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机构地区:[1]贵阳医学院生理学教研室,贵州贵阳550004
出 处:《中国公共卫生》2013年第6期834-836,共3页Chinese Journal of Public Health
基 金:贵州省高层次人才科研条件特助经费(TZJF-2009-38)
摘 要:目的观察p38丝裂原活化蛋白激酶(p38MAPK)、核因子-κBp50(NF-κBp50)在肝纤维化发生发展中作用。方法选取SD大鼠30只,随机分为对照组、肝纤维化4、8周组,每组各10只;肝纤维化组按0.3 mL/100g皮下注射40%CCl4,隔3 d注射1次,造模时间分别为4和8周;于相应时间点处死大鼠并收集肝组织,观察肝组织病理学改变;采用比色法检测肝组织中丙二醛(MDA)及超氧化物歧化酶(SOD)含量;采用免疫组化及western blot检测肝组织中p38MAPK、NF-κBp50蛋白表达变化。结果与对照组比较,肝纤维化4周组大鼠肝组织中p38MAPK(7.9±2.3)、NF-κBp50(16.3±8.1)、MDA[(1.8±0.9)nmol/mgprot]及肝纤维化8周组大鼠肝组织中p38MAPK(11.5±6.8)、NF-κBp50(24.6±13.5)和MDA[(2.9±1.3)nmol/mgprot]的含量均升高(P<0.05);与对照组比较,肝纤维化4、8周组大鼠肝组织中SOD酶活性[(40.6±5.8)、(34.4±3.1)μ/mgprot]均降低(P<0.01)。结论p38MAPK、NF-κBp50及氧化应激可能在肝纤维化的发生发展过程中发挥重要作用。Objective To observe the changes of p38 mitogen-activated protein kinase(p38MAPK) and nuclear factor-κ Bp 50(NF-κBp50) in carbon tetrachloride(CCl4) induced liver fibrosis and to explore their effects on hepatic fibrosis.Methods Thirty Sprague-Dawley rats were randomly divided into normal control group,4 weeks liver fibrosis group and 8 weeks liver fibrosis group.Liver fibrosis model was induced by hypodermic injection of 40% CCl4 at the dosage of 0.3 ml/100 g body weight.The levels of malondialdehyde(MDA) and superoxide dismutase(SOD) in liver tissue were measured with colormtric method and the expressions of p38MAPK and NF-κBp50 protein were detected with immunohistochemical techniques and western blot.Results Compared with the normal control group,the levels of p38MAPK(7.9±2.3),NF-κBp50(16.3±8.1),and MDA(1.8±0.9 nmol/mgprot) in 4 weeks liver fibrosis group and the levels of p38MAPK(11.5±6.8),NF-κBp50(24.6±13.5),and MDA(2.9±1.3 nmol/mgprot) in 8 weeks liver fibrosis group were increased,while the activityies of SOD(40.6±5.8,34.4±3.1 u/mgprot) in 4 weeks and 8 weeks liver fibrosis groups were decreased.Conclusion p38MAPK,NF-κBp50 and oxidative stress may play important roles in CCl4 induced liver fibrosis.
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