Effect of emodin on renal tubular epithelial cell injury and inflammatory respons
10.3760/cma.j.issn.1673-4246.2019.10.013
- VernacularTitle: 大黄素对肾小管上皮细胞损伤及炎症反应的影响
- Author:
Yiran LIU
1
;
Yuqin ZHANG
;
Qizheng ZHU
;
Hongxu ZHANG
Author Information
1. Department of Nephrology, Anhui No.2 Provincial People’s Hospital, Hefei 230000, China
- Publication Type:Journal Article
- Keywords:
Emodin;
Epithelial cells;
Acute kidney injury;
Inflammation;
Oligonucleotide receptor protein 3
- From:
International Journal of Traditional Chinese Medicine
2019;41(10):1091-1095
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of emodin on lipopolysaccharide (LPS)-induced inflammation and damage in HK-2 cells.
Methods:The HK-2 cells were divided into blank group, emodin group, LPS group, and LPS+emodin group. The emodin group was treated with culture medium containing 0.5 μg/ml emodin, the LPS group was treated with culture medium containing 10 μg/ml LPS, the LPS+emodin group was treated with culture medium containing both 0.5 μg/ml emodin and 10 μg/ml LPS, and the blank group was cultured with fresh medium. Twelve hours later, HK-2 cells from each group were harvested for the analysis. The mRNA levels of oligonucleotide receptor protein 3 (NLRP3), IL-1β, IL-18, TNF-α, and neutrophil gelatinase-associated lipocalin (NGAL) in each group were determined by RT-PCR.
Results:Compared to the blank group, the mRNA levels of NLRP3 (2.74 ± 0.38 vs. 1.00 ± 0.14), IL-1β (2.40 ± 0.33 vs. 1.00 ± 0.19), and IL-18 (3.00 ± 0.42 vs. 1.00 ± 0.07), NGAL (31.73 ± 3.41 vs. 1.00 ± 0.07), and TNF-α (9.73±1.60 vs. 1.00 ± 0.11) significantly increased by LPS stimulation (P<0.05). Compared to the LPS group, the mRNA expression of NLRP3 (1.98 ± 0.24 vs. 2.74 ± 0.39), IL-1β (1.54 ± 0.24 vs. 2.40 ± 0.33), and IL-18 (2.09 ± 0.53 vs. 3.00 ± 0.42), NGAL (16.76 ± 1.72 vs. 31.73 ± 3.41) and TNF-α (9.73 ± 1.60 vs. 4.65 ± 1.09) in HK-2 cells of LPS+emodin group significantly decreased (P<0.05).
Conclusions:The emodin protects HK-2 cells from LPS-induced damage and inflammation by inhibiting NLRP3 inflammasome activation.
