织p-JNK、Caspase-9、Caspase-3蛋白表达水平显著高于对照组(P<0.05)。结论镍冶炼烟尘引起大鼠肺组织氧化损伤,同时促进p-JNK、Bax、Caspase-9和Caspase-3蛋白表达,最终产生凋亡。
Objective To investigate the effect of nickel smelt dust on the expression of apoptosis-related protein p-JNK, Bax, Caspase-9 and Caspase-3 in lung tissue of rats. Methods Forty healthy Wistar male rats were randomly divided into five groups: control group and nickel smelting dust 0.50, 1.00, 2.00, 4.00 mg / kg group. On day 1 and day 16, non-exposed intratracheal instillation of test dust , Died 30 days. Hoechst33258 method was used to observe the morphological changes of lung cells. The content of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in lung homogenate were measured by spectrophotometry. The expression of p-JNK, Bax, Caspase-9 and Caspase-3 in lung cells were detected by Western blot. Results Compared with the control group, the apoptotic rates of lung tissue in all the exposed groups were significantly increased (P <0.05). Apoptosis of the cells such as pyknosis was observed in the 4.00 mg / kg group Early morphological characteristics; the activity of SOD, GSH-Px in the lung tissue of each exposure group was significantly lower than that of the control group, MDA content was significantly increased, the difference was statistically significant (P <0.05); the lung tissue (P <0.05). The protein expressions of p-JNK, Caspase-9 and Caspase-3 in lung tissue were significantly higher than those in control group (P <0.05). Conclusion Nickel smelting dust can cause oxidative damage of lung tissue and promote the expression of p-JNK, Bax, Caspase-9 and Caspase-3 protein eventually resulting in apoptosis.