Effect of curcumin on glycerol-induced acute kidney injury in rats

Jindao Wu,Daorong Hou,Qin Chen,Yuan Zheng,Dan Bao,Youjin Dai,Xiongxiong Pan,Yuan Yin,Heling Fu,Qingting Hao

doi:10.1038/s41598-017-10693-4

Abstract

The aim of this study was to investigate the protective role and underlying mechanisms of curcumin on glycerol-induced acute kidney injury (AKI) in rats. Glycerol (10 ml/kg BW, 50% v/v in sterile saline, i.m.) was used to induce AKI, followed by curcumin (200 mg/kg/day, p.o.) administration for 3 days. To confirm renal damage and the effects of curcumin on AKI, serum BUN, Scr, and CK as well as renal SOD, MDA, GSH-Px were measured. Additionally, morphological changes were identified by H&E staining and transmission electron microscopy. The expression of several factors including chemotactic factor MCP-1, proinflammatory cytokines including TNF-α and IL-6, as well as the kidney injury markers, as Kim-1 and Lipocalin-2 were also assessed using q-PCR. Finally, cell apoptosis in renal tissue was detected using in situ TUNEL apoptosis fluorescence staining and expression of proteins associated with apoptotic, oxidative stress and lipid oxidative related signaling pathways were detected using immunohistochemical staining and western blot. The results showed that curcumin exerts renoprotective effects by inhibiting oxidative stress in rhabdomyolysis-induced AKI through regulation of the AMPK and Nrf2/HO-1 signaling pathways, and also ameliorated RM-associated renal injury and cell apoptosis by activating the PI3K/Akt pathway.

Highlights

Acute kidney injury (AKI) is a syndrome characterized by an acute loss of renal function, and is associated with increased mortality, prolonged hospital stays and accelerated chronic kidney disease[1]
There was no significant difference in serum urea and creatinine levels between the acute kidney injury (AKI) and CO + AKI (AKI treated with corn oil) groups
Curcumin treatment resulted in a significant reduction in blood urea nitrogen (BUN), serum creatinine (Scr) and ceatine kinase (CK) levels in CUR + AKI (AKI treated with curcumin) group compared with the AKI and CO + AKI groups, respectively (p < 0.01)

Summary

Introduction

Acute kidney injury (AKI) is a syndrome characterized by an acute loss of renal function, and is associated with increased mortality, prolonged hospital stays and accelerated chronic kidney disease[1]. Despite the reversibility of the loss of renal function in most patients who survive, the mortality of AKI remains alarmingly high (over 50%)[3, 4] and to date, no effective therapies to prevent or treat AKI exist. Myoglobin-induced renal toxicity plays a key role in RM-associated AKI by increasing oxidative stress, inflammation, endothelial dysfunction, vasoconstriction, and apoptosis[10]. The protective role and underlying mechanisms of curcumin on glycerol-induced AKI in rats were investigated

Objectives

Methods

Results

Conclusion