本文選題：小鼠模型 + 狹窄　； 參考：《南昌大學(xué)》2011年碩士論文

【摘要】：背景目的： 前列腺素H合成酶(PGHS),也稱環(huán)氧合酶(COX),是前列腺素類物質(zhì)合成的關(guān)鍵酶,它在動脈粥樣硬化、血管成形術(shù)后狹窄等血管炎性疾病的發(fā)展中扮演著重要的作用。雖然COX-2選擇性抑制劑有增加心臟病發(fā)作和中風(fēng)的危險,但是我們對它在介入治療后血管重塑中的作用知之甚少。本實驗利用COX-2 K0、COX-1COX-2(COX-1基因插入C0X-2位點)轉(zhuǎn)基因小鼠的動脈損傷模型,揭示COX-2來源的前列腺素表達(dá)對血管損傷后內(nèi)膜增生狹窄的影響。 方法結(jié)果： 本實驗通過建立股動脈血管損傷小鼠動物模型,利用免疫熒光和HE染色判斷小鼠股動脈損傷模型是否建立成功,采用HE染色法、Envision免疫組織化學(xué)法、利用image pro plus軟件分析小鼠內(nèi)膜和中膜面積比(I/M ratio),描述COX-2 K0、COX-1＞COX-2轉(zhuǎn)基因小鼠和野生型小鼠股動脈損傷后四周的特征。VSMC標(biāo)記物(α-actin)免疫組化結(jié)果顯示在所有損傷小鼠中,損傷血管內(nèi)膜幾乎全由血管平滑肌組成。COX-2 K0小鼠的股動脈病變中的巨噬細(xì)胞和中性粒細(xì)胞浸潤明顯少于COX-1＞COX-2(P0.05)和WT小鼠(P＜0.01)。COX-2 K0小鼠同COX-1COX-2(4.534±1.274,PK0.05)和WT對照組小鼠(4.534±1.274,P＜0.05)相比內(nèi)膜／中膜比明顯降低。上述結(jié)果表明,COX-2缺失可以防止血管平滑肌細(xì)胞反應(yīng)性增殖。 結(jié)論： COX-2來源前列腺素參與損傷引起的動脈重構(gòu)。這些結(jié)果表明,阻斷COX-2的下游信號可能提供一種方法防止血管成形術(shù)后再狹窄的動脈阻塞。
[Abstract]:Background objectives: Prostaglandin H synthase (PGHSN), also known as cyclooxygenase, is a key enzyme in the synthesis of prostaglandins, which plays an important role in the development of vasculitis such as atherosclerosis, angioplasty and stenosis. Although selective inhibitors of COX-2 may increase the risk of heart attack and stroke, little is known about its role in vascular remodeling after interventional therapy. In this study, the arterial injury model of transgenic mice with COX-2 K0 COX-1COX-1 gene inserted into C0X-2 site was used to reveal the effect of prostaglandin expression derived from COX-2 on intimal hyperplasia and stenosis after vascular injury. Method results: In this experiment, the animal model of femoral artery vascular injury was established, and the success of the model was determined by immunofluorescence and HE staining, and the envision immunohistochemical method was used to determine the success of the model. The image pro plus software was used to analyze the ratio of intima and medial area of COX-2 K0 COX-1 > COX-2 transgenic mice and wild-type mice after femoral artery injury. The immunohistochemical results of 偽 -actinin showed that the expression of 偽 -actinin was found in all the injured mice. The invasion of macrophages and neutrophils in femoral artery lesions of injured vascular intima was almost entirely composed of vascular smooth muscle. The infiltration of macrophages and neutrophils in femoral artery lesions of the injured vascular intima was significantly less than that of COX-1 > COX-2 (P0.05) and WT mice (P < 0.01).COX-2 K0 vs COX-1COX-2(4.534 鹵1.274PK0.05) and WT control mice (4.534 鹵1.274P < 0.05). These results suggest that COX-2 deficiency can prevent reactive proliferation of vascular smooth muscle cells. Conclusion: Prostaglandins derived from COX-2 are involved in arterial remodeling caused by injury. These results suggest that blocking downstream signals of COX-2 may provide a way to prevent restenosis after angioplasty.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2011
【分類號】：R363

【參考文獻(xiàn)】

相關(guān)期刊論文 前2條

1 李曉東;第二代COX-2抑制劑[J];世界臨床藥物;2003年11期

2 武曉靜,黃嵐,宋代良,晉軍,趙剛;內(nèi)皮細(xì)胞生長狀態(tài)對血管平滑肌細(xì)胞增生遷移的影響(英文)[J];生理學(xué)報;2003年05期

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本文編號：1986501