Effects of diammonium glycyrrhizinate on expressions of Rac-1, Claudin-5 and vessel endothelium-Cadherin in rats after cerebral ischemic reperfusion

Abstract

Objective To investigate the effect of diammonium glycyrrhizinate on neurovascular units in rats after cerebral ischemia reperfusion (IR) injury. Methods Two hundred and forty health SD rats were randomly assigned into normal control group (n=30), sham-operated group (n=30), IR group (n=90) and diammonium glycyrrhizinate group (DG, n=90). The rats in the IR group and DG group were divided into 2, 6 and 12 h subgroups after modeling, respectively (n=30). The rats in the IR group and DG group were induced middle cerebral artery occlusion (MCAO) models, and after the models were successfully established, 9.11 mL DG sodium chloride injection was given to DG group, while equal saline to normal group, sham-operated group and IR group via the tail vein. The brain tissues of each group were harvested 2, 6 and 12 h, resperctively, after modeling. The infraction rate was measured by TTC staining; immunohistochemistry was employed to detect the expresions of Claudin-5 and vessel endothelium (VE)-Cadherin; Western blotting was used to detect the protein expression levels of Rac-1 and Claudin-5. Results The DG group had signficantly lower infarction rate than IR group 2, 6 and 12 h after modeling (P<0.05). The Claudin-5 expression rates in the 6 h and 12 h DG subgroups were signficantly higher than those in the 6 h and 12 h IR subgroups (P<0.05). The VE-Cadherin expression rates in the DG group were significantly higher than that in IR group at 2, 6 and 12 h after modeling (P<0.05). Samely, the Claudin-5 relative quantity in DG group was significantly higher than that in IR group at 2, 6 and 12 h after modeling (P<0.05). The Rac-1 quantity in DG group was only statistically higher than IR group at 2 h after modeling (P<0.05). Conclusion The DG can upregulate the Rac-1, VE-Cadherin and Claduin-5 expressions in neurovascular units, and partly protect neurovascular units after cerebral acute IR injury. Key words: Cerebral ischemia reperfusion; Diammonium glycyrrhizinate; Neurovascular unit; Rac-1; Claudin-5; Vessel endothelium-Cadherin