Effect of glycyrrhizin on the spasticity of hemiplegic spasticity in stroke rats by regulating the PI3K/Akt/GSK3β signaling pathway
Objective To investigate the effect of glycyrrhizin(GA)on the spasticity of hemiplegic spasticity in stroke rats by regulating the phosphoinositide 3-kinase(PI3K)/protein kinase B(Akt)/glycogen synthase kinase 3β(GSK3β)signaling pathway.Methods A rat model of post-stroke spasm(PSS)was established by middle cerebral artery occlusion(MCAO).Rats were divided into control group,sham operation group,model group,GA-L group,GA-H group and baclofen group.Rats in the model group,sham operation group and control group were intragastrically administered with the same amount of 0.9％NaCl every day,GA-H group was given 10.8 g·kg-1 GA by gavage daily,GA-L group was given 5.4 g·kg-1 GA by gavage every day,baclofen group was intragastrically administered with 5.4 mg·kg-1 baclofen every day for 4 weeks.Muscle tone was assessed by modified Ashworth scale.The volume of cerebral infarction was analyzed by 2,3,5-triphenyltetrazolium chloride(TTC)staining.The protective effect of GA on neuronal injury after cerebral ischemia-reperfusion injury was observed by Nissl staining and transmission electron microscopy.The expression levels of phosphorylated PI3K(p-PI3K),phosphorylated Akt(p-Akt)and phosphorylated GSK3β(p-GSK3β)in cerebral infarction and peripheral brain stem were detected by immunohistochemical staining.Results The volume of cerebral infarction in sham operation group,model group,GA-L group,GA-H group and baclofen group were 0,(34.23±1.21)％,(24.12±1.03)％,(18.26±1.08)％and(26.38±1.35)％,respectively.The contents of Nissl bodies in control group,sham operation group,model group,GA-L group,GA-H group were(126.23±8.13)％,(131.14±9.62)％,(52.21±6.11)％,(84.29±6.17)％and(112.24±8.21)％,respectively.At 4 weeks,the expressions of p-PI3K in sham operation group,model group,GA-L group,GA-H group and baclofen group in brain tissue surrounding cerebral infarction were 5.45±0.44,4.89±0.34,5.54±0.42,20.59±1.35,25.34±1.46 and 6.47±0.45;the expression of p-PI3K in the brain tissues around brain stem were 14.47±1.48,10.82±1.24,15.39±1.45,13.51±1.32,25.55±1.49 and 8.84±0.74;the expression levels of p-AKT in brain tissue surrounding cerebral infarction were 6.47±0.41,6.18±0.32,5.58±0.51,19.54±1.48,28.56±1.48 and 14.39±1.56;the expression of p-Akt in the surrounding brain tissue were 6.45±1.41,8.09±1.32,6.05±1.12,13.63±1.45,16.58±1.61 and 10.75±1.01;the expression levels of p-GSK3β in brain tissue surrounding cerebral infarction were 8.64±0.52,5.18±0.61,18.54±1.45,39.56±1.63,43.57±1.59 and 18.43±1.48;the expression of p-GSK3β in the surrounding brain tissue were 8.04±1.39,6.91±1.01,6.82±1.16,15.59±1.33,15.65±1.18 and 5.18±0.47.Compared with model group,the expressions of p-PI3K,p-Akt and p-GSK3β in cerebral infarction and peribrainstem brain tissue of rats in GA-L and GA-H groups were significantly up-regulated(all P＜0.05).Conclusion The inhibitory effect of GA on spasticity in PSS rats may be related to the up-regulation of PI3K/Akt/GSK3β pathway,which may be a supplementary treatment strategy for PSS.
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