Role of inflammation induced by the novel immunosuppressant caerulomycin A in kidney inj ury
10.19405/j.cnki.issn1000-1492.2023.09.001
- Author:
Runrun Shan
1
;
Jutao Yu
2
;
Manman Xie
1
;
Xiufeng Luo
1
;
Chunya Xie
1
;
Zongyu Cui
3
;
Xiaoying Liu
1
;
Qi Chen
1
Author Information
1. College of Life Sciences , Anhui Medical University, Hefei 230032
2. School of Pharmacy, Anhui Medical University, Hefei 230032
3. Second Clinical Medical College , Anhui Medical University, Hefei 230032
- Publication Type:Journal Article
- Keywords:
caerulomycin A;
cellular damage;
cellular inflammation;
drug nephrotoxicity
- From:
Acta Universitatis Medicinalis Anhui
2023;58(9):1429-1434
- CountryChina
- Language:Chinese
-
Abstract:
Objective : To investigate the effect of high concentration of Caerulomycin A (Cae A) on HK2 in renal tubular epithelial cells and to explore the role of cytoplasmic nucleotide⁃binding oligomerization domain⁃like receptor protein 3 (NLRP3) in this process.
Methods : The effect of different concentrations of Cae A on the viability of HK2 cells was determined by MTT; the expression of kidney injury molecule (KIM⁃1) and NLRP3 was detected by real⁃time quantitative PCR , Western blot and immunofluorescence , while the effect of Cae A on the mRNA expression of IL⁃1β , IL⁃18 , IL⁃33 , MCP⁃1 , TNF⁃α was also measured by real⁃time quantitative PCR. HK2 cells were divided into control group , high concentration of Cae A group and high concentration of Cae A plus NLRP3 inhibitor
CY⁃09 group , and the expression of KIM⁃1 and NLRP3 protein was detected by Western blot.
Results :The results of MTT showed that high concentration of Cae A could inhibit HK2 cell viability. Real⁃time quantitative PCR , Western blot and immunofluorescence assays showed that high concentration of Cae A upregulated the expression of KIM⁃1 and NLRP3 , as well as the mRNA levels of IL⁃1β , IL⁃18 , IL⁃33 , MCP⁃1 , TNF⁃α , while CY⁃09 could down⁃regulate the expression of NLRP3 and KIM⁃1.
Conclusion : High concentration of Cae A significantly inhibited the viability of HK2 cells and induced damage and inflammatory response to HK2 with some nephrotoxicity that might be achieved via NLRP3 pathway.
- Full text:2024071611154187334新型免疫抑制剂浅蓝霉素A诱导肾损伤炎症的作用_单润润.pdf
