Herbs protect against osteoporosis through anti-inflammation action / 中国组织工程研究

BACKGROUND: The occurrence and development of osteoporosis are shown to be directly related to the inflammatory response induced by immune dysfunction. OBJECTIVE: To summarize the mechanisms of osteoclast differentiation and formation at cellular and molecular levels, as well as the underlying mechanisms of several kinds of medical herbs against osteoporosis, thus paving ways for finding more effective and safe herbs for anti-osteoporosis.METHODS: PubMed database was retrieved using the English keywords of (osteoporosis OR bone loss) AND lipopolysaccharide AND bone resorption", and WanFang database was searched with the Chinese keywords of "osteoarthritis, receptor activator of nuclear factor-κB ligand, lipopolysaccharide,Dendrobium moniliforme,Portulaca oleracea,Ampelopsis sinica,Schizonepeta".The literatures addressing osteoporosis, inflammation and herbal medicine were screened, and those using lipopolysaccharide-induced mouse models were included. Finally, four eligible literatures were enrolled for review. RESULTS AND CONCLUSION:In vivo experiments,CT images and pathological sections of the cancellous bone in the mouse distal femur show that Dendrobium moniliforme,Purslane oleracea,Ampelopsis sinica,and Schizonepeta exert inhibitory effects on lipopolysaccharide-induced osteoporosis.In vitro experiments reveal that these four kinds of herbs fight against osteoporosis by inhibiting osteoclast differentiation and further reducing bone resorption.

Tanshinone IIA down-regulates the expression of MMP-12 and TF in RAW 264.7 cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of tanshinone IIA (TanIIA) on the expression of tissue factor (TF) and matrix metalloproteinase-12 (MMP-12) in RAW264.7 cells and explore the possible mechanism.</p><p><b>METHODS</b>RAW 264.7 cells were incubated with ox-LDL in the presence or absence of different concentrations of tanshinone IIA. At the end of the incubation, the cell proliferation was assessed by MTT assay, and superoxide dismutase (SOD) activity and malondialdehyde (MDA) and TF concentrations in the supernatant were detected by xanthine oxidase method, thiobarbituric acid method and ELISA, respectively. Western blotting was employed to determine MMP-12 expression in the cells.</p><p><b>RESULTS</b>The cell proliferation was dose-dependently inhibited by TanIIA. SOD activity in the supernatant was increased significantly, while the MDA and TF concentration and MMP-12 expression in cells decreased after treatment of the cells with different concentrations of TanIIA.</p><p><b>CONCLUSION</b>TanIIA inhibits the cell proliferation and TF and MMP-12 expressions in RAW264.7 cells stimulated by ox-LDL, and these effects may be related with the anti-oxidation property of TanIIA.</p>

Fenofibrate inhibits tumor necrosis factor-alpha-induced expression of CD40 and matrix metalloproteinase in human vascular endothelial cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the regulatory effects of fenofibrate on TNF-alpha-induced CD40 expression and matrix metalloproteinase (MMP) activity in human vascular endothelial cells (HUVECs).</p><p><b>METHODS</b>Quantitative RT-PCR and flow cytometry were employed to evaluate the effect of fenofibrate on TNF-alpha-induced CD40 mRNA and cell surface CD40 expression in HUVECs, and gelatin zymography was used to determine the effect of fenofibrate on the gelatinolytic activities of MMP-2 and MMP-9 in TNF-alpha-stimulated HUVECs.</p><p><b>RESULTS</b>Fenofibrate at the concentrations of 5x10(-5), 1x10(-4) and 2x10(-4) mol/L significantly reduced TNF-alpha-induced increment of CD40 mRNA and cell surface CD40 expressions (P<0.01), with the maximal inhibition achieved at the concentration of 1x10(-4) mol/L. Fenofibrate at 2x10(-4) mol/L did not further decrease CD40 expression induced by TNF-alpha. Fenofibrate significantly inhibited the stimulatory effect of TNF-alpha on MMP-2 and MMP-9 activities in HUVECs.</p><p><b>CONCLUSION</b>Fenofibrate reduces TNF-alpha-induced increment of CD40 expression and MMP-2 and MMP-9 activities in HUVECs.</p>