本文關(guān)鍵詞： 高糖 落新婦苷 間質(zhì)細(xì)胞衍生因子α 人臍靜脈內(nèi)皮細(xì)胞　出處：《中國(guó)病理生理雜志》2016年04期 　論文類(lèi)型：期刊論文

【摘要】：目的:分析落新婦苷對(duì)高糖刺激的血管內(nèi)皮細(xì)胞間質(zhì)細(xì)胞衍生因子1α(SDF-1α)表達(dá)的影響。方法:SD大鼠腹腔注射鏈脲佐菌素后誘導(dǎo)成急性糖尿病模型,采用硫代巴比妥酸法測(cè)量血漿丙二醛(MDA)濃度,采用紫外分光光度法檢測(cè)血漿H2O2濃度,采用免疫熒光檢測(cè)大鼠胸主動(dòng)脈內(nèi)皮細(xì)胞中SDF-1α的表達(dá)。人臍靜脈內(nèi)皮細(xì)胞(HUVECs)經(jīng)高糖刺激后,用real-time PCR、ELISA和免疫熒光檢測(cè)SDF-1α的表達(dá),流式細(xì)胞術(shù)觀察細(xì)胞周期分布情況,免疫熒光檢測(cè)p65的表達(dá)和細(xì)胞內(nèi)定位。結(jié)果:糖尿病大鼠血漿MDA和H2O2水平均高于正常對(duì)照組,其胸主動(dòng)脈內(nèi)皮細(xì)胞SDF-1α的表達(dá)較正常組減弱;落新婦苷能降低糖尿病大鼠血漿MDA及H2O2的水平并增加胸主動(dòng)脈內(nèi)皮細(xì)胞SDF-1α的表達(dá)。體外高糖刺激呈濃度和時(shí)間依賴(lài)性減少HUVECs中SDF-1α表達(dá),落新婦苷能一定程度地恢復(fù)SDF-1α表達(dá)。高糖刺激增加HUVECs S期比例,而落新婦苷減少其S期分布。高糖刺激HUVECs中p65蛋白核轉(zhuǎn)位,落新婦苷抑制高糖誘導(dǎo)的p65核轉(zhuǎn)位。結(jié)論:落新婦苷能增加高糖刺激下內(nèi)皮細(xì)胞表達(dá)SDF-1α,減少高糖狀態(tài)下的氧化應(yīng)激和NF-κB的活化。
[Abstract]:Objective: to analyze the effect of Acanthrin on vascular endothelial cell mesenchymal cell derived factor-1 偽 (SDF-1 偽) stimulated by high glucose. Methods Acute diabetic model was induced by intraperitoneal injection of streptozotocin into SD rats. Plasma malondialdehyde (MDA) concentration was measured by thiobarbituric acid method and plasma H _ 2O _ 2 concentration was detected by ultraviolet spectrophotometry. The expression of SDF-1 偽 in rat thoracic aortic endothelial cells was detected by immunofluorescence. Human umbilical vein endothelial cells (HUVECs) were stimulated with high glucose and real-time PCR was used. The expression of SDF-1 偽 was detected by ELISA and immunofluorescence, and the distribution of cell cycle was observed by flow cytometry. Results: the levels of MDA and H _ 2O _ 2 in plasma of diabetic rats were higher than those of normal control group. The expression of SDF-1 偽 in the endothelial cells of thoracic aorta was lower than that in the normal group. Acanthrin could decrease the levels of plasma MDA and H2O2 and increase the expression of SDF-1 偽 in thoracic aortic endothelial cells in diabetic rats. In vitro, hyperglycemic stimulation decreased the expression of SDF-1 偽 in HUVECs in a dose-and time-dependent manner. SDF-1 偽 expression. The expression of SDF-1 偽 was restored to some extent by Acanthrin, and the proportion of HUVECs S phase was increased by high glucose stimulation. But Acanthoside reduced its S phase distribution. High glucose stimulated the nuclear translocation of p65 protein in HUVECs. Conclusion: Acanthrin can increase the expression of SDF-1 偽 in endothelial cells stimulated by high glucose, and decrease the oxidative stress and the activation of NF- 魏 B in endothelial cells induced by high glucose.
【作者單位】： 廣東醫(yī)學(xué)院病理學(xué)系;廣東醫(yī)學(xué)院附屬醫(yī)院病理診斷與研究中心;肇慶市第一人民醫(yī)院兒科;廣東醫(yī)學(xué)院基礎(chǔ)醫(yī)學(xué)院病理生理教研室;
【基金】：廣東省大學(xué)生創(chuàng)新訓(xùn)練項(xiàng)目(No.1057112014) 廣東醫(yī)學(xué)院大學(xué)生創(chuàng)新實(shí)驗(yàn)項(xiàng)目(No.2011ZZZF002) 國(guó)家自然科學(xué)基金資助項(xiàng)目(No.81170121)
【分類(lèi)號(hào)】：R587.1
【正文快照】： 糖尿病是危害人群健康的常見(jiàn)病、多發(fā)病。廣東省是中國(guó)的高發(fā)區(qū)之一,發(fā)病率超過(guò)全國(guó)平均水平,且年輕化趨勢(shì)明顯[1-2]。糖尿病的一個(gè)主要特征就是高血糖癥。在長(zhǎng)期的高糖刺激下,血管內(nèi)皮細(xì)胞容易受到損傷。而血管內(nèi)皮細(xì)胞內(nèi)有關(guān)信號(hào)的活化,進(jìn)而導(dǎo)致內(nèi)皮細(xì)胞出現(xiàn)分泌細(xì)胞因子功，

本文編號(hào)：1482016