本文選題：叔丁基對苯二酚　切入點(diǎn)：糖尿病　出處：《眼科新進(jìn)展》2017年03期 　論文類型：期刊論文

【摘要】：目的研究叔丁基對苯二酚(tertiary butyl hydroquinone,tBHQ)對2型糖尿病大鼠視網(wǎng)膜的保護(hù)作用及相關(guān)機(jī)制。方法取雄性Sprague Dawley大鼠60只,分為正常對照組(NC組)、糖尿病組(DM組)和tBHQ組。剔除飼養(yǎng)過程死亡大鼠,最終NC組、DM組、tBHQ組分別為12只、20只、20只大鼠納入研究。造模采用高脂高糖飼料喂養(yǎng)4周后腹腔內(nèi)注射鏈脲佐菌素誘導(dǎo)2型糖尿病模型,tBHQ組于造模后1周在高脂高糖飼料中添加質(zhì)量分?jǐn)?shù)1%tBHQ進(jìn)行干預(yù),于造模后4周和12周心臟采血,檢測血清空腹血糖(fasting plasma glucose,FPG)、血清空腹胰島素(fasting serum insulin,FINs)含量。采用免疫組織化學(xué)法及qRT-PCR法定量檢測各組大鼠視網(wǎng)膜中Nrf2、HO-1、Bcl-2、VEGF蛋白及mRNA的分布和表達(dá)。結(jié)果3組大鼠在4周和12周的FPG水平總體比較差異有統(tǒng)計(jì)學(xué)意義(F分組=78.531,P=0.000);DM組及tBHQ組高于NC組,DM組12周高于4周,tBHQ組12周明顯低于4周,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。3組大鼠在4周和12周的FINs水平總體比較差異有統(tǒng)計(jì)學(xué)意義(F分組=22.480,P=0.000);其中DM組及tBHQ組高于NC組,tBHQ組12周高于4周,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。光學(xué)顯微鏡顯示12周時(shí)NC組無明顯改變;DM組大鼠視網(wǎng)膜組織結(jié)構(gòu)排列疏松,內(nèi)、外核層排列紊亂,細(xì)胞水腫明顯;tBHQ組大鼠視網(wǎng)膜組織結(jié)構(gòu)較清晰,部分細(xì)胞水腫。4周和12周時(shí)各組中均可見Nrf2、HO-1、Bcl-2、VEGF的陽性表達(dá)。Nrf2主要分布于視網(wǎng)膜節(jié)細(xì)胞層、內(nèi)核層,HO-1、Bcl-2主要分布于視網(wǎng)膜節(jié)細(xì)胞層、內(nèi)核層、外核層;VEGF主要分布于神經(jīng)纖維層、節(jié)細(xì)胞層和內(nèi)核層。免疫組織化學(xué)及qRT-PCR檢測顯示,各組大鼠在造模后不同時(shí)間點(diǎn)視網(wǎng)膜中Nrf2、HO-1、Bcl-2、VEGF蛋白及mRNA的相對表達(dá)量的總體比較差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。4周時(shí),DM組Nrf2、HO-1、VEGF的表達(dá)較NC組增加,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05);tBHQ組Nrf2、HO-1、Bcl-2的表達(dá)較DM組增加,VEGF的表達(dá)較DM組降低,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。12周時(shí),DM組Nrf2、HO-1、Bcl-2、VEGF的表達(dá)較NC組增加,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05);tBHQ組Nrf2、HO-1、Bcl-2的表達(dá)較DM組增加,VEGF的表達(dá)較DM組降低,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。12周與4周比較,DM組VEGF的表達(dá)較4周增加,HO-1較4周降低,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05);tBHQ組Nrf2、HO-1、Bcl-2的表達(dá)較4周增加,差異均有統(tǒng)計(jì)學(xué)意義(均為P0.05)。結(jié)論tBHQ對DM大鼠胰島功能具有一定的保護(hù)作用;可促進(jìn)DM大鼠視網(wǎng)膜組織中Nrf2、HO-1、Bcl-2的表達(dá),降低VEGF的表達(dá),對視網(wǎng)膜組織有抗氧化應(yīng)激損傷、減少細(xì)胞凋亡、抑制視網(wǎng)膜血管增殖等作用。tBHQ可能通過Nrf2/HO-1/VEGF及Nrf2/Bcl-2途徑對DM大鼠視網(wǎng)膜起保護(hù)作用。
[Abstract]:Objective to study the protective effect of tertiary Ding Ji butyl hydroquinone tBHQ on retina of type 2 diabetic rats. Methods 60 male Sprague Dawley rats were selected. The rats were divided into normal control group (NC group), diabetic group (DM group) and tBHQ group. Finally, the NC group and DM group were divided into 12 / 20 / 20 rats respectively. The model was fed with high fat and high sugar diet for 4 weeks, and then intraperitoneal injection of streptozotocin (STZ) was used to induce type 2 diabetes mellitus. The tBHQ group was hyperlipidemic and hyperlipidemic 1 week after the establishment of the model, the model was induced by intraperitoneal injection of streptozotocin (streptozotocin). 1 tBHQ was added to the sugar feed to intervene, Heart blood was collected at 4 and 12 weeks after modeling. The contents of serum fasting plasma and fasting serum insulin fins were measured. The distribution and expression of Nrf2HO-1 Bcl-2VEGFin and mRNA in the retina of rats in each group were detected by immunohistochemical method and qRT-PCR method. There was significant difference in FPG level between 12 weeks and 12 weeks. F group (78.531) and tBHQ group (P < 0.05) were significantly lower than those in NC group at 12 weeks and 4 weeks, respectively. There were significant differences in the FINs level between the four and twelve weeks of P0.053.The FINs levels in DM and tBHQ groups were higher than those in NC group at 12 weeks and 4 weeks, respectively, and there were significant differences between the two groups at 12 weeks and 12 weeks, respectively, and there were significant differences between the two groups at 12 weeks and 12 weeks, respectively, and there was no significant difference between DM group and tBHQ group in 12 weeks and 4 weeks after treatment. The difference was statistically significant (P 0.05). Optical microscope showed that the retinal tissue structure in NC group was loose, the inner and outer nuclear layers were disordered, and the retinal tissue structure was clear in TBHQ group at 12 weeks. The positive expression of Nrf2HO-1Bcl-2VEGF2 was found in the retinal ganglion cell layer at the 4th and 12th week of edema. The HO-1 Bcl-2 was mainly distributed in the retinal ganglion cell layer, the nuclear layer and the outer nuclear layer were mainly distributed in the nerve fiber layer. Ganglion cell layer and nuclear layer. Immunohistochemical and qRT-PCR detection. There were significant differences in the expression of Nrf2HO-1Bcl-2VEGF-protein and mRNA in the retina of the rats in each group at different time points after model making (P 0.05 ~ 4 weeks). The expression of Nrf2HO-1VEGFmRNA in DM group was higher than that in NC group. The expression of Nrf2HO-1VEGFmRNA in the retina of the rats in each group was significantly higher than that in the NC group. The expression of Nrf2HO-1Bcl 2 was significantly lower in P0.05THQ group than that in DM group, and the difference was statistically significant (both P0.05 and 12 weeks after treatment), the expression of Nrf2HO-1Bcl-2VEGF in DM group was higher than that in NC group, and the expression of Nrf2HO-1Bcl-2VEGF in DM group was significantly lower than that in DM group. There was significant difference in the expression of Nrf2HO-1Bcl 2 between the two groups. The expression of VEGF in DM group was significantly lower than that in DM group. The expression of VEGF in DM group was significantly lower than that in DM group at week 12 and week 4. The expression of VEGF in DM group was significantly higher than that in DM group at 4 weeks, and the expression of HO-1 in DM group was lower than that in DM group at 4 weeks, and the expression of HO-1Bcl-2 in DM group was significantly lower than that in DM group. There were significant differences in the expression of Nrf2HO-1Bcl 2 between the two groups (P 0.05). Conclusion the expression of Nrf2HO-1Bcl-2 in the retina of DM rats is protected by tBHQ, which can promote the expression of Nrf2HO-1Bcl-2 in the retina of DM rats. TBHQ may protect the retina of DM rats through Nrf2/HO-1/VEGF and Nrf2/Bcl-2 pathway, such as decreasing the expression of VEGF, damaging the retina tissue, reducing apoptosis and inhibiting the proliferation of retinal blood vessels.
【作者單位】： 西南醫(yī)科大學(xué)附屬醫(yī)院眼科;四川省人民醫(yī)院眼科;大理白族自治州人民醫(yī)院眼科;第三軍醫(yī)大學(xué)附屬第二醫(yī)院眼科;
【基金】：四川省科學(xué)技術(shù)廳資助項(xiàng)目(編號:2015SZ0086,LZ-LY-37)~~
【分類號】：R587.2;R774.1

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3 陳果;煙酸對糖尿病視網(wǎng)膜病變保護(hù)作用及其機(jī)制的研究[D];南昌大學(xué)醫(yī)學(xué)院;2015年

4 劉t熡，

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