Research on mechanism of salidroside activating HIF-1 a signaling pathway to promote MOB proliferation / 中国药理学通报

Aim To explore the effeet of salidroside (SAL) on proliferation of osteoblasts and its possible mechanism by using mouse primary osteoblasts ( MOB) as the research object.Methods Alkaline phosphatase ( ALP) staining was used to identify the extracted primary cells.MTT was used to detect the effect of SAL on the proliferation.RT-PCR, Western blot, ELISA were used to investigate the molecular mechanism of SAL.Results The extracted cells generated black-brown deposits by ALP staining, which were shown to be osteoblasts clearly.SAL promoted the pro liferation of MOB.Meanwhile, SAL could up-regulate the mRNA and protein expression levels of hypoxia-inducible factor-lcx ( HIF-1 ex), vascular endothelial growth factor ( VEGF ) , angiopoietin-like protein 4 (ANGPTL4) and interleukin 6 ( IL-6 ) , which were down-regulated by using the HIF-lex blocker YC-1.Conclusions SAL could promote the proliferation of MOB through HIF-1 a/VEGF, ANGPTL4, IL-6 signaling pathway.

Ethanol extract of Ardisiae Japonicae Herba inhibits hepatoma carcinoma cell proliferation in vitro through regulating lipid metabolism / 中草药·英文版

Objective: The aim of this study is to discover the possible working mechanisms of Ardisiae Japonicae Herba (AJH) on hepatoma carcinoma (HCC). Methods: In this study, ethanol extract of AJH was prepared and used to treat HCC cell in vitro. Furthermore, a genomic wide RNA sequencing (RNA-seq) was performed to screen deregulated genes in HCC cells after the treatment of AJH extract. The gene and protein expression related to lipid metabolism in HCC cells were also investigated to validate the results obtained from RNA-seq. Results: AJH extract could inhibit HCC cell proliferation in vitro. RNA-seq analysis has identified 1,601 differentially expressed genes (DEGs, fold change ≥ 2.0 or fold change ≤ 0.5, P < 0.05) in HCC after AJH extract treatment, which included 225 up-regulated genes and 1,376 down-regulated genes. KEGG pathway analysis of DEGs demonstrated that lipid metabolism was a potential pathway related to AJH treatment. In agreement with the RNA-seq data, qPCR and Western-blot analysis indicated that expression of genes and proteins related to lipid metabolism (SREBP1, ACC, ACLY and FASN) were significantly down-regulated in AJH treatment group as compared with the control group. Furthermore, AJH extract could also decrease lipid contents and cellular free fatty acid levels in HCC cells. Conclusion: Ethanol extract of AJH could inhibit HCC cell proliferation in vitro, the possible mechanism may be related to the inhibition of lipid metabolism.