肺气虚模型大鼠介导TNF-α-MAPK信号途径对肾AQP2表达的影响

Influence of Kindey Tissue ΑQP2 by TNF-α-MΑPK Signαling on Lung-Qi Deficency Rats

目的:通过观测肺气虚大鼠血浆中肿瘤坏死因子(TNF-α)含量,肾组织水通道蛋白2(AQP2),丝裂原激活蛋白激酶(p38MAPK)和核因子-κB(NF-κBp65)表达的变化,探讨中医藏象中肺与肾在水液代谢之间关系的现代科学内涵。方法:将SPF级健康雄性Wistar大鼠20只随机分为正常组和模型组,采用ELISA法检测血浆TNF-α含量、Western法检测肾组织AQP2、免疫组化法检测肾组织p38MAPK和NF-κB p65表达变化。结果:与正常组比较,模型组血浆中TNF-α含量升高,肾组织AQP2、p38MAPK和NF-κB p65表达上调(P<0.01)。结论:肺气虚状态下肾组织AQP2表达变化可能是通过TNF-α-MAPK信号转导途径实现的。

To investigate the levels of tumor necrosis factor （ TNF- α） in plasma, kidney aquaporin 2 （ AQP2 ）, mitogenactivated protein kinase （ p38MAPK ）and nuclear factor- κ B （ NF- κ Bp65 ） expression changes in LungQi deficiency rat, reasearch the modern science content in water metabolism of the relationship between lung and kindey. Method： The SPF level of 20 healthy male Wistar rats wererandomly divided into normal group and model group, detected by ELIS A in TNF- α levels, Western detect kindey AQP2, immunohistochemical detection of kindey p38MAPK and NF- K B p65 expression change. Resuhs： Compared with normal group, model group TNF-a levels increased, kindey AQP2 expression increased, p38MAPK and NF- κ B p65 expression increased （ P〈0.01 ）. Conclusion ： High expression of kindey AQP2 in Lung-Qi Deficency state may be through TNF- α -MAPK signal transduction pathway.