中国糖尿病杂志
中國糖尿病雜誌
중국당뇨병잡지
Chinese Journal of Diabetes
2015年
9期
849-852
,共4页
罗格列酮%糖基化终产物%心肌成纤维细胞%胶原蛋白%氧化应激
囉格列酮%糖基化終產物%心肌成纖維細胞%膠原蛋白%氧化應激
라격렬동%당기화종산물%심기성섬유세포%효원단백%양화응격
Rosiglitazone (RGZ )%Advanced glycation end products (AGE )%Cardiac fibroblasts%Collagen%Oxidative stress (OS)
目的:观察AGE诱导心肌成纤维细胞对氧化应激(OS )和胶原蛋白Ⅰ、Ⅲ合成分泌的影响及罗格列酮(RGZ)的干预作用。方法不同浓度AGE与心肌成纤维细胞孵育,予RGZ干预48 h ,收集培养上清液,分别应用超氧化物歧化酶(SOD)、丙二醛(MDA)试剂盒检测SOD活性和MDA含量,采用ELISA检测胶原蛋白Ⅰ、Ⅲ含量。结果 RGZ与200 mg/L AGE共同孵育心肌成纤维细胞48 h ,随RGZ浓度增高(0.1、1、10μmol/L ),心肌成纤维细胞培养上清液中 SOD 活性逐渐增高[(21.564±1.614),(22.323±1.260),(23.661±1.562) vs (19.320±0.896) nU/ml ,P<0.05或 P<0.01];与200 mg/L AGE组比较,MDA含量逐渐降低[(1.325±0.048),(1.279±0.032),(1.229±0.045) vs (1.629±0.043) nmol/ml ,P<0.01];与200 mg/L AGE组比较,胶原蛋白Ⅰ和胶原蛋白Ⅲ含量均呈递减趋势[(79.17±3.25),(60.42±3.58),(42.71±5.11) vs (85.54±2.28) ng/ml ,P<0.01;(37.52±3.43),(27.09±4.75),(20.81±3.26) vs (40.75±2.70) ng/ml ,P<0.01]。结论 AGE诱导心肌成纤维细胞OS ,增加胶原蛋白Ⅰ、Ⅲ合成分泌;RGZ能抑制AGE诱导的心肌成纤维细胞OS ,抑制AGE诱导的胶原蛋白Ⅰ、Ⅲ合成分泌,对糖尿病心肌纤维化的防治有重要意义。
目的:觀察AGE誘導心肌成纖維細胞對氧化應激(OS )和膠原蛋白Ⅰ、Ⅲ閤成分泌的影響及囉格列酮(RGZ)的榦預作用。方法不同濃度AGE與心肌成纖維細胞孵育,予RGZ榦預48 h ,收集培養上清液,分彆應用超氧化物歧化酶(SOD)、丙二醛(MDA)試劑盒檢測SOD活性和MDA含量,採用ELISA檢測膠原蛋白Ⅰ、Ⅲ含量。結果 RGZ與200 mg/L AGE共同孵育心肌成纖維細胞48 h ,隨RGZ濃度增高(0.1、1、10μmol/L ),心肌成纖維細胞培養上清液中 SOD 活性逐漸增高[(21.564±1.614),(22.323±1.260),(23.661±1.562) vs (19.320±0.896) nU/ml ,P<0.05或 P<0.01];與200 mg/L AGE組比較,MDA含量逐漸降低[(1.325±0.048),(1.279±0.032),(1.229±0.045) vs (1.629±0.043) nmol/ml ,P<0.01];與200 mg/L AGE組比較,膠原蛋白Ⅰ和膠原蛋白Ⅲ含量均呈遞減趨勢[(79.17±3.25),(60.42±3.58),(42.71±5.11) vs (85.54±2.28) ng/ml ,P<0.01;(37.52±3.43),(27.09±4.75),(20.81±3.26) vs (40.75±2.70) ng/ml ,P<0.01]。結論 AGE誘導心肌成纖維細胞OS ,增加膠原蛋白Ⅰ、Ⅲ閤成分泌;RGZ能抑製AGE誘導的心肌成纖維細胞OS ,抑製AGE誘導的膠原蛋白Ⅰ、Ⅲ閤成分泌,對糖尿病心肌纖維化的防治有重要意義。
목적:관찰AGE유도심기성섬유세포대양화응격(OS )화효원단백Ⅰ、Ⅲ합성분비적영향급라격렬동(RGZ)적간예작용。방법불동농도AGE여심기성섬유세포부육,여RGZ간예48 h ,수집배양상청액,분별응용초양화물기화매(SOD)、병이철(MDA)시제합검측SOD활성화MDA함량,채용ELISA검측효원단백Ⅰ、Ⅲ함량。결과 RGZ여200 mg/L AGE공동부육심기성섬유세포48 h ,수RGZ농도증고(0.1、1、10μmol/L ),심기성섬유세포배양상청액중 SOD 활성축점증고[(21.564±1.614),(22.323±1.260),(23.661±1.562) vs (19.320±0.896) nU/ml ,P<0.05혹 P<0.01];여200 mg/L AGE조비교,MDA함량축점강저[(1.325±0.048),(1.279±0.032),(1.229±0.045) vs (1.629±0.043) nmol/ml ,P<0.01];여200 mg/L AGE조비교,효원단백Ⅰ화효원단백Ⅲ함량균정체감추세[(79.17±3.25),(60.42±3.58),(42.71±5.11) vs (85.54±2.28) ng/ml ,P<0.01;(37.52±3.43),(27.09±4.75),(20.81±3.26) vs (40.75±2.70) ng/ml ,P<0.01]。결론 AGE유도심기성섬유세포OS ,증가효원단백Ⅰ、Ⅲ합성분비;RGZ능억제AGE유도적심기성섬유세포OS ,억제AGE유도적효원단백Ⅰ、Ⅲ합성분비,대당뇨병심기섬유화적방치유중요의의。
Objective To investigate induction effect of AGE on oxidative stress and type Ⅰ ,Ⅲcollagen synthesis in rat cardiac fibroblasts and interference effect of RGZ during the course. Methods Incubate rat cardiac fibroblasts with AGE of different concentration ,add RGZ to interfere for 48 h ,and then collect supernatant fluid .Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected by SOD kit and MDA kit separately ,and type Ⅰ ,Ⅲ collagen contents were measured by ELISA. Results When incubating cardiac fibroblasts with RGZ and 200 mg/L AGE together for 48 h , with the rise of RGZ concentration(0.1 ,1 and 10 mol/L) ,SOD activity in the supernatant fluid of cultured cardiac fibroblasts gradually increased [(21.564 ± 1.614) ,(22.323 ± 1.260) ,(23.661 ± 1.562) vs (19.320 ± 0.896) nU/ml ,P<0.05 or P<0.01] ,MDA content gradually decreased [(1.325 ± 0.048) ,(1.279 ± 0.032) ,(1.229 ± 0.045 ) vs (1.629 ± 0.043 ) nmol/ml ,P< 0.01 ] and type Ⅰ ,Ⅲ collagen Contents gradually decreased [(79.17 ± 3.25) ,(60.42 ± 3.58) ,(42.71 ± 5.11) vs (85.54 ± 2.28) ng/ml ,P<0.01 ;(37.52 ± 3.43) ,(27.09 ± 4.75) ,(20.81 ± 3.26) vs (40.75 ± 2.70) ng/ml ,P<0.01] as compared with 200 mg/L AGE group. Conclusion AGE can induce oxidative stress in cardiac fibroblasts and increase type Ⅰ ,Ⅲ collagen contents .RGZ can inhibit oxidative stress in cardiac fibroblasts and synthesis and secretion of type Ⅰ ,Ⅲ collagen induced by AGE. This finding indicates that RGZ may play an important role in the prevention of diabetic myocardial fibrosis.