Role of kallikrein kinin system activation in kidney injury induced by trichloroethylene sensitized mice
10.3760/cma.j.issn.1001-9391.2016.03.006
- VernacularTitle:激肽释放酶激肽系统活化在三氯乙烯致敏小鼠肾脏损伤中的作用
- Author:
Min LIU
1
;
Cheng ZHANG
;
Peng YANG
;
Jian HUANG
;
Dandan ZANG
;
Jiaxiang ZHANG
;
Qixing ZHU
Author Information
1. 安徽医科大学公共卫生学院职业卫生与环境卫生学系
- Keywords:
Trichloroethylene;
Kallikrein-kinin system;
Blood urea nitrogen
- From:
Chinese Journal of Industrial Hygiene and Occupational Diseases
2016;34(3):184-188
- CountryChina
- Language:Chinese
-
Abstract:
Objective Through testing the expression of complement C3 fragment C3b and iC3b,C5b-9 as well as indexes of KKS before and after using kallikrein-kinin system inhibitor PKSI-527,observing the relevant between KKS and complement system,we preliminary study on the mechanism how KKS works on the renal injury of sensitized mice model induced by trichloroethylene.Methods Female BALB/c mice (6～8 weeks) were randomly divided into blank control group (5),TCE treated group (15),PKSI-527+TCE treated group (15).Mice were sensitized with TCE in the 1,3,7,10 days,the first and the last challenge were on day 17 and 19.24h before every challenge,mice in PKSI-527 +TCE group were treated with intraperitoneal injection of KKSinhibitor PKSI-527 inhibitor (50mg/kg).Mice were killed 72h after the last challenge.The function of kidney in mice were detected and kidney B1R,B2R expression were detected using real-time quantitative PCR,mice kidney complement C3 fragments C3b,iC3b and C5b-9 deposition were also detected by chemoimmunology.Results Compared with blank control group,all indexes expressions in the solvent control group have no significant change.Compared with the solvent control group,BUN、Cr level and B1R、B2R level have an significant increase (P＜ 0.05) in TCE sensitized group and PKSI-527+TCE sensitized group;There is a sharp decrease in PKSI-527+TCE sensitized group compared to TCE sensitized group (P＜ 0.05).Conclusion The renal damage in the TCE sensitization mouse model may aggravated by upregulate complement system followed by the activation of kallikrein-kinin system.
