歡迎來到天天文庫
瀏覽記錄
ID:54979788
大?。?10.05 KB
頁數(shù):6頁
時間:2020-05-07
《厚樸酚對高脂飼料-STZ 誘導的糖尿病大鼠血糖血脂及肝臟氧化應激損傷的影響 (英文)-論文.pdf》由會員上傳分享,免費在線閱讀,更多相關內容在行業(yè)資料-天天文庫。
1、·476·藥學學報ActaPharmaceuticaSinica2014,49(4):476—481Theantidiabeticandhepat0pr0tectiVeectsofmagnololondiabeticratsinducedbyhigh—fatdietandstreptozotocinWANGJun-jun,ZHAORong,LIANGJichao,CHENYong*(HubeiProvinceKeyLaboratoryofBiotechnologyofChineseTraditi
2、onalMedicine,HubeiUniversity,Wuhan430062,China)Abstract:Theeffectsofmagnolol(Mag)onhyperglycemiaandhyperlipemia,hepaticoxidativestressandcytochromeP4502E1(CYP2E1)activityofdiabeticratsinducedbyhigh—fatdiet(HFD)andstreptozotocin(STZ)werestudied.Aftero
3、raladministrationofMag(25,50and100mg‘kg‘d)forcontinuous10weeks,thebloodglucoseandlipids(TC,TGandLDL—C)levels,aswellasthehepaticCYP2E1activityandMDAcontentofdiabeticrats,decreasedsignificantly(P4、tioxidantenzymaticactivities(CATandGSH—Px)ofdiabeticrats,increasedsignificantly(P<0.05orP5、nhepaticCYP2E1activitycouldbeanimportantmechanismofMagagainsthepaticinsulinresistanceandoxidativedamage.Keywords:magnolol;highfatdiet-streptozotocininduceddiabeticrat;antidiabeticactivity;oxidativestress;CYP2E1activityCLCnumber:R965Documentcode:AArti6、cleID:0513-4870(2014)04.0476—06厚樸酚對高脂飼料.STZ誘導的糖尿病大鼠血糖血脂及肝臟氧化應激損傷的影響王俊俊,趙容,梁繼超,陳勇(湖北大學中藥生物技術省重點實驗室,湖北武漢430062)摘要:本文研究了厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠高血糖、高血脂、肝臟氧化應激和CYP2E1活性的影響。與糖尿病模型組相比,連續(xù)給予厚樸酚(25、50和100mg.kg~.d~,灌胃1l0周后,其血糖、血脂(TC、TG和LDL—C)及肝臟CYP2E1活性和MDA含量顯7、著降低,口服糖耐量和肝臟抗氧化酶(CAT和GSH.Px)活性顯著增加。研究結果不僅證明厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠的高血糖、高血脂、肝臟氧化應激損傷有明顯治療作用,而且厚樸酚對糖尿病大鼠肝臟CYP2E1活性的抑制作用可能是其拮抗糖尿病所致肝臟氧化損傷及胰島素抵抗的重要機制之一。關鍵詞:厚樸酚;高脂一STZ誘導的糖尿病大鼠;抗糖尿病作用;氧化應激:CYP2E1活性Magnoliaofficinalishasbeenusedfortreatmenttraditionalmedic8、inesforalongtime.Magnolol(Mag,ofgastrointestinaldisorders,anxietyandallergicdisease,F(xiàn)igure11isamajorbioactivecompoundwithvariousdiabetessyndromeinJapanese,KoreanandChinesebiologicaleffects.Recently,anti—cancer,anti-stress,anti-anxiety,anti·depressant
4、tioxidantenzymaticactivities(CATandGSH—Px)ofdiabeticrats,increasedsignificantly(P<0.05orP5、nhepaticCYP2E1activitycouldbeanimportantmechanismofMagagainsthepaticinsulinresistanceandoxidativedamage.Keywords:magnolol;highfatdiet-streptozotocininduceddiabeticrat;antidiabeticactivity;oxidativestress;CYP2E1activityCLCnumber:R965Documentcode:AArti6、cleID:0513-4870(2014)04.0476—06厚樸酚對高脂飼料.STZ誘導的糖尿病大鼠血糖血脂及肝臟氧化應激損傷的影響王俊俊,趙容,梁繼超,陳勇(湖北大學中藥生物技術省重點實驗室,湖北武漢430062)摘要:本文研究了厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠高血糖、高血脂、肝臟氧化應激和CYP2E1活性的影響。與糖尿病模型組相比,連續(xù)給予厚樸酚(25、50和100mg.kg~.d~,灌胃1l0周后,其血糖、血脂(TC、TG和LDL—C)及肝臟CYP2E1活性和MDA含量顯7、著降低,口服糖耐量和肝臟抗氧化酶(CAT和GSH.Px)活性顯著增加。研究結果不僅證明厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠的高血糖、高血脂、肝臟氧化應激損傷有明顯治療作用,而且厚樸酚對糖尿病大鼠肝臟CYP2E1活性的抑制作用可能是其拮抗糖尿病所致肝臟氧化損傷及胰島素抵抗的重要機制之一。關鍵詞:厚樸酚;高脂一STZ誘導的糖尿病大鼠;抗糖尿病作用;氧化應激:CYP2E1活性Magnoliaofficinalishasbeenusedfortreatmenttraditionalmedic8、inesforalongtime.Magnolol(Mag,ofgastrointestinaldisorders,anxietyandallergicdisease,F(xiàn)igure11isamajorbioactivecompoundwithvariousdiabetessyndromeinJapanese,KoreanandChinesebiologicaleffects.Recently,anti—cancer,anti-stress,anti-anxiety,anti·depressant
5、nhepaticCYP2E1activitycouldbeanimportantmechanismofMagagainsthepaticinsulinresistanceandoxidativedamage.Keywords:magnolol;highfatdiet-streptozotocininduceddiabeticrat;antidiabeticactivity;oxidativestress;CYP2E1activityCLCnumber:R965Documentcode:AArti
6、cleID:0513-4870(2014)04.0476—06厚樸酚對高脂飼料.STZ誘導的糖尿病大鼠血糖血脂及肝臟氧化應激損傷的影響王俊俊,趙容,梁繼超,陳勇(湖北大學中藥生物技術省重點實驗室,湖北武漢430062)摘要:本文研究了厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠高血糖、高血脂、肝臟氧化應激和CYP2E1活性的影響。與糖尿病模型組相比,連續(xù)給予厚樸酚(25、50和100mg.kg~.d~,灌胃1l0周后,其血糖、血脂(TC、TG和LDL—C)及肝臟CYP2E1活性和MDA含量顯
7、著降低,口服糖耐量和肝臟抗氧化酶(CAT和GSH.Px)活性顯著增加。研究結果不僅證明厚樸酚對高脂飼料一鏈脲佐菌素誘導的2型糖尿病大鼠的高血糖、高血脂、肝臟氧化應激損傷有明顯治療作用,而且厚樸酚對糖尿病大鼠肝臟CYP2E1活性的抑制作用可能是其拮抗糖尿病所致肝臟氧化損傷及胰島素抵抗的重要機制之一。關鍵詞:厚樸酚;高脂一STZ誘導的糖尿病大鼠;抗糖尿病作用;氧化應激:CYP2E1活性Magnoliaofficinalishasbeenusedfortreatmenttraditionalmedic
8、inesforalongtime.Magnolol(Mag,ofgastrointestinaldisorders,anxietyandallergicdisease,F(xiàn)igure11isamajorbioactivecompoundwithvariousdiabetessyndromeinJapanese,KoreanandChinesebiologicaleffects.Recently,anti—cancer,anti-stress,anti-anxiety,anti·depressant
此文檔下載收益歸作者所有