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Keloid is induced by a pathological wound healing response, and hepatocyte growth factor (HGF) is known to be involved in tissue repair viathe activation of its primary receptor, c-Met. We aimed to investigate whether c-Met activation is implicated in keloid pathogenesis. HGF, c-Met, phosphorylated c-Met (p-Met), Ki-67, collagen I protein, and METgene expression were detected in five normal skin and 30 keloid tissues by immunohistochemistry and quantitative real-time polymerase chain reaction analysis, respectively. The influence of p-Met expression on the biological behaviour of keloid fibroblasts was further investigated with regard to cell proliferation, motility, invasiveness, collagen I expression, and intracellular signaling in vitro. p-Met protein and MET gene expression but not HGF or c-Met protein expression showed significant increases in keloid tissues than dermal layer of normal skin tissues. In keloid tissues, p-Met expression was significantly associated with keloid size, Ki-67 and collagen I expression. Moreover, p-Met expression was also related to proliferation, migration, invasiveness, collagen I expression and activation of AKT and Erk in keloid fibroblasts in vitro. c-Met activation may have a strong influence on keloid pathogenesis, and it can be investigated further as a potential molecular target for keloid therapy.

The beneficial cardiac effects of some Ca2channel blockers have been attributed to blood pressure reduction, but these pleiotropic effects require further investigation. We compared the effects of benidipine, which has beneficial cardiac effects, and nitrendipine, which does not, in an animal model of hypertensive diastolic heart failure (DHF).

To investigate the mechanism responsible for the increased cardiac stiffness associated with hypertensive heart failure in Dahl salt-sensitive (DS) rats and the effects of treatment with the combination of a calcium channel blocker [azelnidipine (AZE)] and angiotensin II type 1 receptor blocker [olmesartan (OLM)].

The effect of ginsenoside Rh2 (G-Rh2) on mast cell-mediated anaphylaxis remains unclear. Herein, we investigated the effects of G-Rh2 on OVA-induced asthmatic mice and on mast cell-mediated anaphylaxis.