The effect of hydrosafflower yellow A on the NMDA receptor 1 protein expression in rats with focal cerebral ischemia-reperfusion injury
Aihua Li
Abstract
Aihua Li
Abstract
Objective To study the cerebral protective effect and the mechanism of hydrosafflower yellow A (HSYA) in rats with focal ischemia-reperfusion.Methods The effect of HSYA on the pathological changes and expression of the NMDAR 1 after ischemia-reperfusion was observed in the rat model of MCAO.Results Under HE staining,the changes as follows could be seen:the neuron degeneration and edema could be seen in 0~1 h after reperfusion;some infarction could be seen in 3~6 h after reperfusion and the extent of infarction extended in 12~24 h after reperfusion;the degeneration and necrosis of neurons was obviously decreased and the infarction was also reduced in treatment groups. Under immunohistochemical staining, there was moderate NMDAR 1 positive expression in the cells like neurons in normal rats. The NMDAR 1 expression increased sharply after reperfusion for 0~1 h,and reached the peak in 3 h after reperfusion, then decreased gradually and showed an expression lower than normal in 24~72 h after reperfusion. The expression began to rise in 1~2 weeks but still lower than the normal level.In contrast to the control group, HSYA could largely reduce the NMDAR 1 expression in earlier stage (before 12 h) and increase the expression in later stage (after 24 h).Conclusion The HSYA has the protective effect on cerebral ischemia. The two-phase moderating effect of HSYA on the protein expression of NMDAR 1 after cerebral ischemia-reperfusion may be an important mechanism of cerebral protective effect.
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Objective To study the cerebral protective effect and the mechanism of hydrosafflower yellow A (HSYA) in rats with focal ischemia-reperfusion.Methods The effect of HSYA on the pathological changes and expression of the NMDAR 1 after ischemia-reperfusion was observed in the rat model of MCAO.Results Under HE staining,the changes as follows could be seen:the neuron degeneration and edema could be seen in 0~1 h after reperfusion;some infarction could be seen in 3~6 h after reperfusion and the extent of infarction extended in 12~24 h after reperfusion;the degeneration and necrosis of neurons was obviously decreased and the infarction was also reduced in treatment groups. Under immunohistochemical staining, there was moderate NMDAR 1 positive expression in the cells like neurons in normal rats. The NMDAR 1 expression increased sharply after reperfusion for 0~1 h,and reached the peak in 3 h after reperfusion, then decreased gradually and showed an expression lower than normal in 24~72 h after reperfusion. The expression began to rise in 1~2 weeks but still lower than the normal level.In contrast to the control group, HSYA could largely reduce the NMDAR 1 expression in earlier stage (before 12 h) and increase the expression in later stage (after 24 h).Conclusion The HSYA has the protective effect on cerebral ischemia. The two-phase moderating effect of HSYA on the protein expression of NMDAR 1 after cerebral ischemia-reperfusion may be an important mechanism of cerebral protective effect.
Key concepts: Medicine, Ischemia, Reperfusion injury, NMDA receptor, Immunohistochemistry, Edema, Cerebral infarction, Infarction