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目的探讨蛋白激酶Cδ(PKCδ)在燃煤型砷中毒患者体内的表达及在肝损伤中的作用。方法于贵州省燃煤型砷中毒病区选择156例砷暴露者为砷暴露组,其中包括病区健康组(32例)、无明显肝病组(41例),轻度肝病组(39例),中重度肝病组(44例),选取非病区健康居民36例为非病区健康组。采集所有研究对象的尿液、外周血,测定尿砷含量及外周血PKCδmRNA表达水平,化学法检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、硫氧还蛋白还原酶(TrxR)活力和丙二醛(MDA)含量。结果非病区健康组、病区健康组、无明显肝病组、轻度肝病组、中重度肝病组尿砷含量为(18.92±3.51)、(20.12±3.84)、(46.39±5.47)、(67.98±7.64)、(75.19±8.92)μg/g,PKCδmRNA表达水平mRNA表达量(1.11±0.06)、(1.21±0.08)、(1.23±0.12)、(1.32±0.17)、(1.39±0.21),与非病区健康组、病区健康组、无明显肝病组相比,轻度肝病组与中重度肝病组的尿砷含量明显升高,PKCδmRNA表达水平增高,SOD、GSH-Px和TrxR活力均降低,MDA含量明显升高(P<0.05),尿砷含量与酶活力呈负相关,PKCδmRNA表达与酶活力呈负相关。结论燃煤砷可能通过调控PKCδ蛋白表达,调节机体氧化应激水平,导致燃煤砷中毒肝损伤的发生发展。
Objective To investigate the expression of protein kinase Cδ (PKCδ) in patients with coal-burning arsenism and its role in liver injury. Methods One hundred and sixty-five cases of arsenic exposure were selected as the arsenic-exposed group in Guizhou coal-fired arsenism area, including 32 cases of healthy group, 41 cases of no obvious liver disease, 39 cases of mild liver disease, , Moderate-severe liver disease group (44 cases), select non-ward healthy residents 36 cases of non-ward health group. Urine and peripheral blood was collected from all the subjects. Urinary arsenic levels and peripheral blood PKCδmRNA levels were measured. The levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) TrxR activity and malondialdehyde (MDA) content. Results The urinary arsenic contents in non-ward health group, ward health group, no obvious liver disease group, mild liver disease group and moderate-severe liver disease group were (18.92 ± 3.51), (20.12 ± 3.84), (46.39 ± 5.47), (67.98 (1.11 ± 0.06), (1.21 ± 0.08), (1.23 ± 0.12), (1.32 ± 0.17) and (1.39 ± 0.21), respectively, and (75 ± 8.92) μg / Compared with the non-ward healthy group, the ward healthy group and the non-obvious liver disease group, the urinary arsenic levels were significantly increased in mild hepatopathy group and moderate-severe liver disease group, the expression of PKCδmRNA increased, the activities of SOD, GSH-Px and TrxR decreased , MDA content was significantly increased (P <0.05), urine arsenic content and enzyme activity was negatively correlated, PKCδmRNA expression and enzyme activity was negatively correlated. Conclusion Burning coal arsenic may regulate the expression of PKCδ protein and regulate the level of oxidative stress in the body, resulting in the occurrence and development of hepatic injury induced by burning coal with arsenic poisoning.