Protective Effect of Epigallocatechin Gallate on Acute Kidney Injury Induced by Lipopolysaccharide in Rats via TLR4/Myd88/NF-κB Pathway
10.12007/j.issn.0258-4646.2019.02.004
- VernacularTitle:TLR4/Myd88/NF-κB通路介导表没食子儿茶素没食子酸酯对脓毒血症大鼠急性肾损伤的保护作用
- Author:
Muzi LI
1
;
Keyan CHEN
;
Qian SUN
;
Yuhua QIU
Author Information
1. 辽宁省金秋医院肾内科
- Keywords:
pigallocatechin gallate;
acute kidney injury;
TLR4;
nuclear factor-kappa B;
lipopolysaccharide
- From:
Journal of China Medical University
2019;48(2):109-113
- CountryChina
- Language:Chinese
-
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.
