Intervention Of Huoxue Rongluo Recipe On The Expression Of JAK2/STAT3, IL-1β And TNF-α In Rat Model Of Cerebral Ischemia-reperfusion Injury

Objective:To explore the effect of JAK2/STAT3 in the inflammatory reaction of cerebral ischemia and reperfusion injury,To probe into the influence on the expressions of IL-1β and TNF-α by activation of JAK2/STAT3 after cerebral ischemia and reperfusion injury preliminarily;And to investigate the protective mechanism of Huoxuerongluofang on cerebral ischemia and reperfusion injury.Methods:Rats were divided into sham operation group and modeling group.Rats of the modeling group were divided into model group,Huoxuerongluofang group(model+huoxuerongluofang),AG490 group(model+AG490)after modeling successfully by thread embolism method.Rats of model group,Huoxuerongluofang group and AG490 group were divided into four subgroups-6h,12 h,24h,72 h,there were 6 rats in each subgroup.The corresponding drugs were given to the corresponding group at different time points, the neurological deficits were scored at the corresponding time points,and then the brains were removed and taken for immunohistochemical detection.Results:(1)After reperfusion infarction in rats among experimental groups,neural function defect scores of Huoxuerongluofang group and AG490 group at 24 h,72h were lower than those of the model group(P<0.05);Compared with the AG490 group,nerve function defect score of Huoxuerongluofang group had no significance at each time point(P>0.05).(2)After reperfusion infarction in rats among experimental groups,the expressions of JAK2 in Huoxuerongluofang group were significantly lower than those in model group at 12 h,24h,72h(P<0.01);the expressions of JAK2 in the AG490 group at each point were significantly lower than those in the model group(P<0.01);Compared with the AG490 group,the expressions of JAK2 in Huoxuerongluofang group at 6h were higher(P<0.05),but the expressions of JAK2 in Huoxuerongluofang group and AG490 group were similar at the rest of the time points(P>0.05).(3)After reperfusion infarction in rats among experimental groups,the expressions of STAT3 in Huoxuerongluofang group at 12 h,24h,72 h were obviously lower than those in the model group(P<0.01);the expressions of STAT3 in the AG490 group at each point were significantly lower than those in the model group(P<0.01);Compared with the AG490 group,the expressions of STAT3 in Huoxuerongluofang group at 6h were significantly higher(P<0.01),but the expressions of STAT3 in Huoxuerongluofang group and AG490 group were similar at the rest of the time points(P>0.05).(4)After reperfusion infarction in rats among experimental groups,the expressions of IL-1β in the Huoxuerongluofang group at 12 h,24h,72 h were significantly lower than those in the model group(P<0.01);the expressions of IL-1β in the AG490 group were significantly lower than those in the model group(P<0.01);Compared with the AG490 group,the expressions of IL-1β in Huoxuerongluofang group at 6h were higher(P<0.05),but the expressions of IL-1β in Huoxuerongluofang group and AG490 group were similar at the rest of the time points(P>0.05).(5)After reperfusion infarction in rats among experimental groups,the expressions of TNF-α in Huoxuerongluofang group at each time point were lower than those in the model group(P<0.05),and were significantly lower at 12 h,24h,72h(P<0.01);the expressions of TNF-α at each time point in the AG490 group were significantly lower than those in the model group(P<0.01);Compared with the AG490 group,the expressions of TNF-α in Huoxuerongluofang goup at 6h were significantly higher than those in the AG490 group(P<0.01),but the expressions of TNF-α in Huoxuerongluofang group and AG490 group were similar at the rest of the time points(P>0.05).Conclusion:The activation of JAK2/STAT3 signal pathway can promote the inflammatory reaction of cerebral ischemia reperfusion and aggravate the injury by improving the expressions of IL-1β and TNF-α;AG490 and Huoxuerongluofang can protect the neurological function by reducing the expressions of JAK2,STAT3,IL-1βand TNF-α after cerebral ischemia and reperfusion injury.