Protective Effect of Epigallocatechin Gallate on Acute Kidney Injury Induced by Lipopolysaccharide in Rats via TLR4/Myd88/NF-κB Pathway / 中国医科大学学报

ABSTRACT

Objective To evaluate the protective effect of epigallocatechin gallate (EGCG) on lipopolysaccharide (LPS) -induced acute kidney injury (AKI) in rats and its underlying mechanisms. Methods Sprague-Dawley rats were randomly divided into the Sham group, AKI group, EGCG group and TLR4 group (n = 10 each). To establish the rat model of endotoxemia, serum creatinine (Cr) and urea nitrogen (BUN) levels were detected by biochemical assays; serum interlukin (IL) -6, IL-1β, IL-10, and TNF-α levels were detected by ELISA; kidney histopathology was examined by hematoxylin and eosin (HE) staining method; and expression of TLR4, Myd88 and nuclear factor-kappa B (NF-κB) in rat kidneys at both protein and mRNA levels was detected by Western blotting and qRT-PCR, respectively.Results Kidney injury increased significantly in AKI group compared to the sham group. Serum Cr, BUN, IL-6, IL-1β, and TNF-α levels significantly increased whereas IL-10 levels significantly decreased in AKI group compared to the sham group. Expression levels of TLR4, Myd88, and NF-κB also significantly increased at both protein and mRNA levels in AKI group compared to the sham group. Treatment with EGCG prior to induction of LPS-mediated AKI conferred protection against AKI by significantly reducing the expression of inflammatory markers such as, TLR4, Myd88, and NF-κB. Given TLR4 inhibitor based on this, the protective effect of EGCG on AKI was via inhibition of the TLR4/Myd88/NF-κB pathway. Conclusion EGCG exhibited a protective effect against LPS-induced AKI by inhibiting the activation of TLR4/Myd88/NF-κB pathway.