中国药理学通报
中國藥理學通報
중국약이학통보
Chinese Pharmacological Bulletin
2015年
10期
1388-1393
,共6页
二苯乙烯苷%异丙肾上腺素%心肌纤维化%胶原%转化生长因子-β1%氧化应激
二苯乙烯苷%異丙腎上腺素%心肌纖維化%膠原%轉化生長因子-β1%氧化應激
이분을희감%이병신상선소%심기섬유화%효원%전화생장인자-β1%양화응격
2,3,4 ’,5-tetrahydroxystilbene-2-O-β-D glucoside%isoproterenol%myocardial fibrosis%colla-gen%transforming growth factor-β1%oxidative stress
目的：观察二苯乙烯苷(2,3,4′,5-tetrahydroxystilbene-2-O-β-D glucoside,TSG)对异丙肾上腺素( isoproterenol,ISO)诱导的小鼠心肌纤维化的作用及其相关机制。方法采用连续皮下注射异丙肾上腺素14 d诱导小鼠心肌纤维化模型,同时以TSG (120、60、30 mg · kg-1)和阳性对照卡托普利(40 mg·kg-1)灌胃给药。末次给药12 h后,取心室肌进行苏木精伊红( hematoxylineosin,HE)染色和Masson染色,观察纤维化的程度；测定心肌羟脯氨酸( hydroxyproline,HYP)含量；检测心肌组织中Ⅰ、Ⅲ型胶原,转化生长因子-β1(transforming growth factor-β1,TGF-β1)的蛋白表达水平；测定心肌组织中超氧化物歧化酶( superoxide dismutase,SOD)、谷胱甘肽过氧化物酶( glutathione peroxidase-Px,GSH-Px)活性。结果与正常对照组相比,模型组心肌出现明显纤维化,心肌组织HYP水平明显增高,Ⅰ、Ⅲ型胶原蛋白表达明显增加。与模型组相比, TSG能减轻心肌纤维化程度,降低心肌组织HYP水平及心肌组织中Ⅰ、Ⅲ型胶原蛋白表达。同时,TSG降低心肌组织中TGF-β1的蛋白表达,且能升高损伤心肌组织中SOD和GSH-Px的活性。结论 TSG可抑制ISO诱导的小鼠心肌纤维化,其机制可能与调节TGF-β1蛋白表达及其抗氧化有关。<br> 关键词：二苯乙烯苷；异丙肾上腺素；心肌纤维化；胶原；转化生长因子-β1；氧化应激
目的：觀察二苯乙烯苷(2,3,4′,5-tetrahydroxystilbene-2-O-β-D glucoside,TSG)對異丙腎上腺素( isoproterenol,ISO)誘導的小鼠心肌纖維化的作用及其相關機製。方法採用連續皮下註射異丙腎上腺素14 d誘導小鼠心肌纖維化模型,同時以TSG (120、60、30 mg · kg-1)和暘性對照卡託普利(40 mg·kg-1)灌胃給藥。末次給藥12 h後,取心室肌進行囌木精伊紅( hematoxylineosin,HE)染色和Masson染色,觀察纖維化的程度；測定心肌羥脯氨痠( hydroxyproline,HYP)含量；檢測心肌組織中Ⅰ、Ⅲ型膠原,轉化生長因子-β1(transforming growth factor-β1,TGF-β1)的蛋白錶達水平；測定心肌組織中超氧化物歧化酶( superoxide dismutase,SOD)、穀胱甘肽過氧化物酶( glutathione peroxidase-Px,GSH-Px)活性。結果與正常對照組相比,模型組心肌齣現明顯纖維化,心肌組織HYP水平明顯增高,Ⅰ、Ⅲ型膠原蛋白錶達明顯增加。與模型組相比, TSG能減輕心肌纖維化程度,降低心肌組織HYP水平及心肌組織中Ⅰ、Ⅲ型膠原蛋白錶達。同時,TSG降低心肌組織中TGF-β1的蛋白錶達,且能升高損傷心肌組織中SOD和GSH-Px的活性。結論 TSG可抑製ISO誘導的小鼠心肌纖維化,其機製可能與調節TGF-β1蛋白錶達及其抗氧化有關。<br> 關鍵詞：二苯乙烯苷；異丙腎上腺素；心肌纖維化；膠原；轉化生長因子-β1；氧化應激
목적：관찰이분을희감(2,3,4′,5-tetrahydroxystilbene-2-O-β-D glucoside,TSG)대이병신상선소( isoproterenol,ISO)유도적소서심기섬유화적작용급기상관궤제。방법채용련속피하주사이병신상선소14 d유도소서심기섬유화모형,동시이TSG (120、60、30 mg · kg-1)화양성대조잡탁보리(40 mg·kg-1)관위급약。말차급약12 h후,취심실기진행소목정이홍( hematoxylineosin,HE)염색화Masson염색,관찰섬유화적정도；측정심기간포안산( hydroxyproline,HYP)함량；검측심기조직중Ⅰ、Ⅲ형효원,전화생장인자-β1(transforming growth factor-β1,TGF-β1)적단백표체수평；측정심기조직중초양화물기화매( superoxide dismutase,SOD)、곡광감태과양화물매( glutathione peroxidase-Px,GSH-Px)활성。결과여정상대조조상비,모형조심기출현명현섬유화,심기조직HYP수평명현증고,Ⅰ、Ⅲ형효원단백표체명현증가。여모형조상비, TSG능감경심기섬유화정도,강저심기조직HYP수평급심기조직중Ⅰ、Ⅲ형효원단백표체。동시,TSG강저심기조직중TGF-β1적단백표체,차능승고손상심기조직중SOD화GSH-Px적활성。결론 TSG가억제ISO유도적소서심기섬유화,기궤제가능여조절TGF-β1단백표체급기항양화유관。<br> 관건사：이분을희감；이병신상선소；심기섬유화；효원；전화생장인자-β1；양화응격
Aim To study the effects of 2 ,3 ,4 ’ ,5-tet-rahydroxystilbene-2-O-β-D glucoside ( TSG ) on myo-cardial fibrosis ( MF) induced by isoproterenol ( ISO) in mice and its possible mechanism. Methods MF in mice was induced by subcutaneous injection of isoprot-erenol for 14 days. TSG (30,60,120 mg·kg-1 ) and captopril ( 40 mg · kg-1 ) were then administered by gavage to mice. The experiment was stopped 12 h after the last administration of the drugs. Hematoxylin-eosin ( HE) and Masson staining were used to estimate the extent of MF. Level of hydroxyproline in myocardial tissues was measured. Protein expressions of collagenⅠ, collagen Ⅲ and transforming growth factor-β1 (TGF-β1) in myocardial tissues were measured. Lev-els of superoxide dismutase ( SOD ) and glutathione peroxidase ( GSH-Px ) were determined. Results Compared with control mice, the level of hydroxypro-line in myocardial tissues was significantly increased in isoproterenol treated mice. Histological sections of iso-proterenol-treated hearts showed extensive myocardial fibrosis. And protein expressions of collagenⅠand col-lagen Ⅲwere markedly increased in isoproterenol trea-ted mice. However, therapy with TSG decreased the level of hydroxyproline in myocardial tissues, ameliora-ted the degree of myocardial fibrosis, and reduced the collagen expressions induced by isoproterenol adminis-tration. Moreover, treatment with TSG decreased TGF-β1 protein expression and elevated the myocardial SOD and GSH-Px activity. Conclusion TSG can inhibit MF formation induced by ISO in mice which might be due to regulating TGF-β1 protein expression and its an-tioxidant effect.
