Cathepsin L aggravated kidney injury by activating PKC signal in TCE-sensitized mice
10.19405/j.cnki.issn1000-1492.2022.07.019
- Author:
Yican Wang
1
;
Yiting Hong
1
;
Meng Huang
1
;
Jiaxiang Zhang
1
;
Feng Wang
2
;
Jiale Peng
1
;
Qixing Zhu
3
,
4
Author Information
1. Dept of Occupational Hygiene and Environmental Hygiene，School of Public Health，Anhui Medical University，Hefei 230032
2. Dept of Dermatology，The Second Affiliated Hospital of Anhui Medical University，Hefei 230601
3. Dept of Occupational Hygiene and Environmental Hygiene，School of Public Health，Anhui Medical University，Hefei 230032
4. Institute of Dermatology，the First Affiliated Hospital of Anhui Medical University，Hefei 230022
- Publication Type:Journal Article
- Keywords:
trichloroethylene;
occupational medicamentosa-like dermatitis due to trichloroethylene;
cathepsin L;
protein kinase C;
kidney damage
- From:
Acta Universitatis Medicinalis Anhui
2022;57(7):1116-1121
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the mechanism of cathepsin L(CTSL)-mediated kidney injury in trichloroethene(TCE)-sensitized mice.
Methods:41 BALB/C mice were randomly divided into blank group(n=5), solvent group(n=5), TCE treatment group(n=15) and TCE+CTSLi treatment group(n=16). TCE percutaneous sensitization mouse model was established, and the mice were evaluated as positive group and negative group according to skin sensitization score. The renal pathology of mice was observed by electron microscopy and HE staining, the renal function level of mice was assessed by serum urea nitrogen(BUN). The expression of CTSL was detected by immunofluorescence, the apoptosis of renal cells was assessed by TUNEL staining, and the activation of renal protein kinase C(PKC) signal molecule was detected by Western blot.
Results:The sensitization rates of TCE treatment group and TCE+CTSLi treatment group were 53.3%(8/15) and 50.0%(8/16), respectively, and there was no statistical difference in sensitization rates(P>0.05). Pathological results showed that TCE sensitized-mice showed edema and vacuolar degeneration of renal tubular cells, thickening of glomerular basement membrane, fusion of podocytes and mitochondria vacuolar degeneration. The results of renal function showed that the serum BUN level of TCE sensitized mice was higher than that of other groups. Immunofluorescence results showed that the expression level of CTSL in the kidney of TCE-sensitized positive mice increased(P<0.05,F=82.438), and the apoptosis level of renal structure cells was also higher than that of other groups(P<0.05). Western blot showed that the phosphorylation of PKC protein in the kidney of TCE-sensitized mice increased, while the expression of PKC protein in TCE+CTSLi sensitized mice was down-regulated after CTSLi pretreatment(P<0.05,F=35.686), the level of renal cell apoptosis decreased, and renal damage was improved.
Conclusion:CTSL might aggravate renal damage via activation of PKC signaling in TCE-sensitized mouse.
- Full text:2025022709244243667组织蛋白酶L激活PKC信号加重TCE致敏小鼠肾脏损害_王燚灿.pdf
