Abstract
The activation of hepatic stellate cells (HSC) plays a key role in the progression of hepatic fibrosis, it is essential to remove activated HSC through apoptosis to reverse hepatic fibrosis. Schisandrin B (Sch B) is the main chemical component of schisandrin lignan, and it has been reported to have good hepatoprotective effects. However, Schisandrin B on HSC apoptosis remains unclear. In our study, we stimulated the HSC-T6 and LX-2 cell lines with TGF-β1 to induce cell activation, and the proliferation and apoptosis of the activated HSC-T6 and LX-2 cells were detected after treatment with different doses of Schisandrin B. Flow cytometry results showed that Sch B significantly reduced the activity of activated HSC-T6 and LX-2 cells and significantly induced apoptosis. In addition, the cleaved-Caspase-3 levels were increased, the Bax activity was increased, and the Bcl-2 expression was decreased in HSC-T6 and LX-2 cells treated with Sch B. Our study showed that Sch B inhibited the TGF-β1-induced activity of hepatic stellate cells by promoting apoptosis.
Highlights
Maria Ciudad-Mulero, Liver fibrosis is caused by a variety of pathological factors associated with intrahepatic connective tissue dysplasia, which results in the pathological process of intrahepatic diffuse extracellular matrix deposition [1,2]
These results suggest that Schisandrin B (Sch B) inhibits the proliferation of activated hepatic stellate cells (HSC)-T6 and LX-2 in a dose-dependent manner
Activation of HSCs is driven by a variety of mediators, such as reactive oxygen species, chemokines, growth factors, matrix hardness, stromal cell proteins, and injury-related molecular patterns, which are secreted by adjacent cells and signal HSC scar formation in an autosecretory and/or paracrine manner [20,21]
Summary
Maria Ciudad-Mulero, Liver fibrosis is caused by a variety of pathological factors associated with intrahepatic connective tissue dysplasia, which results in the pathological process of intrahepatic diffuse extracellular matrix deposition [1,2]. In the pathological progression of hepatic fibrosis, a large number of activated HSCs are thought to undergo one of two processes: one process is the transition from an “activated type” to a “static type”, and the other process is apoptosis [9]. Drugs designed to inhibit HSC activation, induce cell apoptosis and prevent ECM deposition have achieved certain effects in the treatment of experimental liver fibrosis. Activated HSC is an important marker for the development of liver fibrosis, and many attempts have been made to identify drugs that reduce the number of activated proliferating HSCs by inducing HSC apoptosis; this strategy can be considered a feasible approach the treatment of fibrosis
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