Paeoniflorin alleviates cisplatin and lansoprazole-induced acute kidney injury by inhibiting necroptosis
10.19405/j.cnki.issn1000-1492.2025.11.015
- VernacularTitle:芍药苷通过抑制程序性坏死 减轻顺铂及兰索拉唑诱导的急性肾损伤
- Author:
Qi Xu
1
;
Xiaomei Luo
1
;
Wei Zhu
1
;
Yuanyuan Li
1
;
Yonggui Wu
1
Author Information
1. Dept of Nephropathy , The First Afiliated Hospital of Anhui Medical University , Hefei 230022
- Publication Type:Journal Article
- Keywords:
acute kidney injury;
lansoprazole;
cisplatin;
paeoniflorin;
necroptosis;
renal tubular epithelial cells
- From:
Acta Universitatis Medicinalis Anhui
2025;60(11):2096-2105
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of paeoniflorin (Pae) on acute kidney injury ( AKI) and mouse renal tubular epithelial cell ( mRTEC) damage induced by lansoprazole (LPZ) and cisplatin (CIS) through in vivo and in vitro experiments .
Methods :The C57BL/6J mice or mRTECs were divided into four groups : normal control (NC) group , NC + LPZ group , CIS group , and CIS + LPZ group . Serum creatinine (CRE) and blood urea nitro- gen (BUN) levels in mice were measured , and kidney pathology was observed with HE staining. Western blot , im- munohistochemistry , and immunofluorescence were used to detect the expression levels of kidney injury molecule-1 (KIM-1) and receptor-interacting protein kinase (RIPK) 1 , RIPK3 , and mixed lineage kinase domain-like protein (MLKL) . Subsequently , C57BL/6J mice or mRTECs were divided into six groups : NC group , NC + Pae group , CIS + LPZ (M) group , and CIS + LPZ + Pae ( M + Pae) group . Serum CRE and BUN levels in each group were measured , kidney pathology was observed with HE staining , and ultrastructural changes in the kidney were observed with transmission electron microscopy. The KIM-1 and necroptosis-related protein expression levels were detected by Western blot , immunohistochemistry , and immunofluorescence .
Results:Compared with the NC group , CRE and BUN levels were elevated in the CIS group , and these levels were further increased after LPZ in- tervention (all P < 0. 001) . Compared with the CIS group , renal tubular dilation and brush border loss were evi- dent in the CIS + LPZ group based on HE staining of kidney tissue (P < 0. 001) . Compared with the NC group , the expression levels of KIM-1 , RIPK1 , RIPK3 , and MLKL in the renal tissues of mice in the CIS group increased ( all P < 0. 001) , and compared with the CIS group , The expression levels of KIM-1 , RIPK1 , RIPK3 and MLKL in the renal tissues of mice in the CIS + LPZ group increased (all P < 0. 001) . After Pae treatment , compared with group M , the expression levels of CRE , BUN , KIM-1 , RIPK1 , RIPK3 and MLKL in each group of mice decreased significantly and in a dose-dependent manner (all P < 0. 001) .
Conclusion:LPZ promotes CIS-induced AKI by enhancing necroptosis in renal tubular epithelial cells , and Pae can improve CIS and LPZ-induced AKI by inhibi- ting necroptosis .
- Full text:2026030511203774168芍药苷通过抑制程序性坏死减轻顺铂及兰索拉唑诱导的急性肾损伤_徐起.pdf
