| BackgroundIschemic cerebrovascular disease is a common neurological disease.Clinical recanalization after cerebral embolization,correction of heart failure,correction of shock,recanalization of microcirculation and cardiopulmonary resuscitation may cause cerebral ischemia and restore blood supply to the ischemic area.Reperfusion injury may aggravate brain dysfunction,which is called cerebral ischemia reperfusion injury.Stellate ganglion block is a common clinical sympathetic nerve block method,can make the increased blood flow to the disposal area,circulation,and can be adjusted in the nervous system,endocrine system and immune system function,but whether it can inhibit M1 microglia activation relieve cerebral ischemia reperfusion injury remains to be explored.ObjectiveThis research adopts the line switch block middle cerebral artery of 90 min restore perfusion method preparation of cerebral ischemia reperfusion injury model of rats as the research object,explore the cervical sympathetic trunk from broken nerve protection of ischemia reperfusion injury in rats and mechanism of action,for the clinical application of star festival block in the treatment of cerebral ischemia reperfusion injury risk patients to provide experimental basis.Methods1.54 SPF healthy male SD rats,aged 8 to 10 weeks and weighing 240 to 270 g,were divided into 3 groups by random number table(n=18): Sham group,cerebral ischemia reperfusion group,and cervical sympathetic trunk severation group(TCST group).2.Sham group operated but did not have inserted cable thrombus,IR group line bolt obstruction middle cerebral artery model to establish cerebral ischemia reper fusion injury,TCST group immediately after middle cerebral artery obstruction.2.The Sham group underwent surgical operation without inserting the thread plug,the IR group underwent the method of restoring the perfusion of the middle cerebral artery occlusion for 90 minutes to establish the cerebral ischemia reperfusion injury model,and the TCST group underwent the cervical sympathetic trunk dissection immediately after the middle cerebral artery occlusion.3.Serum levels of TNF-α,IL-6 and IL-1β were determined by ELISA at 6,12 and 24 h after cerebral ischemia reperfusion,respectively.At 24 h after cerebral ischemia reperfusion,Zealonga score was used to record the neurological deficit score,TTC staining was used to measure the cerebral infarct volume ratio,TUNEL staining was used to detect the apoptosis rate of cerebral cortical region cells,and Western blot was used to detect the expression levels of CD68 and Iba-1 protein in brain tissues,HE staining was used to observe the morphological changes of cortical region of brain tissue and MRI was used to detect the degree of pathological injury of brain tissue.Results1.Compared with Sham group,serum concentrations of TNF-α,IL-6 and IL-1β in IR group and TCST group were increased at each time and time point(P <0.05);Compared with IR group,the serum concentrations of TNF-α,IL-6 and IL-1β in TCST group were decreased at each time point(P <0.05).2.Compared with Sham group,neurological deficit score and cerebral infarct volume ratio were increased in IR group and TCST group(P <0.05).Compared with IR group,neurological deficit score and cerebral infarct volume ratio were decreased in TCST group(P <0.05).3.TUNEL assay was used to detect the apoptosis of cortical cells in each group.Compared with Sham group,the apoptosis rate of cortical cells in IR group and TCST group was significantly increased(P <0.05).Compared with IR group,the apoptosis rate of cortical region cells in TCST group was significantly decreased(P <0.05).4.Compared with Sham group,the expression of CD68 and Iba-1 in brain tissues of IR group and TCST group were up-regulated(P <0.05);Compared with IR group,the expression of CD68 and Iba-1 in brain tissue of TCST group was down-regulated(P <0.05).5.Compared with Sham group,the morphological changes of nerve cells and pathological damage of brain tissue were aggravated in IR group and TCST group.Compared with IR group,the morphological changes of nerve cells and pathological damage of brain tissue were significantly reduced in TCST group.Conclusion1.Cervical sympathetic trunk dissection has a neuroprotective effect on cerebral ischemia-reperfusion injury in rats.Stellate ganglion block can reduce the production /release of proinflammatory factors and reduce inflammatory response.2.The mechanism of cervical sympathetic trunk dissection alleviating cerebral ischemia-reperfusion injury in rats may be related to inhibiting the activation of M1-type microglia and alleviating inflammatory response. |
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