【摘要】：目的觀察生長素對(duì)載脂蛋白E基因敲除(ApoE~(-/-))小鼠血漿白細(xì)胞介素8(IL-8)、單核細(xì)胞趨化因子1(MCP-1)、腫瘤壞死因子α(TNF-α)水平和血管壁核轉(zhuǎn)錄因子κBp65(NFκBp65)表達(dá)及動(dòng)脈粥樣斑塊的影響。方法8周齡雄性ApoE~(-/-)小鼠12只飼以西方類型膳食12周建立動(dòng)脈粥樣硬化模型,遺傳背景相同的6只8周齡雄性C57BL/6J小鼠飼以同類型膳食作對(duì)照。第8周時(shí)模型組分為腹腔內(nèi)注射生長素(100μg/kg)組(n=6)和注射生理鹽水(0.1mL)組(n=6),C57BL/6J小鼠亦給予生理鹽水(0.1mL)腹腔內(nèi)注射。第12周時(shí)眼眶取血,分離血漿,酶聯(lián)免疫吸附試驗(yàn)(ELISA)法檢測(cè)IL-8、MCP-1、TNF-α水平。取小鼠主動(dòng)脈進(jìn)行蘇丹Ⅳ染色,觀察主動(dòng)脈粥樣硬化病變面積占主動(dòng)脈內(nèi)膜面積的比例,行主動(dòng)脈竇HE及油紅O染色,觀察主動(dòng)脈竇動(dòng)脈粥樣斑塊面積占管腔總面積的比例,行主動(dòng)脈免疫組化染色,觀察NFκBp65的表達(dá)。結(jié)果與C57BL/6J小鼠比較,ApoE~(-/-)小鼠和ApoE~(-/-)+生長素小鼠總膽固醇和低密度脂蛋白膽固醇高[(6.7±0.5),(7.6±2.0)比(5.5±0.2)mmol/L,(5.6±0.3),(6.0±0.5)比(2.2±0.1)mmol/L,均P0.05],ApoE~(-/-)+生長素小鼠高密度脂蛋白膽固醇比ApoE~(-/-)組高[(0.5±0.1)比(0.3±0.1)mmol/L,P0.05]。與C57BL/6J小鼠比較,ApoE~(-/-)小鼠主動(dòng)脈粥樣硬化病變面積占主動(dòng)脈內(nèi)膜面積比例增加[(15.1±1.7)%比0],ApoE~(-/-)+生長素小鼠主動(dòng)脈粥樣病變面積占主動(dòng)脈內(nèi)膜面積比例較ApoE~(-/-)小鼠降低[(10.1±0.5)%比(15.1±1.7)%,P0.05];C56BL/6J小鼠主動(dòng)脈竇無動(dòng)脈斑塊形成(0%),ApoE~(-/-)組和ApoE~(-/-)+生長素組均有動(dòng)脈斑塊形成,但ApoE~(-/-)+生長素組小鼠主動(dòng)脈竇斑塊面積占管腔總面積的比例較ApoE~(-/-)組低[(22.6±2.2)%比(32.4±3.2)%,P0.01]。ApoE~(-/-)小鼠TNF-α、IL-8和MCP-1水平較C57BL/6J小鼠增高[分別為(24.5±1.7)比(10.1±0.5)ng/L,(33.5±16.7)比(16.8±8.8)ng/L,(78.0±5.6)比(13.5±1.8)ng/L;均P0.05],ApoE~(-/-)+生長素組TNF-α、IL-8和MCP-1水平較ApoE~(-/-)組降低[分別為(15.5±1.0)比(24.5±1.7)ng/L,(22.0±1.2)比(33.5±16.7)ng/L,(45.5±4.5)比(78.0±5.6)ng/L;均P0.05]。ApoE~(-/-)小鼠血管壁NF-κBp65表達(dá)較C57BL/6J增高,ApoE~(-/-)小鼠+生長素組血管壁NF-κBp65表達(dá)較ApoE~(-/-)小鼠組降低(P0.05)。結(jié)論生長素通過抑制炎癥反應(yīng)減少ApoE~(-/-)小鼠動(dòng)脈粥樣斑塊形成。
[Abstract]:Objective to observe the effect of auxin on plasma interleukin 8 (IL-8) and monocyte chemokine 1 (MCP-1) in apolipoprotein E knockout (ApoE~ (- / -) mice. The levels of tumor necrosis factor 偽 (TNF- 偽), the expression of transcription factor 魏 Bp65 (NF 魏 Bp65) and the effects of atherosclerotic plaques. Methods Twelve 8-week-old male ApoE~ (- / -) mice were fed with 12 Zhou Jianli's atherosclerosis model with western type diet, and 6 8-week-old male C57BL/6J mice with the same genetic background were fed with the same type of diet as control. At the 8th week, the model group was divided into two groups: intraperitoneal injection of growth hormone (100 渭 g/kg) and saline (0.1mL). C57BL/6J mice were also given intraperitoneal injection of normal saline (0.1mL). At the 12th week, the blood was taken from the orbit and the plasma was isolated. The level of IL-8,MCP-1,TNF- 偽 was detected by (ELISA) assay. The aorta of mice was stained with Sudan 鈪，

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