Effect of Buyang Huanwu decoction on expression of silent information regulator 1 in cortical area of rats after cerebral ischemia/reperfusion injury / 中国药理学通报

ABSTRACT

Aim To investigate the effect of Buyang Huanwu decoction on the expression of silencing regulation factor 1(SIRT1)protein in cortical area and the possible mechanism of cerebral ischemia/reperfusion injury(CIRI)via establishing middle cerebral artery occlusion(MCAO)model. Methods SD rats were randomly divided into sham group(Sham), model group(MCAO/R), Buyang huanwu decoction group(BYHWT), and atorvastatin group(Atorvastatin), with 15 rats in each group. After 2 h ischemia/reperfusion for 72 h and drug intervention, the model was successfully constructed by using laser speckle blood flow monitoring video system. Zea Longa neurological function score was used to evaluate the neurological defects of rats after modeling. TTC staining was used to detect infarct volume. Nissl staining was used to observe the injury of nerve cells. Western blot was employed to detect the SIRT1 protein expression level. Immunofluorescence was applied to detect the fluorescence expression of SIRT1. Results Compared with sham group, the neurological deficits of MCAO/R group were serious(P<0.05). Cerebral infarction volume increased(P<0.05). The nerve cells were severely damaged, disordered, with the nucleus pyknosis(P<0.05). SIRT1 protein expression was reduced(P<0.05). The fluorescence intensity of SIRT1 decreased(P<0.05). Compared with MCAO/R group, the neurological impairment degree of rats in BYHWT and Atorvastatin groups was reduced(P<0.05). The proportion of cerebral infarction volume decreased(P<0.05). The injury of nerve cells was significantly reduced and the number of nerve cells increased(P<0.05). The expression of SIRT1 protein was up-regulated(P<0.05). Fluorescence intensity of SIRT1 increased(P<0.05). Conclusions Buyang huanwu decoction can effectively alleviate brain injury in cerebral ischemia/reperfusion rats, and its protective effect may be related to the increase of SIRT1 protein expression in the ischemic cortical region.