| BackgroundIf timely after cerebral ischemia reperfusion recovery time windowpenumbra of oxygen supply, can save neurons physiological functions,improve patient prognosis. However, with the restoration of the bloodsupply to the ischemic area may also lead to further tissue damage anddysfunction that ischemia-reperfusion injury.Therefore, how to reducecerebral ischemia-reperfusion injury become the key to the treatment ofischemic cerebrovascular disease. Recent studies have shown that afterischemia and hypoxia, brain tissue can upregulate the expression ofintracellular signal transduction pathways, start their own angiogenesismechanism,and gradually establish their own collateral circulation toaccommodate or resist cerebral ischemia and hypoxia, reduce reperfusioninjury. After ischemic stroke involved in angiogenesis intracellular signaltransduction pathways and mechanisms are more complicated, whichPI3K/Akt signaling pathway and brain microvascular ischemic penumbrageneration and is closely related to the establishment of collateralcirculation, express their signal effector molecules, is regulated by avariety of factors both inside and outside the cells, and thus play animportant role in the development of disease. However, this endogenousangiogenesis mechanism means oxygen supply is insufficient to compensatethe ischemic area, the need to promote angiogenesis drug intervention,which is the role of traditional Chinese medicine research in angiogenesisand signaling pathways, provides a broad prospects. The issue on the basis of preliminary studies, from the rat model of ischemic region andexpression changes penumbra α-SMA, PI3K, Akt1to explore the aged ratswith cerebral ischemia/reperfusion angiogenesis characteristics andtraditional Chinese medicine preparation for aged rats with cerebralischemia/reperfusion angiogenesis effects and possible mechanisms ofaction, which is characterized by senile depth pathophysiology of ischemiccerebrovascular disease, explore traditional Chinese medicine treatment ofischemic cerebrovascular disease pathways, with great social significanceand scientific value.Objective1By observing the youth group,age group,nimodipine groupNaomaitong rat cerebral ischemia(I)3h reperfusion(I/R)24h,3d,6d,12dpathological changes in brain tissue damage,revealing a large agingFeatures mouse brain I/R injury and cerebral protective effects on themNaomaitong;2By studying youth group,aging group,nimodipine group Naomaitongrat cerebral ischemia (I)3h reperfusion (I/R)24h,3d,6d,12d cerebral cortexpenumbra microvascular α-SMA expression,revealing aged rats I/R brainangiogenesis Naomaitong characteristics and its impact;3By studying youth group,aging group,nimodipine group Naomaitongrat cerebral ischemia (I)3h reperfusion (I/R)24h,3d,6d,12d cerebral cortexpenumbra PI3K,Akt1expression changes reveal possible mechanisms ofaging rats I/R angiogenesis and Naomaitong on them.Method1Copy MCA suture method using focal cerebral ischemia (I)3hreperfusion (I/R)24h,3d,6d,12d animal model of rats was observed byoptical microscopy techniques in cerebral I/R pathological features of thecerebral cortex at different time points after brain injury,to further exploreNaomaitong aged rats with brain ischemia reperfusion injury in brain tissuepathological changes.2Copy MCA suture method using focal cerebral ischemia (I)3hreperfusion (I/R)24h,3d,6d,12d animal models,using immunohistochemicalmethods compare cerebral ischemia in rats3h reperfusion1d,3d,6d,12dafter cerebral cortex penumbra microvascular expression of α-SMA,the study of aging Naomaitong ischemia reperfusion microvascular α-SMAexpression of change.3Copy MCA suture method using focal cerebral ischemia (I)3hreperfusion (I/R)24h,3d,6d,12d animal models,using immunohistochemicalmethods compare cerebral ischemia3h and then each group perfusion1d,3d,6d,12d posterior cerebral cortex penumbra PI3K, Akt1expressionchanges of aging research Naomaitong ischemia reperfusion brain tissuePI3K,Akt1expression.Result1Aged rats I/R brain microvascular pathology observed and its impactNaomaitongBy conventional HE staining, light microscopy model of ischemiccerebral cortex and the central area of penumbra pathological changes ofbrain tissue damage found in I3h began edema; I/R24h, I/R3d day moreserious degree of edema, nerve fiber disorders, vascular gap widened;peaked when I/R6d edema, and seen a lot of nerve cells, glial celldegeneration and necrosis, capillary wall damage; disappeared when I/R12dedema, neuronal, glial cells, nerve fibers reduce liquefaction necrosis fociappear. Compared with the model group, the same time the youth, agingmodel edema early group were severely injured, recovery is slow; agingmodel group compared with the same point in time, Naomaitong nimodipinegroup and pathological tissue damage lighter.2The aged rat brain I/R α-SMA protein schedule change impacts and itsexpression Naomaitong expressionBy immunohistochemistry results showed: α-SMA weak expression ofyouth and aging sham group were seen; youth model group I24h expressionbegan to rise, with the changes I/R time points, the positive upward trend,I/R6d,12d at a higher level; compared with the model group, youth, agingmodel group I3h, I/R24h, I/R3d, I/R12d model group were significantlylower than the young (P <0.05, P <0.01); and aging model group at the sametime point, Naomaitong group and α-SMA expression nimodipine groupwere higher than the aging model group (P <0.05). 3Aged rats brain I/R PI3K drive change and influence its expressionNaomaitong when Akt1protein expressionBy immunohistochemistry results showed: PI3K weak expression ofyouth and aging sham group were seen; youth model group I24h expressionbegan to rise, with the changes I/R time points, the positive upward trend,I/R6d reach peak, I/R12d is decreasing; compared with the same timeyoung model group, the positive aging model group were lower (P <0.05);aging model group compared with the same point in time, Naomaitong groupand nimodipine group at each time point PI3K expression were higher thanthe aging model group (P <0.01).Akt1weakly positive expression of youth and aging sham group wereseen;youth model group I24h expression began to rise,with the changesI/R point in time,the positive upward trend, I/R6d peaked, I/R12d wasdecreasing trend; compared with the same time young model group, thepositive expression of Akt1aging model group were lower (P <0.05); agingmodel group compared with the same point in time, the positive expressiongroup and Naomaitong nimodipine group at each time point aging modelgroup were higher than (P <0.01); positive Naomaitong nimodipine groupcompared with the same set of time points, higher than the nimodipinegroup (P <0.01).Conclusion1suffering from the same condition I/R injury, aging model rats therewas a young rat model group earlier injury, damage heavy, slow recovery.With the extension of rat I/R time, each model group, the degree of tissuerepair after injury is different, Naomaitong can significantly improve brainaging rats after I/R tissue damage.2after cerebral I/R injury in the brain tissue of the models seenangiogenesis, and with the extension of rat I/R time gradually increasedangiogenesis. Pharmacological interventions can promote angiogenesis,which went role Naomaitong significantly.3Naomaitong aged rats after cerebral I/R injury has a protective effect,the mechanism may increase the ischemic penumbra PI3K, Akt1signaleffector molecule expression, activation PI3K/Akt1signal transduction pathway. |
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