醫(yī)學(xué)論文范文:rAAV2/1�睞crp30對(duì)動(dòng)脈粥樣硬化的GK大鼠NF�拨蔅及黏附分子的影響

醫(yī)學(xué)論文范文:rAAV2/1�睞crp30對(duì)動(dòng)脈粥樣硬化的GK大鼠NF�拨蔅及黏附分子的影響

【摘要】 目的 觀察rAAV2/1�睞crp30對(duì)動(dòng)脈粥樣硬化GK大鼠模型血清可溶性細(xì)胞間黏附分子(sICAM��1)、可溶性血管內(nèi)皮黏附分子(sVCAM��1)水平和NF�拨蔅表達(dá)的影響，從血管炎癥的角度探討脂聯(lián)素對(duì)糖尿病大血管病變的作用。方法 將造模成功的30只動(dòng)脈粥樣硬化的GK大鼠分為三個(gè)處理組：①模型1組，后肢肌肉注射鹽水;②模型2組，后肢肌肉注射空病毒rAAV2/1;③治療組，后肢肌肉注射 rAAV2/1�睞crp30。治療8周后處死所有大鼠，比較三組之間血清sICAM��1，sVCAM��1及主動(dòng)脈處NF�拨蔅p65 mRNA的表達(dá)水平。結(jié)果 治療組和模型1組、模型2組比較，血清sVCAM��1、sICAM��1顯著降低(P<0.05)。治療組和模型1組、模型2組比較，主動(dòng)脈NF�拨蔅p65 mRNA表達(dá)顯著下調(diào)(P<0.05)。結(jié)論 rAAV2/1�睞crp30可通過抑制NF�拨蔅的表達(dá)，減輕炎癥反應(yīng)而對(duì)糖尿病大血管病變產(chǎn)生保護(hù)作用。

【關(guān)鍵詞】 脂聯(lián)素;2型糖尿病大血管病變;核轉(zhuǎn)錄因子;可溶性細(xì)胞間黏附分子;可溶性血管內(nèi)皮黏附分子

Effects of rAAV2/1�睞crp30 on NF�拨蔅 and adhesion molecule

in GK rats with atherosclerosisZHONG Hui�瞛u1, ZHANG Ying1, LI Qiang�瞲iang2, LI Guo1

(1. Department of Endocrinology, Xiangya Hospital, Central South University, Changsha 410008;

2. Institute of Political Science and Administration, Central South University, Changsha 410083, China)ABSTRACT: Objective To study the effects of rAAV2/1�睞crp30 on sICAM��1 and sVCAM��1 level as well as NF�拨蔅 expression in GK rats with diabetic arteriosclerosis so as to explore the effect of adiponectin on diabetic macroangiopathy. Methods A total number of 30 atherosclerotic GK rat models were randomly divided into three groups: ① Model group one (M1): hind limb intramuscular injection of normal saline; ② Model group two (M2): hind limb intramuscular injection of vacuity virus rAAV2/1; ③ Treatment group (T): hind limb intramuscular injection of rAAV2/1-Acrp30 at a dose of 1×1012mg/L. After 8 weeks�� treatment, the rats were killed, and serum sVCAM��1 and sICAM��1 level as well as aortic NF�拨蔅p65mRNA expression were measured in each group. Aortic NF�拨蔅p65mRNA expression was measured by RT�睵CR.Results Compared with those in control model groups (M1 and M2), sVCAM��1 and sICAM��1 levels were decreased significantly in the treatment (T) group (P<0.05). Aortic NF�拨蔅p65 mRNA expression was significantly down�瞨egulated in the treatment (T) group compared with that in control model groups (M1 and M2) (P<0.05). Conclusion rAAV2/1�睞crp30 may produce protective effects on diabetic atherosclerosis by decreasing inflammatory reactions醫(yī).學(xué)全.在.線網(wǎng)站m.quanxiangyun.cn.

KEY WORDS: adiponectin; diabetic macroangiopathy; nuclear factor�拨蔅 (NF�拨蔅); soluble intercellular adhesion molecule (sICAM��1); soluble vascular cell adhesion molecule (sVCAM��1)

炎癥發(fā)病學(xué)說是近年來2型糖尿病病因與發(fā)病機(jī)制的重大進(jìn)展。該學(xué)說認(rèn)為：炎癥反應(yīng)在2型糖尿病及大血管病變的發(fā)生、發(fā)展中具有重要作用。核因子NF�拨蔅(nuclear factor)是調(diào)控基因轉(zhuǎn)錄的重要因子，它可與許多蛋白質(zhì)基因啟動(dòng)子和增強(qiáng)子部位的κB序列結(jié)合，誘導(dǎo)這些蛋白表達(dá)增強(qiáng)，從而參與炎癥反應(yīng)及動(dòng)脈粥樣硬化等多種疾病的病理過程。NF�拨蔅的活化會(huì)極大的刺激炎癥因子如血管細(xì)胞黏附分子��1(vascular cell adhesion molecule��1, VCAM��1)、細(xì)胞間黏附分子��1(intracellular adhesion molecule��1, ICAM��1)、E選擇素(E�瞫electin)等細(xì)胞黏附分子的轉(zhuǎn)錄與表達(dá)。上述細(xì)胞因子的增多可趨使單核巨噬細(xì)胞、淋巴細(xì)胞的侵入和聚集在動(dòng)脈內(nèi)膜下，內(nèi)膜下的細(xì)胞活化后可合成及分泌前炎癥介質(zhì)如白介素6、白介素8、腫瘤壞死因子(tumor necrosis factor, TNF�拨�)等[1]。NF�拨蔅是動(dòng)脈粥樣硬化前炎癥介質(zhì)、炎癥因子和炎癥產(chǎn)物的中樞調(diào)節(jié)者[2]。

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