| Objectives: Spontaneous subarachnoid hemorrhage(SAH) is a serious fatal disease, 80-90% of the rupture caused by intracranial aneurysms. Delayed cerebral vasospasm is related with high mortality and morbidity caused by delayed cerebral ischemia after spontaneous subarachnoid hemorrhage. DCVS produce specific mechanism is still not clear, a variety of pathological mechanism may be relevant. Which vascular smooth muscle cells(VSMCs) proliferation, phenotype switching and apoptosis play an important role in DCVS. Cardmonin(CAR) has conformed anti-inflammatory, anti-viral and anti-tumor effects. At the same time can dilate blood vessels, anti-arterial vascular smooth muscle cell proliferation.However,there is no report about CAR treatment on delayed cerebral vasospasm after subarachnoid hemorrhage. The object of our study is to detect the mechanism of animal experiments CAR intervents delayed cerebral vasospasm after subarachnoid hemorrhage.Methods: Puncturing internal carotid artery in rats as the model of delayed cerebral vasospasm after subarachnoid hemorrhage. subarachnoid hemorrhage model in rats, Cardmonin(7.5 mg/kg) intraperitoneal injection per day from 1 day to 7 days aftersurgery, control group injected amount of saline solution. SD rats were randomly divided into four groups, namely the control group(group A), SAH group(group B), SAH + vehicle group(group C), Cardmonin groups(group D). Each group of animals and neurological scores to compare changes in nerve function between their respective groups.Hematoxylin and eosin(HE) staining calculates the wall thickness of basilar atrery, immunohistochemistry to detect the phosphorylation of protein kinase B(p-Akt), and immunofluorescence staining to detect the Akt pathway downstream protein C-myc expression and α- smooth muscle actin(α-SM actin) change. Td T-mediated d UTP nick end labeling(Tunel) staining were detected among groups of vascular endothelial cells and vascular smooth muscle cell apoptosis. And calculate the number of positive cells per unit area average as intravascular measurement standard with p-Akt, C-myc, α-SM actin expression and Tunel.Results: 1.Each group of neurological scores result: group D compared with groups B, C had statistically significance(P <0.01), but groups B and C had not statistically significant difference(P>0.05). 2.Vascular wall thickness of the basilar artery in HE staining; A group average of basal artery wall thickness(9.43 ± 0.69) μm, group B(20.53 ± 2.97) μm, group C(19.56 ± 0.64) μm, group D(12.60 ± 0.85) μm. No statistically significant difference was(P>0.05) between group B and group C.But group D compared with B and C groups had statistically significant difference(P <0.05). 3.The p-Akt, C-myc, α-SM actin expression and Tunel Results: A group of vascular unit area p-Akt, C-myc, α-SM actin and Tunel positive cells(103 / mm2), respectively(2.38 ± 0.51,0.75 ± 0.08,0.24 ± 0.02,2.55 ± 0.29), group B(5.58 ± 0.65,2.56 ± 0.34,0.14 ± 0.02,5.45 ± 0.56), group C(5.41 ± 0.56,2.67 ± 0.56,0.15 ± 0.02,5.53 ± 0.40), D group(2.36 ± 0.58,0.96 ± 0.20,0.23 ± 0.02,2.77 ± 0.29), group B and group C were no significant difference(P> 0.05), D group and group B and group C were statistically significant(P <0.01), A group and D group was not statistically significant(P> 0.05).Conclusions: Cardmonin can promote the recovery of neurological function after SAH. Witch probably by inhibiting Akt pathway,reduced C-myc protein expression and upregulation the expression of α-SM actin. That effects in smooth muscle phenotypic phenotype switching and proliferation.As well as,reducing apoptosis of endothelial cells and smooth muscle cells.and promote the recovery of DCVS after subarachnoid hemorrhage. |
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