Effects of AstragalosideⅣon delayed cerebral vasospasm after subarachnoid hemorrhage

ZHAO Jian-wu; YU Yao-yu; YU Tian-lei; LI Yan-liang; TANG Zhu; GUI Zheng; ZHOU Xin; JI Wen-jie

doi:10.13798/j.issn.1009-153X.2015.06.010

Abstract：Objective To explore the effect of Astragaloside Ⅳ(AS-Ⅳ) on delayed cerebral vasospasm after subarachnoid hemorrhage (SAH) and its mechanism. Methods Forty male SD rats were randomly were divided into 4 groups of 10 animals each, i.e. normal, SAH+AS-Ⅳ, SAH+dimothyl sulfoxide (DMSO) and SAH groups. The SAH model was made by endovascularly puncturing the internal carotid artery. The rats were given daily by intraperitoneal injection of AS-Ⅳsuspension in SAH+AS-Ⅳgroup 30 minutes after the establishment of the model, equal volume of 0.1%DMSO in SAH+DMSO group, and equal volume of saline in the normal and SAH groups. The morphological changes in the basilar arteries were observed by a microscope, the expressions of TLR4 and NF-κB p65 in the basilar arteries were determined by immunohistochemical technique, and the plasma levels of TNF-αand IL-6 were determined by enzyme-linked immunosorbent assay. Results The thickness of the basilar artery wall was significantly thinner in the normal group than that in SAH+AS-Ⅳgroup (P<0 .05), which was significantly thinner than that those in SAH and SAH+DMSO groups (P<0.05). The area of transverse section of the basilar artery was significantly bigger in the normal group than that in SAH+AS-Ⅳgroup (P<0.05), which was significantly bigger than those in SAH and SAH+DMSO groups (P<0.05). The levels of TLR4 and NF-κB p65 expressions in the basilar arteries were significantly lower in the normal group than those in SAH+AS-Ⅳgroup (P<0.05), which were significantly lower in SAH and SAH+DMSO groups (P<0.05). The plasma levels of TNF-αand IL-6 were significantly lower in the normal group than those in SAH+AS-Ⅳgroup (P<0.05), which were significantly lower in SAH and SAH+DMSO groups (P<0.05). Conclusion AS-Ⅳcan alleviate the delayed cerebral vasospasm after SAH via inhibiting TLR4 and NF-κB-mediated inflammatory signaling pathways.