Our results showed that miR-181b expression was increased much higher than miR-181a expression in vitro in transforming growth factor-β1-induced HSC activation as well as in vivo in carbon tetrachloride-induced rat liver fibrosis.
However, whether serum glycosylation isomer of M2BP (M2BPGi) was associated with the regression of liver fibrosis in patients with chronic hepatitis B (CHB) during IFN-α add-on therapy is still unknown.
Hepatic stellate cell-targeted delivery of hepatocyte growth factor transgene via bile duct infusion enhances its expression at fibrotic foci to regress dimethylnitrosamine-induced liver fibrosis.
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.
TGF-β1 and α-SMA showed a progressive increase with advancing severity of hepatic fibrosis (mean TGF-β1: 2,058.4 in F1-F2 and 1,583.8 in F3-F4, p ≤ 0.04; mean α-SMA: 13.59 in F1-F2 and 16.62 in F3-F4, p ≤ 0.05).
Clinical studies have reported that LWWL can also be used for the treatment of liver fibrosis with associated treatment regimens resulting in a concomitant reduction in transforming growth factor β1 (TGF-β1) levels in the serum of patients with hepatic fibrosis.
Serum glycosylated Wisteria floribunda agglutinin-positive Mac-2 binding protein (WFA<sup>+</sup> -M2BP) is a novel marker for staging liver fibrosis and predicting hepatocellular carcinoma (HCC) occurrence.
To avoid the impact of schistosomicidal activity of PZQ against liver fibrosis induced by S. japonicum infection, we established a mouse model of carbon tetrachloride (CCl<sub>4</sub> )-induced liver fibrosis for in vivo studies and used TGF-β1-stimulated human hepatic stellate cell line (LX-2) in addition to other fibroblast-like cell line (MES13) and fibroblast cell line (NIH3T3) in vitro.
Collectively, our results reveal that SEPT6 regulates various biological behaviors in HSCs through TGF-β1/Smad, mitogen-activated protein kinases and phosphatidylinositol-3-kinase/protein kinase B signaling pathways, thus promoting liver fibrosis.
Compared with controls, both TGF-beta1 and TGF-beta2 mRNA expression increased in the liver during the progress of liver fibrosis in patients with KP and LT on the array.
Lower albumin was also associated with increased levels of several inflammatory biomarkers, markers of liver fibrosis, albuminuria, and greater arterial stiffness, diastolic dysfunction and pulmonary hypertension.
In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF-β1-mediated Smad pathway activation, EMT occurrence, and ECM deposition.
Here we have further investigated the downstream effects of phagocytosis by studying NADPH oxidase activation and its link to procollagen alpha1 (I) and TGF-beta1 expression in an immortalized human stellate cell line and in several models of liver fibrosis.
After intravenous injection, CSLN/siCTGF complex was target specifically delivered to the liver and resulted in a significant reduction in collagen content and pro-fibrogenic factors like tumor necrosis factor alpha (TNF-α), transforming growth factor beta (TGF-β), interleukin-6 (IL-6), and CTGF with the dramatic improvement of patho-physiological symptoms in liver fibrosis model rats.
To investigate the modulating effects of date fruits on pro- and anti-apoptotic markers, cytochrome P450 2E1 (CYP2E1) and hepatocyte growth factor (HGF) in liver fibrosis.
Taken together, activation of I<sub>1</sub>R negatively regulates the progression of liver fibrosis in the Nrf2-dependent pathway, which suggests that specifically targeting I<sub>1</sub>R may be a potential therapeutic strategy for the treatment of liver fibrosis.
These findings suggested that AKF-PD attenuated the progression of hepatic fibrosis by suppressing HSCs activation via the TGF-β1/Smad and MAPK signaling pathways, and therefore that AKF-PD may be suitable for use as a novel therapeutic agent against liver fibrosis.
After 4 weeks of intravenous tail vein injection into CCl<sub>4</sub>-injured mouse liver, LEPCs engrafted into liver parenchyma, differentiated into ALB positive hepatocytes, and could alleviate liver fibrosis through down regulating fibrosis genes-Tgfb1 and α-SMA as well as decreasing expression of collagen gene Col1a1, Col3a1, and Col4a1, and regain liver function by recovering ALT and AST.