Fermented soshiho-tang with Lactobacillus plantarum enhances the antiproliferative activity in vascular smooth muscle cell

• Published in: BMC complementary and alternative medicine 2014-02, Vol.14 (1), p.78-78, Article 78
• Main Authors: Lee, Jung-Jin, Kwon, Hyeeun, Lee, Ji-Hye, Kim, Dong-Gun, Jung, Sang-Hyuk, Ma, Jin Yeul
• Format: Article
• Language: English
• Subjects: Analysis; Animals; Cell cycle; cell cycle checkpoints; Cell Cycle Checkpoints - drug effects; Cell Proliferation - drug effects; Cell Survival - drug effects; Cells, Cultured; chronic hepatitis; Colleges & universities; complement; Cyclin-dependent kinases; cyclins; dose response; Fermentation; Hepatitis; hepatotoxicity; Kinases; Lactobacillus plantarum; Lactobacillus plantarum - metabolism; liver cirrhosis; liver regeneration; Medical research; Muscle, Smooth, Vascular - cytology; Muscle, Smooth, Vascular - drug effects; Myocytes, Smooth Muscle - cytology; Myocytes, Smooth Muscle - drug effects; phosphorylation; Physiological aspects; Plant Extracts - metabolism; Plant Extracts - pharmacology; Rats; smooth muscle; traditional medicine; viability
• ISSN: 1472-6882; 1472-6882
• DOI: 10.1186/1472-6882-14-78

Soshiho-tang (SST) is a traditional medicine widely used for the treatment of chronic hepatitis. SST has been shown to confer a variety of pharmacological activities, including prevention of hepatotoxicity, promotion of liver regeneration, and modulation of liver fibrosis. In this study, we investigated the antiproliferative activity of native and fermented (FSST) formulations of SST in vascular smooth muscle cells (VSMCs) and examined the potential underlying mechanisms driving these effects. SST, along with preparations fermented with Lactobacillus plantarum KFRI-144 (S-A144), L. amylophilus KFRI-161 (S-A161) and L. bulgaricus KFRI-344 (S-A344), were investigated to determine their effects on the proliferation and viability of VSMCs, along with the signalling pathways underlying these effects. S-A144 exhibited a strong, dose-dependent inhibition of VSMC proliferation relative to untreated controls, but the others did not affect. In addition, S-A144 significantly decreased the phosphorylation of Akt and PLCγ1 in a dose-dependent manner and induced cell cycle arrest at the G0/G1 phase characterised by decreased expression of CDKs, cyclins and PCNA. The findings suggest that S-A144 exhibit enhanced inhibition of PDGF-BB-induced VSMC proliferation comparison to S-AOR through the suppression of cell cycle progression and expression of cell cycle-related proteins, along with the downregulation of Akt phosphorylation.