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Resveratrol attenuates lipopolysaccharide‐induced acute kidney injury by suppressing inflammation driven by macrophages
Author(s) -
Chen Liang,
Yang Sixing,
Zumbrun Elizabeth E.,
Guan Hongbing,
Nagarkatti Prakash S.,
Nagarkatti Mitzi
Publication year - 2015
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201400819
Subject(s) - resveratrol , inflammation , lipopolysaccharide , pharmacology , acute kidney injury , medicine , kidney , sepsis , cytokine , immunology
Scope Acute kidney injury (AKI) is the most frequent and serious complication in sepsis, a potentially deadly inflammatory response induced by bacterial, viral, or fungal infection. LPS‐induced AKI is associated with an abnormal inflammatory response, including renal endothelial dysfunction and renal inflammation. Resveratrol, a natural phytoalexin with low toxicity and anti‐inflammatory properties, is known to protect endothelial cells and modulate the immune response in sepsis. Methods and results This study investigates the potential protective effects of resveratrol on AKI induced by LPS exposure of mice. Resveratrol was administered as a pre‐ and posttreatment, or as a posttreatment alone following LPS injection and compared to control groups. Resveratrol significantly improved kidney function and lowered serum and kidney tissue inflammatory cytokine levels. Consistently, resveratrol prevented endotoxin‐induced disruption of endothelial cell permeability and inhibited inflammation of kidney tissue. Resveratrol treatment attenuated the effects of LPS on macrophages, with significant inhibition of activation, cytokine release, and Toll‐like receptor 4 activation. Resveratrol treatment also resulted in decreased expression of iNOS, Bcl‐2, and Bcl‐xL in macrophages, which was linked with induction of apoptosis in macrophages. Conclusion Our studies suggest that resveratrol might represent a novel therapeutic agent to prevent and treat sepsis‐induced AKI.