中国中医眼科杂志
中國中醫眼科雜誌
중국중의안과잡지
JOURNAL OF TRADITIONAL CHINESE OPHTHALMOLOGY
2015年
2期
82-86
,共5页
马栋%王静波%郭承伟%吕璐
馬棟%王靜波%郭承偉%呂璐
마동%왕정파%곽승위%려로
络治法%糖尿病视网膜病变%NF-κB%大鼠
絡治法%糖尿病視網膜病變%NF-κB%大鼠
락치법%당뇨병시망막병변%NF-κB%대서
collaterals therapy%diabetic retinopathy%NF-κB%rats
目的：观察络治法对链佐脲菌素（STZ）诱导的糖尿病大鼠视网膜组织中核转录因子κB （NF-κB）表达的影响，探讨络治法对糖尿病视网膜病变微血管损伤的保护作用及作用机制。方法60只雌性Wistar大鼠随机分成正常组、模型组、羟苯磺酸钙对照药物组、络治组四组。除正常组不做处理外，其它各组均采用STZ腹腔注射制作糖尿病大鼠模型。给药24周后每组大鼠取右眼做眼球壁石蜡切片，行NF-κB免疫组织化学染色，计算机图像定量分析灰度值。左眼取视网膜组织，Western blot法检测视网膜中NF-κB p65蛋白含量。结果免疫组化结果显示络治组视网膜中NF-κB表达明显低于模型组及对照组（P＜0.05），灰度值与空白组大体相当（P>0.05）。 Western blot结果显示络治组NF-κB p65表达较模型组及对照组显著降低（P＜0.05）。结论络治法可明显抑制视网膜组织中NF-κB的活化，甚至接近正常大鼠水平。这可能是络治法对糖尿病大鼠视网膜微血管病变发挥防治作用的重要机理之一。
目的：觀察絡治法對鏈佐脲菌素（STZ）誘導的糖尿病大鼠視網膜組織中覈轉錄因子κB （NF-κB）錶達的影響，探討絡治法對糖尿病視網膜病變微血管損傷的保護作用及作用機製。方法60隻雌性Wistar大鼠隨機分成正常組、模型組、羥苯磺痠鈣對照藥物組、絡治組四組。除正常組不做處理外，其它各組均採用STZ腹腔註射製作糖尿病大鼠模型。給藥24週後每組大鼠取右眼做眼毬壁石蠟切片，行NF-κB免疫組織化學染色，計算機圖像定量分析灰度值。左眼取視網膜組織，Western blot法檢測視網膜中NF-κB p65蛋白含量。結果免疫組化結果顯示絡治組視網膜中NF-κB錶達明顯低于模型組及對照組（P＜0.05），灰度值與空白組大體相噹（P>0.05）。 Western blot結果顯示絡治組NF-κB p65錶達較模型組及對照組顯著降低（P＜0.05）。結論絡治法可明顯抑製視網膜組織中NF-κB的活化，甚至接近正常大鼠水平。這可能是絡治法對糖尿病大鼠視網膜微血管病變髮揮防治作用的重要機理之一。
목적：관찰락치법대련좌뇨균소（STZ）유도적당뇨병대서시망막조직중핵전록인자κB （NF-κB）표체적영향，탐토락치법대당뇨병시망막병변미혈관손상적보호작용급작용궤제。방법60지자성Wistar대서수궤분성정상조、모형조、간분광산개대조약물조、락치조사조。제정상조불주처리외，기타각조균채용STZ복강주사제작당뇨병대서모형。급약24주후매조대서취우안주안구벽석사절편，행NF-κB면역조직화학염색，계산궤도상정량분석회도치。좌안취시망막조직，Western blot법검측시망막중NF-κB p65단백함량。결과면역조화결과현시락치조시망막중NF-κB표체명현저우모형조급대조조（P＜0.05），회도치여공백조대체상당（P>0.05）。 Western blot결과현시락치조NF-κB p65표체교모형조급대조조현저강저（P＜0.05）。결론락치법가명현억제시망막조직중NF-κB적활화，심지접근정상대서수평。저가능시락치법대당뇨병대서시망막미혈관병변발휘방치작용적중요궤리지일。
OBJECTIVE To observe the expression of nuclear factor kappa B (NF-κB) in the retina of streptozotocin (STZ) induced diabetic rats treated with collaterals therapy, and to investigate the protective effects and mechanism of collaterals therapy on diabetic retinopathy microvascular injury. METHODS Sixty female Wistar rats were randomly divided into 4 group including blank group, model group, control group and collaterals therapy group. Except the blank group rats all were made into models of diabetic rats and treated according to the scheme. After 24 weeks each ratˊs right eye was made into parafin section and treated by immunohistochemical staining to detect NF-κB content. While by western blot method detect the NF-κB p65 protein content in left eyeˊs retina was detected. RESULTS Immunohistochemical results showed that the NF-κB expression in the collaterals therapy group was obviously lower than that of model group and control group (P<0.05), and was almost the same with the blank group (P>0.05). Western blot results showed that the NF-κB p65 expression in collaterals therapy group decreased significantly compared with model group and control group (P<0.05). CONCLUSIONS Collaterals therapy could obviously inhibit the expression of NF-κB in retinal tissue, which may be an important mechanism on how collaterals therapy could prevent retinal microvascular lesions.
