本文關(guān)鍵詞： Roscovitine 核因子κB 頸動(dòng)脈內(nèi)膜 炎性增生　出處：《中國(guó)病理生理雜志》2017年02期 　論文類型：期刊論文

【摘要】：目的:探討roscovitine通過(guò)影響核因子κB(nuclear factor-κB,NF-κB)活化抑制大鼠頸動(dòng)脈內(nèi)膜損傷導(dǎo)致炎性增生的作用及其分子機(jī)制。方法:隨機(jī)將SD大鼠分成對(duì)照組、模型組和治療組3組,每組20只。模型組采用胰蛋白酶消化法制作頸動(dòng)脈內(nèi)膜損傷模型;對(duì)照組采用假手術(shù)用生理鹽水代替胰蛋白酶消化步驟,其他同模型組操作;治療組在分離的頸動(dòng)脈血管外壁均勻涂抹終濃度為2 g/L roscovitine緩釋凝膠0.5 mL,其他同模型組。各組大鼠術(shù)后常規(guī)飼養(yǎng)4周后取材備檢。采用HE染色觀察各組形態(tài)學(xué)變化,采用Western blot法檢測(cè)IκB的表達(dá)變化和磷酸化降解,檢測(cè)NF-κB的表達(dá)變化、磷酸化激活以及其下游環(huán)氧合酶2(cyclooxygenase-2,COX-2)、血管細(xì)胞黏附分子1(vascular cell adhesion molecule-1,VCAM-1)、腫瘤壞死因子α(tumor necrosis factor-α,TNF-α)和白細(xì)胞介素6(interleukin-6,IL-6)的表達(dá)變化。結(jié)果:Roscovitine通過(guò)抑制胰蛋白酶損傷誘導(dǎo)的IκB-α磷酸化降解,阻斷NF-κB-p65的磷酸化活化,進(jìn)而下調(diào)COX-2表達(dá),抑制VCAM-1、TNF-α和IL-6的表達(dá),從而發(fā)揮抑制損傷血管內(nèi)膜增生的作用。結(jié)論:Roscovitine通過(guò)影響NF-κB活化抑制大鼠頸動(dòng)脈內(nèi)膜損傷導(dǎo)致的炎性增生。
[Abstract]:Objective: to investigate the effect of roscovitine on nuclear factor- 魏 B (NF- 魏 B). Effects of NF- 魏 B activation on inflammatory hyperplasia induced by carotid intimal injury in rats and its molecular mechanism. Methods: SD rats were randomly divided into three groups: control group, model group and treatment group. There were 20 rats in each group. The model group was treated with trypsin digestion method to make carotid intima injury model. The control group was treated by sham operation with normal saline instead of trypsin digestion step, and the other model group was operated with normal saline instead of trypsin. In the treatment group, the final concentration of 2 g / L roscovitine sustained release gel was 0. 5 mL on the external wall of the isolated carotid artery. Other same model groups. The rats in each group were routinely fed for 4 weeks after operation. The morphological changes of each group were observed by HE staining. I 魏 B expression and phosphorylation degradation and NF- 魏 B expression were detected by Western blot assay. Phosphorylation and its downstream cyclooxygenase-2 cyclooxygenase-2 (COX-2). Vascular cell adhesion molecule-1 (VCAM-1). Tumor necrosis factor- 偽 (TNF- 偽) and interleukin-6 (IL-6). Results the phosphorylation of NF- 魏 B-p65 was blocked by inhibiting the phosphorylation of I 魏 B- 偽 induced by trypsin injury. The expression of COX-2 was down-regulated and the expression of TNF- 偽 and IL-6 in VCAM-1 was inhibited. Conclusion: Roscovitine inhibits inflammatory hyperplasia induced by carotid intima injury by affecting NF- 魏 B activation.
【作者單位】： 河北中醫(yī)學(xué)院基礎(chǔ)醫(yī)學(xué)院生物化學(xué)與生物學(xué)教研室;河北省心腦血管病中醫(yī)藥防治重點(diǎn)實(shí)驗(yàn)室;河北省人民醫(yī)院;
【基金】：國(guó)家自然科學(xué)基金資助項(xiàng)目(No.31271466;No.81573698) 河北省科技支撐計(jì)劃(No.13277739D) 河北省教育廳科技類重點(diǎn)項(xiàng)目(No.ZD2014005) 河北省自然科學(xué)基金資助項(xiàng)目(No.2009001053)
【分類號(hào)】：R543.4
【正文快照】： 隨著社會(huì)的老齡化,動(dòng)脈粥樣硬化性疾病的發(fā)病率逐年升高,已經(jīng)成為嚴(yán)重危害人類健康的主要疾病。雖然動(dòng)脈粥樣硬化性疾病的發(fā)病機(jī)理尚未完全闡明,但經(jīng)多年的發(fā)展,血管搭橋術(shù)、動(dòng)脈球囊擴(kuò)張術(shù)及支架置入術(shù)等多種形式的血管重建術(shù)已經(jīng)成為治療這類疾病常用而有效的方法[1];然而,

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