TGF-β1/Smad7 signaling pathway and cell apoptosis: Two key aspects of Selenium-biofortified soybean peptide attenuating liver fibrosis

2019 ◽  
Vol 63 ◽  
pp. 103583
Author(s):  
Weiwei Liu ◽  
Tao Hou ◽  
Xing Zhang ◽  
Hui He
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Cell Apoptosis ◽  
Key Aspects ◽  
Tgf Β1

Effects of Siniruangan Recipe on Proliferation, Apoptosis and Activation of Human Hepatic Stellate Cell Line LX-2

Pharmacology ◽  
2019 ◽  
Vol 104 (5-6) ◽  
pp. 342-351 ◽  
Author(s):  
Jinming Liu ◽  
Guorong Zhao ◽  
Bichen Ai ◽  
Yirong He ◽  
Ming Mei ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Cell Apoptosis ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Cell Activity ◽  
Relative Content ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Cell Counting ◽  
Tgf Β1

Background: Experimental and clinical evidence suggests that liver fibrosis is potentially reversible. Hepatic stellate cells (HSCs) play a key role in the development of hepatic fibrosis. Previous clinical applications and researches showed that Siniruangan recipe (SNRG) reversed liver fibrosis and even liver cirrhosis. This experimental study aimed to elucidate the effects of SNRG on the proliferation, apoptosis and activation of HSCs. Methods: The human HSCs line LX-2 was cultured with normal culture medium and multi-dose SNRG water decoction for 48 h. Cell Counting Kit-8 assay was used to detect the proliferation and cytotoxicity of LX-2 cells. Annexin V-FITC/PI double staining was performed to identify apoptotic cells. Immunofluorescence staining was used to determine the relative content of cleaved caspase-3, tissue inhibitor of metalloproteinase-1 (TIMP-1) and transforming growth factor-β1 (TGF-β1) in LX-2 cells. Western blot was used to detect the relative content of Bcl-2, Bax, α-smooth muscle actin, β-catenin and TIMP-1 protein expression in LX-2 cells. Results: The SNRG inhibited the proliferation of LX-2 and induced cell apoptosis through caspase-dependent and mitochondrial-dependent pathways. SNRG may inhibit the activation of LX-2 through the β-catenin pathway. The decrease in TIMP-1 and TGF-β1 protein induced by SNRG promoted the degradation of the extracellular matrix (ECM). Conclusions: SNRG induced LX-2 cell apoptosis, inhibited cell proliferation, decreased LX-2 cell activity and promoted the degradation of ECM in vitro, which may be important mechanisms for reversing liver fibrosis and liver cirrhosis.

Role of MiR-146a in Cartilage Repair in Osteoarthritis of the First Metatarsophalangeal Joint by Influencing the TGF- β1/Smads Signaling Pathway

2020 ◽  
Vol 10 (4) ◽  
pp. 493-499
Author(s):  
Liming Wang ◽  
Juqing Guo ◽  
Chongbin Fang ◽  
Haibin Yan ◽  
Lukuan Du
Keyword(s):  
Signaling Pathway ◽  
Cartilage Repair ◽  
Cell Apoptosis ◽  
Transfection Efficiency ◽  
Metatarsophalangeal Joint ◽  
Inflammatory Factors ◽  
Serum Samples ◽  
First Metatarsophalangeal Joint ◽  
Proliferation Activity ◽  
Tgf Β1

Objective: To investigate miR-146a's role in cartilage repair in osteoarthritis of the first metatarsophalangeal joint (OFMJ). Methods: The serum samples of 30 OFMJ patients diagnosed in our hospital and 30 healthy people receiving physical examination were enrolled. The expression of miR-146a in those subjects was measured by qRT-PCR. Articular cartilage cells were isolated and transfected with lentivirus to silence or overexpress miR-146a. RT-PCR was performed to detect the transfection efficiency and the content of inflammatory factors. CCK-8 assay was to test cell proliferation activity and TUNEL assay was to detect cell apoptosis. The expressions of genes and proteins related to apoptosis and the TGF- β1/Smads signaling pathway were determined by RTPCR and Western blotting. Results: The serum miR-146a level in the patients with osteoarthritis of the first metatarsophalangeal joint was decreased significantly (p < 0.05). miR-146a showed a high expression in mimics group and was significantly lower in inhibitors group. The content of inflammatory factors in miR-146a mimics group was significantly reduced compared with other two groups (p < 0.05), and significantly higher level of inflammatory factors was detected in miR-146a inhibitors group (p < 0.05) along with increased number of cells and proliferation activity (p < 0.05) as well as increased cell apoptosis (p < 0.05). Bcl-2 was upregulated in miR-146a mimics group and Caspase-3 level was decreased. The expression of TGF-β 1/Smads was elevated in miR146a inhibitors group. Conclusion: MiR-146a can participate in the cartilage repair in osteoarthritis of the first metatarsophalangeal joint possibly through regulating TGF-β1/Smads signaling pathway.

scholarly journals Indole-3-propionic Acid-aggravated CCl4-induced Liver Fibrosis via the TGF-β1/Smads Signaling Pathway

2021 ◽  
Vol 000 (000) ◽  
pp. 000-000
Author(s):  
Fei Liu ◽  
Changfeng Sun ◽  
Yuanfang Chen ◽  
Fei Du ◽  
Yuxiang Yang ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Propionic Acid ◽  
Tgf Β1

scholarly journals Dioscin alleviates alcoholic liver fibrosis by attenuating hepatic stellate cell activation via the TLR4/MyD88/NF-κB signaling pathway

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Min Liu ◽  
Youwei Xu ◽  
Xu Han ◽  
Lianhong Yin ◽  
Lina Xu ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Type I Collagen ◽  
Transforming Growth Factor ◽  
Stellate Cell ◽  
Pyrrolidine Dithiocarbamate ◽  
Type I ◽  
Tgf Β1

Abstract The present work aimed to investigate the activities and underlying mechanisms of dioscin against alcoholic liver fibrosis (ALF). In vivo liver fibrosis in mice was induced by an alcoholic liquid diet and in vitro studies were performed on activated HSC-T6 and LX2 cells treated with lipopolysaccharide. Our results showed that dioscin significantly attenuated hepatic stellate cells (HSCs) activation, improved collagen accumulation and attenuated inflammation through down-regulating the levels of myeloid differentiation factor 88 (MyD88), nuclear factor κB (NF-κB), interleukin (IL)-1, IL-6 and tumour necrosis factor-α by decreasing Toll-like receptor (TLR)4 expression both in vivo and in vitro. TLR4 overexpression was also decreased by dioscin, leading to the markedly down-regulated levels of MyD88, NF-κB, transforming growth factor-β1 (TGF-β1), α-smooth muscle actin (α-SMA) and type I collagen (COL1A1) in cultured HSCs. Suppression of cellular MyD88 by ST2825 or abrogation of NF-κB by pyrrolidine dithiocarbamate eliminated the inhibitory effects of dioscin on the levels of TGF-β1, α-SMA and COL1A1. In a word, dioscin exhibited potent effects against ALF via altering TLR4/MyD88/NF-κB signaling pathway, which provided novel insights into the mechanisms of this compound as an antifibrogenic candidate for the treatment of ALF in the future.

Synergistic anti-liver fibrosis actions of total astragalus saponins and glycyrrhizic acid via TGF-β1/Smads signaling pathway modulation

2016 ◽  
Vol 190 ◽  
pp. 83-90 ◽  
Author(s):  
Yuping Zhou ◽  
Xin Tong ◽  
Shuang Ren ◽  
Xiaoling Wang ◽  
Jiamei Chen ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Glycyrrhizic Acid ◽  
Tgf Β1

Deltamethrin induces liver fibrosis in quails via activation of the TGF-β1/Smad signaling pathway

2020 ◽  
Vol 259 ◽  
pp. 113870 ◽  
Author(s):  
Bing Han ◽  
Zhanjun Lv ◽  
Xiaoya Zhang ◽  
Yueying Lv ◽  
Siyu Li ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Smad Signaling ◽  
Smad Signaling Pathway ◽  
Tgf Β1

scholarly journals Honokiol Acts as a Potent Anti-Fibrotic Agent in the Liver through Inhibition of TGF-β1/SMAD Signaling and Autophagy in Hepatic Stellate Cells

2021 ◽  
Vol 22 (24) ◽  
pp. 13354
Author(s):  
Seita Kataoka ◽  
Atsushi Umemura ◽  
Keiichiro Okuda ◽  
Hiroyoshi Taketani ◽  
Yuya Seko ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathway ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Smad Signaling ◽  
Smad Signaling Pathway ◽  
Tgf Β1

Chronic liver injury may result in hepatic fibrosis, which can progress to cirrhosis and eventually liver failure. There are no drugs that are specifically approved for treating hepatic fibrosis. The natural product honokiol (HNK), a bioactive compound extracted from Magnolia grandiflora, represents a potential tool in the management of hepatic fibrosis. Though HNK has been reported to exhibit suppressive effects in a rat fibrosis model, the mechanisms accounting for this suppression remain unclear. In the present study, the anti-fibrotic effects of HNK on the liver were evaluated in vivo and in vitro. In vivo studies utilized a murine liver fibrosis model, in which fibrosis is induced by treatment with carbon tetrachloride (CCl4). For in vitro studies, LX-2 human hepatic stellate cells (HSCs) were treated with HNK, and expression of markers of fibrosis, cell viability, the transforming growth factor-β (TGF-β1)/SMAD signaling pathway, and autophagy were analyzed. HNK was well tolerated and significantly attenuated CCl4-induced liver fibrosis in vivo. Moreover, HNK decreased HSC activation and collagen expression by downregulating the TGF-β1/SMAD signaling pathway and autophagy. These results suggest that HNK is a new potential candidate for the treatment of hepatic fibrosis through suppressing both TGF-β1/SMAD signaling and autophagy in HSCs.

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