Key result
HMH completely suppressed B2-kinin receptor expression in response to high glucose and inhibited bradykinin-induced MAPK phosphorylation and CTGF protein increases in vascular smooth muscle cells.
HMH may confer vascular protection against high glucose and bradykinin stimulation through its anti-oxidant properties, ameliorating vascular injury and remodeling.
A creatinine metabolite, 5-hydroxy-1-methylhydantoin (HMH: NZ-419), a hydroxyl radical scavenger, has previously been shown to confer renoprotection by inhibiting the progression of chronic kidney disease in rats. In the current study, we demonstrate that HMH modulates the effects of glucose and bradykinin (BK) in vascular smooth muscle cell (VSMC). HMH a novel anti-oxidant drug completely suppressed the expression of B2-kinin receptors (B2KR) in response to high glucose (25 mM) stimulation in VSMC and was also shown to attenuate the effects of BK on VSMC remodeling. HMH inhibited the BK-induced increase in MAPK phosphorylation and attenuated the increase in connective tissue growth factor (CTGF) protein levels in VSMC. These findings suggest that HMH may confer vascular protection against high glucose concentrations and BK-stimulation to ameliorate vascular injury and remodeling through its anti-oxidant properties.
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Ienaga et al. (2014) studied Vascular injury and remodeling (in vitro model). 5-hydroxy-1-methylhydantoin (HMH: NZ-419) was evaluated on Expression of B2-kinin receptors, MAPK phosphorylation, and connective tissue growth factor protein levels. HMH completely suppressed B2-kinin receptor expression in response to high glucose and inhibited bradykinin-induced MAPK phosphorylation and CTGF protein increases in vascular smooth muscle cells.
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