ABSTRACT
This study aimed to investigate apoptosis induction of ginsenoside compound K (ginsenoside CK) in human liver cancer SMMC-7721 cells and the involvement of TGF-β1/Smads signaling pathway. MTT assay was used to detect cell viability following ginsenoside CK treatment in SMMC-7721 cells. Annexin V-FITC/PI assay was used to detect apoptosis. After ginsenoside CK, or TGF-β1/Smads pathway activator TGFβ1 and inhibitor LY2109761 treatment, the TGF-β1/Smads pathway proteins and apoptosis proteins were detected by Western blot. The results showed that ginsenoside CK inhibited the proliferation of SMMC-7721 cells in a dose- and time-dependent manner. Annexin V-FITC/PI showed that ginsenoside CK induced apoptosis in SMMC-7721 cells. Meanwhile, ginsenoside CK inhibited the expression of Smad2/3, p-Smad2/3, Smad4, but promoted Smad7 expression, cleavage of caspase-3 and down-regulated Bcl-2/Bax. Compared with TGFβ1 treatment alone, levels of Smad2/3, p-Smad2/3, Smad4 and the ratio of Bcl-2/Bax were down-regulated, whereas Smad7 or cleaved caspase-3 was up-regulated in the ginsenoside CK+TGF-β1 group. In addition, Smad2/3, p-Smad2/3 and Smad4 expression were decreased in LY2109761 group. Compared with LY2109761 group, cleaved caspase-3 expression and Bcl-2/Bax have no significant change in ginsenoside CK+LY2109761 group. Taken together, our results showed that ginsenoside CK induced apoptosis in SMMC-7721 cells, and such induction is related to inhibiting TGF-β1/Smads signaling pathway.
ABSTRACT
The study was designed to test the role of 5,2',4'-trihydroxy-6,7,5'-trimethoxy flavone nanoparticle (TTF1-NP) on lipopoiysaccharide (LPS)-induced inflammatory response, and to explore the anti-inflammatory mechanism in human hepatocellular carcinoma cells. Inflammatory responses were induced in human hepato-cellular carcinoma HepG2 cells with LPS; Proliferation effect of TTF1-NP in LPS-stimulated HepG2 cells were detected by MTT assay; The expression of TLR4, AKT/mTOR signaling related proteins and IL-6 were detected by Western blot assay. The results showed that TTF1-NP inhibited the proliferation of HepG2 cells induced by LPS in a dose-dependent manner; TTF1-NP inhibited the expression of TLR4, the activation of AKT and mTOR, and expression of IL-6 in a dose-dependent manner; TTF1-NP inhibited the activation of AKT/mTOR signaling pathway and TLR4 proteins leading to suppression of IL-6 expression in HepG2 cells stimulated by insulin. These results suggest that TTF1-NP inhibited inflammatory responses from LPS treatment with a potential mechanisms in the inhibition of AKT/mTOR pathway.