首页> 外文期刊>Graefe's archive for clinical and experimental ophthalmology: Albrecht von Graefes Archiv fur klinische und experimentelle Opthalmologie >Shifts in renin–angiotensin system components, angiogenesis, and oxidative stress-related protein expression in the lamina cribrosa region of streptozotocin-induced diabetic mice
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Shifts in renin–angiotensin system components, angiogenesis, and oxidative stress-related protein expression in the lamina cribrosa region of streptozotocin-induced diabetic mice

机译:在链脲佐菌素诱导的糖尿病小鼠的椎板克里泽地区的肾素 - 血管紧张素系统组分,血管生成和氧化应激相关蛋白表达中的转变

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Abstract Purpose This study aimed to analyse shifts in renin–angiotensin system (RAS) components, angiogenesis, and oxidative stress-related protein expression in the lamina cribrosa (LC) region in streptozotocin (STZ)-induced diabetic mice. Methods Six months after diabetes induction, the retinal vessels of male C57BL/6?J mice were observed by colour photography, fundus fluorescein angiography (FFA), and immunofluorescent staining following incubation with CD31. Immunofluorescence for glial fibrillary acidic protein (GFAP), alpha-smooth muscle actin (α-SMA),and NG2 was also performed. Angiotensin-converting enzyme 1 (ACE1), angiotensin II type I receptor (AT1R), renin, hypoxia-inducible factor 1-alpha (HIF-1α), vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGFR2), and haeme oxygenase 1 (HO-1) expression levels were confirmed by immunohistochemical and western blotting analyses. Results Compared with control mice, diabetic mice had significantly higher blood glucose concentrations ( p ? p ? + pericytes were observed in diabetic mice than in control mice. ACE1, AT1R, renin, HIF-1α, VEGF, VEGFR2, and HO-1 expression were up-regulated in the LC of the STZ-induced diabetic mice. Conclusions Collectively, ACE 1, AT1R, HIF-1α, VEGF, VEGFR2, and HO-1 activation in the LC region in diabetic mice may be involved in diabetes via the RAS and induction of angiogenesis and oxidative stress.
机译:摘要目的本研究旨在分析在链脲佐菌素(STZ)诱导的糖尿病小鼠的椎板克里泽(LC)区中肾素 - 血管紧张素系统(RAS)组分(RAS)组分,血管生成和氧化应激相关蛋白表达的转变。方法糖尿病诱导术后六个月,通过彩色摄影,眼底荧光素血管造影(FFA)观察雄性C57BL /6βJ小鼠的视网膜血管,并在与CD31孵育后免疫荧光染色。还进行了胶质纤维酸性蛋白(GFAP),α-平滑肌肌动蛋白(α-SMA)和NG2的免疫荧光。血管紧张素转化酶1(ACE1),血管紧张素II型受体(AT1R),肾素,缺氧诱导因子1-α(HIF-1α),血管内皮生长因子(VEGF),血管内皮生长因子受体2(VEGFR2)通过免疫组织化学和蛋白质印迹分析证实了HAEME氧酶1(HO-1)表达水平。结果与对照小鼠相比,糖尿病小鼠具有显着更高的血糖浓度(p≤P≤p≤P≤P≤P≤P≤P≤p≤P≤pryte。在对照小鼠中观察到糖尿病小鼠。ACE1,AT1R,Renin,HIF-1α,VEGF,VEGFR2和HO-1表达在STZ诱导的糖尿病小鼠的LC中调节。结论在糖尿病小鼠中的LC区域中的统一性1,AT1R,HIF-1α,VEGF,VEGFR2和HO-1活化可以通过糖尿病患者参与糖尿病Ras和诱导血管生成和氧化应激。

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