The combination of piR-823 and EIF3B increased TGF-β1 expression, which activates HSCs in liver fibrosis. piR-823 may be a new target in the treatment of liver fibrosis.
These results suggest that TGF-β1-induced autophagy is required for the fibrogenic response in LX-2 cells and that ASPP2 may both inhibit TGF-β1-induced autophagy and decrease liver fibrosis.
This study focused on the effects of evodiamine on carbon tetrachloride (CCl<sub>4</sub>)-induced liver fibrosis in rats and HSCs in vitro via the TGF-β1/Smad signaling pathway.
The probable modes of action of these plants include immunomodulation, stimulation of hepatic DNA synthesis, simulation of superoxide dismutase and glutathione reductase to inhibit oxidation in hepatocytes, reduction of intracellular reactive oxygen species by enhancing levels of antioxidants, suppression of ethanol-induced lipid accumulation, inhibition of nucleic acid polymerases to downregulate viral mRNA transcription and translation, free radical scavenging and reduction of hepatic fibrosis by decreasing the levels of transforming growth factor beta-1, and collagen synthesis in hepatic cells.
We conclude that Cav1 is an important inhibitor of TGF-β1/Smad signaling in HSCs activation and collagen production, which might make it a promising target for therapy of liver fibrosis.
Furthermore, gmNK1 inhibited protein expression levels of fibrosis-related type I collagen (Col I) and α-smooth muscle actin (α-SMA) genes in TGF-β1-activated HSC-T6 cells and CCl<sub>4</sub>-induced liver fibrosis in rat.
The present study aimed to investigate the protective effects of OCT on carbon tetrachloride (CCl<sub>4</sub>)-induced rat liver fibrosis and activation and proliferation of transforming growth factor-β1 (TGF-β1)-treated hepatic stellate cells (HSCs) and explore its anti-hepatofibrotic mechanisms.
Vitamin D plays a critical role in the development of liver fibrosis as it inhibits transforming growth factor β1 (TGFβ1)-induced excessive deposition of ECM in activated hepatic stellate cells (HSCs).
Exposure to environmental levels of Phe decreased body weight and liver-somatic index; impaired histology of liver; influenced the peroxisome proliferator-activated receptor gamma (PPARγ) signaling and lipid metabolism in liver; stimulated oxidative stress in the rats' liver; induced the variation of NFκB pathway and liver inflammatory response; and caused liver fibrosis via transforming growth factor β1 (tgfβ1).
Hepatic stellate cell (HSC) line CFSC-8B was stimulated by transforming growth factor β1 (TGF-β1) or platelet-derived growth factor BB (PDGF-BB) to induce liver fibrosis in vitro.
These results demonstrated that TGFβ-1 receptor inhibitor improved the repair potential of hUC-MSCs against hepatic injury through TGFβ-1/Smad pathway, which contributed to improving the therapeutic efficiency of liver fibrosis.
Furthermore, IGFBPrP1 likely participates in liver fibrosis in a TGFβ1-depedent manner, and may act as an upstream regulatory factor of TGFβ1 in the Smad pathway.
Both the in vitro and in vivo results clearly showed that, morin by acting on Hippo/Yap and TGF-β1/Smad pathways, ameliorated experimental liver fibrosis, indicating that morin has potential for effective treatment of liver fibrosis.
These results suggested that CT6 inhibited HSC-T6 activation induced by TGF-β1, indicating the potential therapeutic effect of these extracts against liver fibrosis.
The results of this proof-of-concept study suggest that active immunization against TGF-β1 is a worthwhile strategy to pursue in efforts to prevent hepatic fibrosis associated with chronic liver disease.
These data indicates that metformin could mitigate CCl<sub>4</sub>-induced liver fibrosis and these beneficial effects might result from suppressed TGF-β1/Smad3 signaling.
Quercetin attenuated liver damage by suppressing the TGF-β1/Smads signaling pathway and activating the PI3K/Akt signaling pathway to inhibit autophagy in BDL- or CCl<sub>4</sub>- induced liver fibrosis.
We analyzed miR-200a regulation of SIRT1 expression in CCl<sub>4</sub>-induced liver fibrosis and TGF-β1-mediated activation of HSC. miR-200a, SIRT1, α-SMA, Col1A1, Notch1 and NICD expression were estimated by Western blotting, qRT-PCR and Immunohistochemistry.
This study explored the effects of CGA on miR-21-regulated TGF-β1/Smad7 liver fibrosis in the hepatic stellate LX2 cell line and in CCl4-induced liver fibrosis in Sprague-Dawley rats.