国际眼科杂志
國際眼科雜誌
국제안과잡지
International Eye Science
2015年
10期
1695-1699
,共5页
脂联素%氧诱导视网膜病变%氧化应激%内皮型一氧化氮合酶%一氧化氮
脂聯素%氧誘導視網膜病變%氧化應激%內皮型一氧化氮閤酶%一氧化氮
지련소%양유도시망막병변%양화응격%내피형일양화담합매%일양화담
adiponectin%oxgen-induced retinopathy%oxidative stress%endothelial nitric oxide synthase%nitric oxide
目的：观察脂联素对C57 BL/6 J小鼠氧诱导视网膜病变的影响。<br> 方法：将新生C57 BL/6 J小鼠随机分为3组,分别为常氧对照组、生理盐水注射氧诱导视网膜病变( oxygen-induced retinopathy,OIR)组和脂联素注射OIR组。将后两组小鼠于生后第7 d ( P7)至P12置于体积分数75%±2%高氧氧箱中以诱导OIR模型。脂联素注射OIR模型组在P7~ P15每天接受腹腔注射重组鼠脂联素蛋白(3.0μg/g),生理盐水注射OIR组则于上述相同时间点注射同等剂量的生理盐水。三组小鼠均于P17时取右眼行视网膜铺片和Lectin染色,观察视网膜中央无血管区及病理性新生血管的情况；取左眼行视网膜切片和 HE染色,观察视网膜组织病理学变化；应用Western-blot测定左眼视网膜组织中iNOS、nNOS、eNOS的表达；取右眼视网膜组织定量检测ROS/RNS含量以及NO水平。<br> 结果：脂联素注射OIR组小鼠视网膜中央无血管区面积较生理盐水注射OIR组明显减少(t=7.304,P<0.01),病理性新生血管数目明显减少(t=2.654,P<0.01)；脂联素注射OIR组小鼠视网膜组织ROS含量较生理盐水注射组明显降低(t=13.349,P<0.01)；脂联素注射OIR组小鼠视网膜组织 NO 含量明显高于生理盐水注射组( t=3.023,P<0.01),iNOS表达明显低于生理盐水注射组(t=5.112,P<0.01),eNOS表达明显高于生理盐水注射组(t=7.421,P<0.01),nNOS的表达无统计学差异(t=1.074,P>0.01)。<br> 结论：脂联素可以通过激活内源性eNOS促进生理性NO生成,同时又能抑制ROS/RNS的产生,在OIR进程中发挥视网膜血管的保护作用。
目的：觀察脂聯素對C57 BL/6 J小鼠氧誘導視網膜病變的影響。<br> 方法：將新生C57 BL/6 J小鼠隨機分為3組,分彆為常氧對照組、生理鹽水註射氧誘導視網膜病變( oxygen-induced retinopathy,OIR)組和脂聯素註射OIR組。將後兩組小鼠于生後第7 d ( P7)至P12置于體積分數75%±2%高氧氧箱中以誘導OIR模型。脂聯素註射OIR模型組在P7~ P15每天接受腹腔註射重組鼠脂聯素蛋白(3.0μg/g),生理鹽水註射OIR組則于上述相同時間點註射同等劑量的生理鹽水。三組小鼠均于P17時取右眼行視網膜鋪片和Lectin染色,觀察視網膜中央無血管區及病理性新生血管的情況；取左眼行視網膜切片和 HE染色,觀察視網膜組織病理學變化；應用Western-blot測定左眼視網膜組織中iNOS、nNOS、eNOS的錶達；取右眼視網膜組織定量檢測ROS/RNS含量以及NO水平。<br> 結果：脂聯素註射OIR組小鼠視網膜中央無血管區麵積較生理鹽水註射OIR組明顯減少(t=7.304,P<0.01),病理性新生血管數目明顯減少(t=2.654,P<0.01)；脂聯素註射OIR組小鼠視網膜組織ROS含量較生理鹽水註射組明顯降低(t=13.349,P<0.01)；脂聯素註射OIR組小鼠視網膜組織 NO 含量明顯高于生理鹽水註射組( t=3.023,P<0.01),iNOS錶達明顯低于生理鹽水註射組(t=5.112,P<0.01),eNOS錶達明顯高于生理鹽水註射組(t=7.421,P<0.01),nNOS的錶達無統計學差異(t=1.074,P>0.01)。<br> 結論：脂聯素可以通過激活內源性eNOS促進生理性NO生成,同時又能抑製ROS/RNS的產生,在OIR進程中髮揮視網膜血管的保護作用。
목적：관찰지련소대C57 BL/6 J소서양유도시망막병변적영향。<br> 방법：장신생C57 BL/6 J소서수궤분위3조,분별위상양대조조、생리염수주사양유도시망막병변( oxygen-induced retinopathy,OIR)조화지련소주사OIR조。장후량조소서우생후제7 d ( P7)지P12치우체적분수75%±2%고양양상중이유도OIR모형。지련소주사OIR모형조재P7~ P15매천접수복강주사중조서지련소단백(3.0μg/g),생리염수주사OIR조칙우상술상동시간점주사동등제량적생리염수。삼조소서균우P17시취우안행시망막포편화Lectin염색,관찰시망막중앙무혈관구급병이성신생혈관적정황；취좌안행시망막절편화 HE염색,관찰시망막조직병이학변화；응용Western-blot측정좌안시망막조직중iNOS、nNOS、eNOS적표체；취우안시망막조직정량검측ROS/RNS함량이급NO수평。<br> 결과：지련소주사OIR조소서시망막중앙무혈관구면적교생리염수주사OIR조명현감소(t=7.304,P<0.01),병이성신생혈관수목명현감소(t=2.654,P<0.01)；지련소주사OIR조소서시망막조직ROS함량교생리염수주사조명현강저(t=13.349,P<0.01)；지련소주사OIR조소서시망막조직 NO 함량명현고우생리염수주사조( t=3.023,P<0.01),iNOS표체명현저우생리염수주사조(t=5.112,P<0.01),eNOS표체명현고우생리염수주사조(t=7.421,P<0.01),nNOS적표체무통계학차이(t=1.074,P>0.01)。<br> 결론：지련소가이통과격활내원성eNOS촉진생이성NO생성,동시우능억제ROS/RNS적산생,재OIR진정중발휘시망막혈관적보호작용。
AIM:To investigate the role of adiponectin ( APN ) in C57BL/6J mice model of oxygen-induced retinopathy ( OIR) . <br> METHODS: Neonatal C57BL/6J mice were divided randomly into three groups: normoxic control group, physiological saline injection of OIR group and adiponectin injection of OIR group. The mice of the latter two groups were exposed to 75%±2% oxygen from 7d (P7) ~ P12 to induced OIR. Recombinant APN ( rAPN) was injected intraperitoneally ( i. p. , 3. 0μg/g) in a mice model of OIR from P7 ~P15. Another set of mice model of OIR were received a similar treatment with physiological saline. All eyes were collected at P17. The right eyes were whole mounted and stained with Lectin to observe central retinal avascular area and the growth of pathological neovascularization; The left eyes were performed histopathological cross sections stained with HE to analyzed the histopathological changes in the retina. The eyes were enucleated to assess the levels of reactive oxygen species ( ROS ) and NO. The protein expression of iNOS, nNOS, eNOS were detected by Western-blot. <br> RESULTS: The central retinal avascular area, neovascular area were markedly decreased after the APN injection compared with physiological saline injection of OIR group (t = 7. 304, P<0. 01; t = 2. 654, P<0. 01). Compared with physiological saline injection of OIR group, the levels of ROS were lower ( t= 13. 349, P<0.01), the levels of NO were higher (t=3. 023, P<0. 01), the expression of iNOS were decreased ( t= 5. 112, P<0.01), the expression of eNOS were decreased ( t =7.421, P<0. 01). nNOS expression had no significant difference (t=1. 074, P>0. 01). <br> CONCLUSION:The realtus demonstrate that APN can promote physiological NO by acting endogenous eNOS, while suppress ROS/RNS generation and play a protective role in retinal vessels in OIR process.
