| ObjectiveTo observe the protective effect of HNG on cerebral ischemia-reperfusion injury in rats,and to investigate the effect of Janus protein tyrosine kinase 2/signal transducers and transcription activator 3(JAK2/STAT3)signaling pathway on myeloid leukemia-1(B-cell lymphoma/leukemi2,Bcl-2)in global cerebral ischemia-reperfusion injury and JAK2/ STAT3 signal transduction Pathways in ischemic brain injury.Effects of HNG on expression of JAK2,STAT3,Mcl-1 and Bcl-2 in frontal lobe of rats with global cerebral ischemia and reperfusion.Method:The model used in this study is: modified Pulsineli4 vascular occlusion method of rat cerebral ischemia-reperfusion model.10% chloral hydrate(300-350 mg /kg body weight)intraperitoneal injection anesthesia.Prone position of the rat limbs and head fixed to the control panel,povidone-iodine will be local skin disinfection.Along the midline of the back of the neck to cut the skin,blunt separation fascia,muscle,to the first cervical spinous process after the separation of the two sides can be revealed on the first cervical vertebral lamellar wing,The vertebral artery of the deep wing of the two flanks is electro coagulated so that the vertebral artery is permanently occluded.Suture the muscles and skin layer by layer.After 24 hours,the rats were anesthetized,cut the skin along the anterior part of the anterior neck,bluntly separated fascia and anterior cervical muscles,free from both sides of the common carotid artery,wearing a No.1 silk thread,Clamp the bilateral common carotid artery for 10 minutes and then suture the skin.The rats in the Sham operation group were subjected to vertebral artery coagulation alone,and the common carotid artery was exposed but not caught.Forty-seven SD rats were randomly divided into Sham group,global cerebral ischemia group,global cerebral ischemia+HNG treatment group(GI+HNG).Including Sham group 6,GI group,GI+HNG group 36.GI group and GI + HNG group were divided into 6 subgroups at 1h,3h,6h,12 h,24h and 72 h after reperfusion,6 rats in each subgroup.The rats in the GI+HNG group were treated with HNG(50?g/kg body weight)and the frontal lobes were detected by real-time quantitative PCR(RT-PCR)JAK2,STAT3,MCL-1 and BCL-2 mRNA expression levels.Result1.JAK2/STAT3 signaling pathway may be involved in the mechanism of cerebral ischemia-reperfusion injury after cerebral ischemia-reperfusion injury.2.HNG on the neurological changes of cerebral ischemia-reperfusion injury in rats: Sham rats had no significant neurological impairment and no significant changes in behavior,the whole cerebral ischemia group(GI)(GI+HNG)in the whole cerebral ischemia + HNG group(GI+HNG)were different from those in the neurological deficits(GI+HNG)(GI+HNG)in the whole cerebral ischemia group was significantly higher than that in the control group(P<0.05),and the neurological impairment was significantly higher in the whole cerebral ischemia group(P<0.05)Significant difference(P<0.05),suggesting that HNG can improve neurological deficits.3.The effect of global cerebral ischemia+HNG on the pathological changes of ischemic frontal cortex after 24 hours of cerebral ischemia-reperfusion injury in rats: the structure of brain tissue of Sham rats was normal,the morphology of endothelial cells Normal,nerve cell structure is complete,cytoplasm and nuclei clearly visible.In the ischemia-reperfusion group(GI group),the volume of the frontal cortex was decreased,the cytoplasm was loose,the cytoplasm and the nucleus were concentrated and fixed,and the chromatin was concentrated in the vicinity of the nucleus of the nucleus to form apoptotic bodies.The extent of neuronal degeneration in the whole brain ischemic + HNG group(GI+HNG group)was significantly higher than that in the whole cerebral ischemia group(GI group),and the difference was significant(P<0.05)HNG can reduce the pathological damage of cranial nerve cells.4.GI + HNG treatment of the frontal lobe JAK2,STAT mRNA expression levels after this injury a certain influence: sham group(sham-operated group)a small amount of JAK2,STAT3 mRNA expression,ischemia-reperfusion group(The expression of JAK2 and STAT3 mRNA in the brain tissue of the whole group was significantly higher than that of the control group(P<0.05).The expression of JAK2 and STAT3 mRNA in the cerebral ischemia group and the whole cerebral ischemia + HNG group was significantly higher than that in the control group(P<0.05),which indicated that this treatment could improve the expression of JAK2 and STAT3 mRNA in the group of cerebral ischemia + HNG treatment group.5.Effects of Cerebral Ischemia+HNG on MCL-1 and BCL-2mRNA: MCL-1 and BCL-2 mRNA were mainly expressed in neurons.Apoptotic cells were brown and normal cells were blue-violet.The Sham operation group had a small amount of MCL-1 and BCL-2 positive cells,which may be normal anti-apoptotic cells.The levels of MCL-1 and BCL-2 mRNA in the whole cerebral ischemia group were significantly different from those in the Sham-operated group(P<0.05).The expression of MCL-1 and BCL-2 mRNA in the whole cerebral ischemia + HNG group was significantly higher than that in the whole cerebral ischemia group(P<0.05).Suggesting that global cerebral ischemia+HNG treatm-ent can increase the expression of MCL-1 and BCL-2 mRNA.Conclusions1.The global cerebral ischemia and reperfusion neurologic defects in rats,brain tissue pathological changes significantly,increase the number of brain cells.2.Increased expression of JAK2,STAT3 MCL-1 and BCL-2 genes in rat cerebral ischemia-reperfusion.MCL-1 and BCL-2 are involved in the formation of anti-apoptotic cells in ischemic regions,while JAK2,STAT3 activation and over expression may regulate the expression of MCL-1 and BCL-2 after ischemia.3.Global cerebral ischemia+HNG treatment can improve neurological deficit after ischemia and reperfusion,reduce brain cell necrosis and reduce brain cell apoptosis.The protective mechanism may be related to the activation of JAK2/STAT3 pathway to increase the expression of MCL-1 and BCL-2 genes in brain tissue. |
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