Abstract
Platycodi radix is a widely sold health food worldwide, which contains numerous phytochemicals that are beneficial to health. Previously, we reported that saponin from the roots of Platycodi radix-derived saponin inhibited toxicant-induced liver diseases. Nevertheless, the inhibitory effect of platyconic acid A (PA), the active component of Platycodi radix-derived saponin, on the anti-fibrotic activity involving the SMAD pathway remains unclear. We investigated the inhibitory effects of PA on TGF-β1-induced activation of hepatic stellate cells (HSCs). PA inhibited TGF-β1-enhanced cell proliferation, as well as expression of α-SMA and collagen Iα1 in HSC-T6 cells. PA suppressed TGF-β1-induced smad2/3 phosphorylation and smad binding elements 4 (SBE4) luciferase activity. Reversely, PA restored TGF-β1-reduced expression of smad7 and peroxisome proliferator-activated receptor (PPAR)γ. PA also repressed TGF-β1-induced phosphorylation of Akt and MAPKs. In summary, the results suggest that the inhibitory effect of PA on HSCs occurs through the blocking of SMAD-dependent and SMAD-independent pathways, leading to the suppression of α-SMA and collagen Iα1 expression.
Highlights
Liver diseases constitute one of the world’s major health problems, causing serious morbidity and mortality [1]
The results showed that platyconic acid A (PA) decreased hepatic fibrogenesis by blocking SMAD and activating PPARγ, suggesting that PA could be developed as an alternative treatment for patients with chronic liver fibrosis
We examined the inhibitory effect of PA on Transforming growth factor (TGF)-β1-induced cell proliferation using the WST-1 assay, which showed that PA suppressed TGF-β1-induced cell proliferation in a concentration-dependent manner (Figure 1D)
Summary
Liver diseases constitute one of the world’s major health problems, causing serious morbidity and mortality [1]. Hepatic fibrosis can progress to liver cirrhosis accompanied by severe liver disease, leading to disorders of normal liver architecture and nodule formation, liver cancer, and liver failure. Hepatic fibrosis is generally prognostic for chronic liver injury caused by alcoholic abuse, obesity, and viral infection [2]. Various risk factors have been reported and disease progress has been well studied, the mechanisms of therapeutic targets for various forms of chronic liver disease remain unclear. Hepatic stellate cells (HSCs), a nonparenchymal cell type within the perisinusoidal space of Disse, contribute to key homeostatic functions of the liver, including regeneration, immunoregulation, drug metabolism, and detoxification. HSCs are stored as non-proliferative, quiescent cells
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