Mechanism Research Of Glycyrrhizin In Preventing Vasospasm After Experimental Subarachnoid Hemorrhage

Objective:To observe whether or not glycyrrhizin could relieve rats’ cerebral vasospasm after subarachnoid hemorrhage(SAH), and explore the mechanism of glycyrrhizin in preventing cerebral vasospasm.Methods:36 male SD rats were randomly divided into three groups: control group(n=12), SAH group(n=12) and glycyrrhizin treatment group(treatment group, n=12). The control group did not receive any treatment. SAH group and treatment group were shares of building models by autologous femoral arterial blood injection into the cisterna magna twice, and treatment group received intraperitoneal injection of glycyrrhizin once a day in a dose of 10mg/kg. All groups of rats were killed on the third day and the brain pontine basilar arteries were removed to observe inner diameter and thickness of blood vessels after slicing. HMGB1 in basal artery tissue were measured by western blot analysis, and RNA level of proinflammation cytokines such as IL-1β, IL-6 and TNF-α were measured by RT-PCR.Results: Glycyrrhizin treatment significantly increased the luminal inner perimeter and reduced the thickness of the basilar artery wall(P<0.05). Western blot analysis showed that the expression level of HMGB1 significantly increased in basal artery tissue in SAH group and treatment group compared with that of control group(P <0.05); the expression level of HMGB1 in treatment group significantly decreased compared with that of SAH group(P <0.05). RT-PCR analysis showed the RNA level of IL-1β, IL-6 and TNF-α were expressed lower in the basal artery tissue of control group compared with that of SAH group and treatment group(P <0.05), and the RNA expression level of these proinflammation cytokines in treatment group significantly decreased compared with that of SAH group(P <0.05).Conclusions: Glycyrrhizin could effectively alleviate rats’ vasospasm after subarachnoid hemorrhage. The underlying mechanism was that glycyrrhizin inhibited the expression of HMGB1 and further reduced the expression of IL-1β, IL-6 and TNF-α to relieve inflammation.