Individuals with diabetes have high concentration of methylglyoxal (MGO) and have advanced glycation end-products (AGEs) which play an important role in vascular complications, such as stroke. Our previous data demonstrated that hydroxysafflor yellow A (HSYA), a major active chemical component of the safflower yellow pigment, had antiglycation effect on the AGEs formation in vitro. It is not known whether HSYA can protect against MGO-induced injury in cultured human brain microvascular endothelial cells (HBMEC). Using cultured HBMEC, cell injury was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formation, lactate dehydrogenase (LDH) release and AnnexinV/PI staining. Advanced glycogen end-products and caspase-3 formation were measured by Western blotting. Incubation of MGO for 24h concentration-dependently induced HBMEC injury, which was protected by HSYA from 10 to 100 μmol/l. Caspase-3 expression and AnnexinV/PI staining illustrated that the protection of HSYA was probably associated with inhibiting cell apoptosis. What's more, MGO promoted AGEs accumulation in the cultured HBMEC, which was also inhibited by 100 μmol/l HSYA. Thus, our results proved that HSYA could inhibit MGO-induced injury in the cultured HBMEC, which was associated with its antiglycation effect.
Keywords: Advanced glycation end-products; Apoptosis; Human brain microvascular endothelial cells; Hydroxysafflor yellow A; Methylglyoxal.
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