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Leukamenin F suppresses liver fibrogenesis by inhibiting both hepatic stellate cell proliferation and extracellular matrix production

   
@article{APS6727,
	author = {Qiong Liu and Xu Wang and Chen-jing Li and Li-hong Hu and Xu Shen},
	title = {Leukamenin F suppresses liver fibrogenesis by inhibiting both hepatic stellate cell proliferation and extracellular matrix production},
	journal = {Acta Pharmacologica Sinica},
	volume = {31},
	number = {7},
	year = {2016},
	keywords = {},
	abstract = {Aim: To investigate the inhibitory effect of the natural product Leukamenin F on liver fibrosis and explore its potential underlying mechanisms.
Methods: Carbon tetrachloride (CCl4)-treated mouse model in vivo and in hepatic stellate cells (HSC) in vitro were used. The effect on CCl4-induced liver fibrosis was studied using histochemical and biochemical analysis, while the inhibition on HSC was assessed using cell proliferation/apoptosis assay and collagen I production using real-time PCR. The inhibitory effects of Leukamenin F on Akt/mTOR/p70S6K and TGFβ/Smad pathways was studied using Western blot and cell image analysis.
Results: Leukamenin F (0.1–1 mg/kg, ip, q.d.×28) significantly reduced α-SMA and collagen specific Sirius red staining areas in CCl4 -treated mouse livers. This compound at 1–2 μmol/L dose-dependently inhibited α-SMA expression, cell proliferation and type I procollagen mRNA expression in activated HSC. Furthermore it inhibited the Akt/mTOR/p70S6K pathway and suppressed TGFβ -induced Smad2/Smad3 phosphorylation and nuclear translocation in HSC.
Conclusion: Our results demonstrated that Leukamenin F could attenuate CCl4-induced liver fibrogenesis in mice as an efficient inhibitor against both HSC proliferation and ECM production. This natural product provides a valuable structural hint for the development of anti-liver fibrosis reagents.},
	issn = {1745-7254},	url = {http://www.chinaphar.com/article/view/6727}
}