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Cerebral Ischemia And Reperfusion Injury In Tgf-beta1 Link Analysis And Qing Kai Ling Injection Of The Role

Posted on:2008-08-12Degree:MasterType:Thesis
Country:ChinaCandidate:Y WangFull Text:PDF
GTID:2204360212488878Subject:Integrative basis
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The mechanism of encephalopathy is one of modern medical research hot spots. Among them, imflammation of cerebral ischemia becomes an important reseach domain. Treatment of traditiongal Chinese medicine expresses good effect to many kinds of brains source disease. Especially, it is remarkable to the curative effect on cerebral ischemia. Its cilinic superiority is dominant. In the paper it puts in transforming growth factor-β1(TGF-β1) which produces in the procedure of cerebral ischemia-reperfusion injury, blocks TGF-β1 in blood circulation with mono-antibody of TGF-β1, and discusses the mechanism of cerebral ischemia -reperfusion.This paper includes two parts: documental research and experimental research.The documental research discusses the inflammation mechanism in the procedure of cerebral ischemia-reperfusion injury and how the cytokines affect. In this part, we overview the function of TGF-β1 in the cerebral ischemia and the research development of other research area.The experimental research includes two parts:The first part studys on the expression of TGF-β1 after cerebral ischemia -reperftsion, and discusses the effect of Qingkailing(QKL). Adult male Wistar rats received double common carotid clamping. These rats were divided into 17 groups randomly: normal group, model groups, treatment gruops(QKL), anti-TGF-β1 groups. The later four were divided into 12h, 24h, 48h, 72h respectively. We obeserved the expression of TGF-β1 and glial fibrillay acidic protein(GFAP) which is the marker of astrocyte. Furthermore, we observed the pathological changes after HE staining.The second part studys on changes of related cytokine expression after cerebral ischemia-reperftsion by blocking TGF-β1, and effect of QKL. Model and animals are same as Part1. Indexes include TNF-α, sICAM-1, IL-1βand VEGF. It studys on changes of related cytokine expression after cerebral ischemia reperftsion, and the effects of QKL.The results showed:Part 1①Blocking TGF-β1 and using QKL on serum NSE after ischemia-reperftsionAfter ischemia-reperftsion, compared with the model groups (group M), the groups of anti-TGF-β1(group MT) and QKL(group MQ) can reduce serum NSE content, the groups combined anti-TGF-β1 and QKL (group MQT)are worse than QKL. This shows that QKL has a dependability with TGF-β1.②Blocking TGF-β1 and using QKL on brain tissue TGF-β1 after ischemia reperftsionOn the domain of the ischemia brain, there is noticeable expression of TGF-β1. Compared with group N, the expression is more in group M and it is decreased in group MT and MQ. But in group MQT, their effect is not built up.③Blocking TGF-β1 and using QKL on the activation of AST. GFAP is the single marker of AST. Compared with group N, reperfusion 12h later, in group M the expression of GFAP is enhanced. But in group MT and MQ, it is reduced. IN group MQT, its expression is between in MQ and MT.④Blocking TGF-β1 and using QKL on the brainmorph after cerebral ischema eperftsion.When cerebral ischemia reperftsion accurs, anti-TGF-β1 is given. The brain tissue of the groups of anti-TGF-β1 and QKL have the superiority compared with the model groups, the groups of QKL still exists red blood cell which shape is like coin gathering in the microvessel. Improving the microvessel unobstructed degree can be get by united using QKL and anti- TGF-β1.Part 2①Blocking TGF-β1 and using QKL on TNF-αafter ischemia-reperftsionAfter ischemia-reperftsion, compared with group M, group MT and group MQ can reduce serum TNF-αcontent, group MQT are worse than QKL.②Blocking TGF-β1 and using QKL on IL-1βafter ischemia-reperftsionAfter ischemia-reperftsion, compared with group M, group MT can reduce IL-1βcontent. In group MQT it is lower than group M, but it seems that QKL has no effect on it. In group MQT, it is reduced than group M. And its content is similar to group MT.③Blocking TGF-β1 and using QKL on sICAM-1 after ischemia -reperftsionAfter ischemia-reperftsion, sICAM-1 is increased in group M. Compared with group M, group MT and group MQ can reduce its content and group MQT are higer than group MT and group MQ.④Blocking TGF-β1 and using QKL on VEGF after ischemia-reperftsionAfter ischemia-reperftsion, VEGF is increased in group M. Compared with group M, group MT and group MQ can reduce its content. In group MQT, it is reduced 12h later and its content is less than in group M. Totally, it is lower than group MQ.Conclusion:①Cerebral ischemia-reperfusion injury causes the endothelial cell disarrange -ment of the structure and the function suffers injury is one of again core damages. QKL has some treatment on the early time.②On the ealy time of cerebral ischemia-reperfusion , using TGF-β1mAb can reduce the injury , the activision of AST, the content of CKS .③QKL can reduce the content of the CKS which take part in the inflammation and reduce the expression of TGF-β1.④QKL may have effect on TGF-β1→TNF-α,sICAM-1,VEGF and it is not sure on TGF-β1→IL-1β.⑤QKL may have effect on AST→TGF-β1.
Keywords/Search Tags:cerebral ischemia-reperfusion injury, qingkailing, cytokine, transforming growth factor-β1
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