本文關鍵詞： 動脈粥樣硬化 肝細胞生長因子 間質-上皮轉化因子 炎癥因子 M1型巨噬細胞 M2型巨噬細胞　出處：《安徽醫(yī)科大學》2017年碩士論文　論文類型：學位論文

【摘要】：目的通過對動脈粥樣硬化(AS)模型兔多次肌肉注射重組腺病毒-肝細胞生長因子(Ad-HGF),探討肝細胞生長因子(HGF)對AS模型兔巨噬細胞M1型標志物精氨酸酶II(Arg II)及誘導性一氧化氮合酶(i NOS)的表達、巨噬細胞M2型標志物CD163及精氨酸酶I(Arg I)的表達、血清炎癥因子、血脂和AS斑塊成分的影響。方法40只4月齡雄性新西蘭大耳兔隨機分為正常組、AS模型組、空載體腺病毒(null-Ad)組,Ad-HGF組,正常組給予普通飼料,其余各組均給予高膽固醇飼料。于喂養(yǎng)第4周、5周、6周時,Ad-HGF組肌肉注射1 ml Ad-HGF(5×109PFU/m L·只),null-Ad組肌肉注射1 ml null-Ad(5×109PFU/m L·只),正常組和AS模型組注射等量生理鹽水。12周留取血液標本后處死動物取出主動脈,分別測定血清炎癥因子IL-6、IL-10、血脂水平,主動脈內膜/中膜厚度比值(IMT),血管平滑肌細胞(VSMCs)、膠原纖維和巨噬細胞的含量,主動脈HGF、間質-上皮轉化因子(c-Met)、Arg-II、i NOS、CD163、Arg I的蛋白表達。結果與正常組比較,AS模型組血清IL-6、血脂水平、主動脈Arg II、i NOS的蛋白表達、IMT、膠原纖維及巨噬細胞含量明顯增加(P0.05),血清IL-10水平、主動脈HGF、c-Met、CD163、Arg I的蛋白表達、VSMCs含量明顯降低(P0.05);與AS模型組相比,null-Ad組血清炎癥因子IL-6、IL-10、血脂水平,IMT,VSMCs、膠原纖維和巨噬細胞的含量,主動脈HGF、c-Met、Arg II、i NOS、CD163、Arg I的蛋白表達無明顯差別(P0.05);與AS模型組相比,Ad-HGF組血脂水平無明顯差別(P0.05),血清IL-6水平、主動脈Arg II、i NOS的蛋白表達、IMT及巨噬細胞含量明顯降低(P0.05),血清IL-10水平、主動脈HGF、c-Met、CD163、Arg I的蛋白表達、VSMCs含量、膠原纖維含量明顯增加(P0.05)。結論HGF降低AS模型兔促炎因子水平,增加抗炎因子水平,抑制M1型巨噬細胞浸潤、誘導M2型巨噬細胞分化、增加斑塊VSMCs和膠原纖維含量而促進斑塊穩(wěn)定、抑制AS進展。
[Abstract]:Objective to intramuscularly inject recombinant adenovirus-hepatocyte growth factor (HGF) into the atherosclerotic atherosclerotic model rabbits. To investigate the expression of hepatocyte growth factor (HGF) on argininase type 1 (II(Arg II) and inducible nitric oxide synthase (iNOS) in macrophages of as model rabbits. Expression of macrophage M2 marker CD163 and argininase Ig Arg I, serum inflammatory factors. Methods Forty 4-month-old male New Zealand rabbits were randomly divided into normal as model group and empty vector adenovirus null-Ad-Ad-HGF group. The normal group was given normal diet and the other groups were given high cholesterol diet. Ad-HGF group was intramuscularly injected with 1 ml Ad-HGF(5 脳 109 PFU / mL 路mouse. Null-Ad group was intramuscularly injected with 1 ml null-Ad(5 脳 109 PFU / mL 路mouse. The normal group and as model group were injected with the same amount of normal saline for 12 weeks, then the rats were sacrificed to take out the aorta, and the serum levels of IL-6, IL-10 and lipids were measured respectively. The ratio of intima-media thickness to intima-media thickness of aorta (IMT), vascular smooth muscle cell (VSMC), collagen fiber and macrophage content, aortic HGF, interstitial epithelium transforming factor c-Metals. Results compared with the normal group, the level of serum IL-6, serum lipids and aortic Arg II in the as model group were higher than those in the control group. The protein expression of I NOS, the content of collagen fiber and macrophage were significantly increased (P 0.05), the level of serum IL-10 and aortic HGF c-Mett CD163 were also significantly increased. The protein expression of Arg I significantly decreased the content of P0.05C. Compared with as model group, the levels of serum inflammatory factor IL-6 and IL-10, serum lipids level and the contents of collagen fibers and macrophages, HGF of aorta were measured in null-Ad group. There was no significant difference in the protein expression of c-Meta Arg II-NOSU CD163 and Arg I between the two groups (P 0.05). Compared with as model group, there was no significant difference in blood lipid level, serum IL-6 level and protein expression of aortic Arg III NOS in Ad-HGF group. The content of IMT and macrophage decreased significantly, the level of serum IL-10 and the protein expression of aorta HGFC-MetCD163 / Arg I were significantly decreased. Conclusion HGF can decrease the level of proinflammatory factor, increase the level of anti-inflammatory factor, inhibit the infiltration of M1 macrophage and induce the differentiation of M2 macrophage. Increased plaque VSMCs and collagen fibers increased plaque stability and inhibited as progression.
【學位授予單位】：安徽醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R543.5

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