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Spironolactone rescues renal dysfunction in obstructive jaundice rats by upregulating ACE2 expression
Er-Liang Kong1, Jin-Min Zhang1, Ni An1
1Department of Anesthesiology & Intensive Care, Shanghai Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, Shanghai, 200438, China.
Journal of Cell Communication and Signaling
|June 9, 2018
Summary
Obstructive jaundice in rats impairs kidney function and reduces angiotensin-converting-enzyme-2 (ACE2) expression. Spironolactone treatment improved renal function, reduced fibrosis, and increased ACE2 levels, highlighting its therapeutic potential.
Area of Science:
- Nephrology
- Endocrinology
- Gastroenterology
Background:
- Postoperative acute renal failure is a serious complication of obstructive jaundice, with unclear mechanisms.
- The renin-angiotensin-aldosterone system (RAAS) is implicated in renal disease, and angiotensin-converting-enzyme-2 (ACE2) acts as a renal protector.
- Understanding ACE2's role and the effects of spironolactone is crucial for managing obstructive jaundice-induced renal injury.
Purpose of the Study:
- To investigate the role of ACE2 in obstructive jaundice (OJ)-induced renal injury in rats.
- To evaluate the therapeutic effect of spironolactone on renal function and ACE2 expression in OJ rats.
- To explore the correlation between ACE2 expression and renal injury markers.
Main Methods:
- Obstructive jaundice was induced in rats via bile duct ligation.
- Kidney tissue and serum samples were analyzed for total bilirubin, serum creatinine, and ACE2 expression.
- Levels of RAAS components (renin, AngII, Ang-(1-7), aldosterone) and ICAM-1 were measured post-spironolactone treatment.
- Renal histology was assessed using HE and Masson staining to evaluate necrosis, inflammation, and fibrosis.
Main Results:
- Obstructive jaundice led to increased total bilirubin and serum creatinine, with decreased renal ACE2 expression.
- Spironolactone intervention altered RAAS component expression, reduced renal necrosis, inflammation, and fibrosis.
- ACE2 mRNA expression showed a moderate negative correlation with total bilirubin and serum creatinine levels.
- Spironolactone treatment upregulated ACE2 expression and improved renal function in OJ rats.
Conclusions:
- The RAAS plays a significant role in renal damage associated with obstructive jaundice.
- Spironolactone effectively ameliorates renal fibrosis and dysfunction in obstructive jaundice by upregulating ACE2 expression.
- Targeting ACE2 and utilizing spironolactone may offer a promising therapeutic strategy for obstructive jaundice-induced renal injury.
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