Dietary Flavonoid Hyperoside Induces Apoptosis of Activated Human LX-2 Hepatic Stellate Cell by Suppressing Canonical NF-κB Signaling.
Li-Wen WangZhiwei YueMengzheng GuoLianying FangLiang BaiXinyu LiYongqing TaoSuying WangQiang LiuDexian ZhiHui ZhaoPublished in: BioMed research international (2016)
Hyperoside, an active compound found in plants of the genera Hypericum and Crataegus, is reported to exhibit antioxidant, anticancer, and anti-inflammatory activities. Induction of hepatic stellate cell (HSC) apoptosis is recognized as a promising strategy for attenuation of hepatic fibrosis. In this study, we investigated whether hyperoside treatment can exert antifibrotic effects in human LX-2 hepatic stellate cells. We found that hyperoside induced apoptosis in LX-2 cells and decreased levels of α-smooth muscle actin (α-SMA), type I collagen, and intracellular reactive oxygen species (ROS). Remarkably, hyperoside also inhibited the DNA-binding activity of the transcription factor NF-κB and altered expression levels of NF-κB-regulated genes related to apoptosis, including proapoptotic genes Bcl-Xs, DR4, Fas, and FasL and anti-apoptotic genes A20, c-IAP1, Bcl-X L , and RIP1. Our results suggest that hyperoside may have potential as a therapeutic agent for the treatment of liver fibrosis.
Keyphrases
- induced apoptosis
- oxidative stress
- endoplasmic reticulum stress
- signaling pathway
- cell cycle arrest
- transcription factor
- pi k akt
- dna binding
- reactive oxygen species
- cell death
- anti inflammatory
- liver fibrosis
- smooth muscle
- endothelial cells
- dna damage
- genome wide
- genome wide identification
- lps induced
- single cell
- induced pluripotent stem cells
- poor prognosis
- cell therapy
- bioinformatics analysis
- dna methylation
- pluripotent stem cells
- inflammatory response
- bone marrow
- stem cells
- smoking cessation
- binding protein
- high resolution
- single molecule
- editorial comment
- mass spectrometry
- atomic force microscopy