1. Emodin weakens liver inflammatory injury triggered by lipopolysaccharide through elevating microRNA-145 in vitro and in vivo.
- Author
-
Xie R, Liu M, and Li S
- Subjects
- Animals, Apoptosis drug effects, Apoptosis genetics, Chemical and Drug Induced Liver Injury metabolism, Chemical and Drug Induced Liver Injury pathology, Emodin therapeutic use, Female, Inflammation chemically induced, Inflammation genetics, Inflammation pathology, Liver drug effects, Liver metabolism, Liver pathology, Male, NF-kappa B metabolism, Rats, Rats, Wistar, Chemical and Drug Induced Liver Injury drug therapy, Chemical and Drug Induced Liver Injury genetics, Emodin pharmacology, Lipopolysaccharides adverse effects, MicroRNAs genetics
- Abstract
Hepatitis is a severe liver disease with worldwide distribution. This study explored the anti-inflammatory influence of Emodin on LPS-triggered liver injury in vitro and in vivo. In vitro, we discovered that LPS treatment triggered L-02 cell and primary hepatocyte inflammatory injury. Emodin weakened the LPS-triggered cell inflammatory injury and NF-κB pathway activation. Emodin alleviated LPS-stimulated decrease of miR-145 expression. Moreover, miR-145 participated in the regulation of pro-inflammatory factors expression and negatively regulated IRAK1. Besides, IRAK1 exert regulatory roles in the activation of NF-κB pathway. In vivo, we found that Emodin pre-treatment weakened the LPS-triggered increases of pro-inflammatory factors expression, up-regulations of AST and ALT level, liver cell apoptosis, reduction of miR-145 and enhancement of IRAK1. Our research verified that Emodin weakened LPS-triggered liver cell inflammatory injury in vitro and in vivo might be achieved by elevating miR-145, decreasing IRAK1 and then suppressing NF-κB pathway.
- Published
- 2019
- Full Text
- View/download PDF