| BackgroundIschemic cerebral vascular disease (ICVD), as a clinical risk, urgent, seriousillness, have a pathological basis of chronic disease, and the evolution process iscomplex and changeable. its mortality increases with age, and seriouslyendangering the health of aged people. In our country, with the increase of the agedand the arrival of aging society, the research of pathogenesis of ischemic stroke inaged is urgent to seek the effective treatment. In recent years, introduced theconcept of therapeutic angiogenesis, and provides a new idea for the treatment ofICVD. Angiogenesis is not only science and biological processes in a complexorganization, at the same time, a process in dynamic balance of complex signaltransduction change, an important way to study is a comprehensive understandingof vascular and the regulation mechanism of generation of complex processes, butalso enable us to further clarify the pathophysiological characteristics of ICVD,and for the open up a new way for the treatment of ischemic cerebral vasculardiseases. With the research on signal transduction pathway in cerebralischemia/reperfusion angiogenesis mechanism, gradually realize the signaltransduction pathways that regulate angiogenesis in vascular networkreconstruction of the new role, but the brain injury after ischemia/reperfusionangiogenesis, especially older angiogenesis research is rare. This paper on thebasis of previous studies, from the changes of the expression of α-SMA, SDF-lα,CXCR4protein of cerebral ischemia/reperfusion in the aged rats brain mechanismof angiogenesis, and taking it as the breakthrough point to explain the Chineseherbal compound Naomaitong on angiogenesis promoting effect and possiblemechanism of action.Objective1By comparing the youth group, aging control group (referred to as the aginggroup), nimodipine aging group (referred to as nimodipine group) and Naomaitong aging group (referred to as the Naomaitong group) score, pathologic changes ofcerebral ischemia and ischemic brain areas of rat brain nerve dysfunction after I/R,to explore the Naomaitong the protective effect on brain tissue of aged rats withI/R.2By observing the expression of youth group, aged group, nimodipine group andNaomaitong group rats brain tissue I/R α-SMA, SDF-lα, CXCR4protein, to studythe Naomaitong on angiogenesis in brain tissue of aged rats I/R role.Method1The comprehensive scores of nerve function method, TTC staining and lightmicroscopy observation of each group were compared in rats with cerebral ischemiareperfusion state (I)3h (I/R)24h,3d,6d,12d neurological dysfunction score, brainischemia area and ischemic brain tissue pathological change.2Immunohistochemical method was used to observe the cerebral ischemiareperfusion (I)3h (I/R)24h,3d,6d,12d in brain tissue of α-SMA, SDF-1α, CXCR4protein expression.Result1Comparing of neurological function score and neural infarct area and brainmicrovascular pathology of cerebral ischemia-reperfusion injury in each groupof rats.1.1Each group rats neurological function scoreThe neurological score of sham operation group was significantly higher thanin model group at each time (P<0.01); the young model group12d neural functionscores than the6d group,3D group increased（P<0.05）, group12d neural functionscore than the old model6d group,3d group increased (P<0.05), compared with themodel group, nimodipine group12d neural function score increased (P<0.05),Naomaitong group3d, group6d, group12d neural function score was significantlyincreased (P<0.01, P<0.05), wherein the Naomaitong group12d respectively.Compared with12d group and model group, nimodipine group12d increased(P<0.01); nimodipine12d group,6d group than in the3d group increased (P<0.05),Naomaitong group12d increased than those of the3d group and6d group (P<0.01,P<0.05).1.2Each group rats neural infarct area of cerebral ischemia-reperfusion injury.The model group compared with the sham operation group increased at eachtime point(P<0.01), model group12d cerebral infarction area compared with the model group6d decreased significantly (P<0.05); compared with the model group,the nimodipine group rats cerebral infarction area visible point decreasedsignificantly (P<0.05), Naomaitong group at different time points in rats withcerebral infarction area compared with the model group decreased significantly(P<0.01, P<0.05), and nimodipine in comparison, Naomaitong6d of cerebralinfarction group and12d group rats area was significantly reduced (P<0.01,P<0.05); Naomaitong group12d and group6d were significantly lower in3d groupreduced the area of cerebral infarction (P<0.05).1.3Brain microvascular pathology of aged I/R rats and the effect of Naomaitongon itRoutine HE stain, the cerebral cortex ischemic core and penumbra injury ofbrain tissue pathological changes under light microscope showed: compared withthe young model group in the same time, the aged model group were severelyinjured, and the recovery was slow; compared with the same time point of agedmodel group, nimodipine group and Naomaitong group the damage is light; thesame time compared with nimodipine group, Naomaitong group had slight injury;2The α-SMA expression process after I/R in aged rats brain and the effect ofNaomaitong on its expressionThe results of immunohistochemistry showed: blank control group showed aweak expression of α-SMA; compared with the young model group, aged modelgroup, ischemia3h, reperfusion24h,3d,6d,12d α-SMA expression were lowerthan the young model group (P<0.01), aged model group, ischemia, reperfusion24h,3h,3d positive expression of α-SMA expression increased, peak at6d ofreperfusion,12d positive expression of α-SMA began to decrease, but still at ahigher level; compared with the same time point of aged model group, nimodipinegroup and Naomaitong group, the positive expression of α-SMA were higher thanthat in aged model group (P<0.01); compared with the at the same time thenimodipine group, Naomaitong group, ischemia3h, reperfusion24h,3d,6d,12dα-SMA positive expression was higher than that of nimodipine group (P<0.05,P<0.01).3The expression of SDF-lα, CXCR4protein in the brain of I/R rats and theinfluence of Naomaitong on its expressionThe results of immunohistochemistry showed: blank control group showedweakly positive expression of SDF-lα, CXCR4; compared with the same time young model group, aged model group, ischemia3h, reperfusion24h,3d,6d,12d,SDF-lα, CXCR4expression were decreased (P<0.05, P<0.01), aged in SDF-lα,CXCR4model group, the positive expression of SDF-lα, CXCR4peak at24h ofreperfusion, ischemia reperfusion3d~12d trend was gradually reduced; comparedwith the aging model group in the same time, Naomaitong group and nimodipinegroup at each time point of SDF-lα, CXCR4positive expression was higher thanthat in aged model group (P<0.05, P<0.01); compared with nimodipine group inthe same time points: Naomaitong group, ischemia3h, reperfusion24h,3d,6d,12din rat SDF-lα, CXCR4, the positive expression of SDF-lα and CXCR4was higherthan that of nimodipine group (P<0.01).Conclusion1With the increase of age, aged rats with I/R induced brain damage occurs early,severity, slow recovery after cerebral ischemia injury, a reduced expression of-SMA, microvessel density decreased, brain microvessel quantity compared toyoung rats was significantly reduced, this may and the expression of SDF-l α,CXCR4protein is related to the reduction of. May also is old ICVD the condition isserious, one of the pathophysiological mechanisms of morbidity and high mortality2Naomaitong could significantly alleviate the pathology of I/R after brain injuryin aging rats, decrease the change of I/R of aged rats after nerve dysfunction score,reduce infarct area and up regulation of I/R in rats brain tissue of α-SMA proteinexpression, and its mechanism may be related to Naomaitong promoting SDF-l α,CXCR4protein expression the relevan.3Naomaitong could facilitate the activation of SDF-lα/CXCR4signaltransduction pathway, collect a large number of blood vessel growth factors to theischemic brain tissue, promote angiogenesis, has a protective effect on the injury ofbrain I/R in aged rats. |
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