中华普通外科杂志
中華普通外科雜誌
중화보통외과잡지
CHINESE JOURNAL OF GENERAL SURGERY
2008年
10期
791-793
,共3页
郭晏同%赵景明%宋磊%周迈%焦岗军%彭吉润%李涛%冷希圣
郭晏同%趙景明%宋磊%週邁%焦崗軍%彭吉潤%李濤%冷希聖
곽안동%조경명%송뢰%주매%초강군%팽길윤%리도%랭희골
肝硬化%胶原%过氧化物酶体增殖物激活受体
肝硬化%膠原%過氧化物酶體增殖物激活受體
간경화%효원%과양화물매체증식물격활수체
Liver cirrhosis%Collagen%Peroxisome proliferator activated receptors
目的 研究过氧化物酶体增殖物激活受体γ(peroxisome proliferator activated receptorgamma,PPARγ)配体对大鼠肝纤维化的作用.方法 将Wistar大鼠40只随机分为两组,对照组(20只)和罗格列酮组(20只).所有动物使用饮水中加人质量比0.3‰硫代乙酰胺的方法 制作肝纤维化模型.对照组喂饲普通颗粒饲料.罗格列酮组喂饲含200 ppm罗格列酮的颗粒饲料.喂饲6个月后,用RT-PCR方法 检测肝纤维化大鼠肝脏PPARγ、TGF-β 1 及Ⅰ型前胶原mRNA表达,用Westernblot法检测PPARγ、TGF-β 1 、Ⅰ型胶原及α平滑肌肌动蛋白(α-SMA)表达,用Van Gieson(VG)染色的方法 检测肝组织切片的胶原表达情况.结果 罗格列酮组与对照组相比,PPARγmRNA表达显著增强(t=6.93,P<0.01),TGF-β 1 mRNA(t=3.89,P<0.01)和Ⅰ型前胶原mRNA表达显著降低(t=5.67,P<0.01).PPARγ、TGF-β 1 及Ⅰ型胶原蛋白表达所得结果 与RT-PCR结果 相一致.罗格列酮组与对照组相比,α-SMA表达显著降低(t=3.12,P<0.01).罗格列酮组肝组织切片的胶原染色低于对照组(t=3.47,P<0.01).结论 PPARγ配体能够抑制大鼠纤维化肝脏的胶原产生,在体内具有一定的抗肝纤维化作用.
目的 研究過氧化物酶體增殖物激活受體γ(peroxisome proliferator activated receptorgamma,PPARγ)配體對大鼠肝纖維化的作用.方法 將Wistar大鼠40隻隨機分為兩組,對照組(20隻)和囉格列酮組(20隻).所有動物使用飲水中加人質量比0.3‰硫代乙酰胺的方法 製作肝纖維化模型.對照組餵飼普通顆粒飼料.囉格列酮組餵飼含200 ppm囉格列酮的顆粒飼料.餵飼6箇月後,用RT-PCR方法 檢測肝纖維化大鼠肝髒PPARγ、TGF-β 1 及Ⅰ型前膠原mRNA錶達,用Westernblot法檢測PPARγ、TGF-β 1 、Ⅰ型膠原及α平滑肌肌動蛋白(α-SMA)錶達,用Van Gieson(VG)染色的方法 檢測肝組織切片的膠原錶達情況.結果 囉格列酮組與對照組相比,PPARγmRNA錶達顯著增彊(t=6.93,P<0.01),TGF-β 1 mRNA(t=3.89,P<0.01)和Ⅰ型前膠原mRNA錶達顯著降低(t=5.67,P<0.01).PPARγ、TGF-β 1 及Ⅰ型膠原蛋白錶達所得結果 與RT-PCR結果 相一緻.囉格列酮組與對照組相比,α-SMA錶達顯著降低(t=3.12,P<0.01).囉格列酮組肝組織切片的膠原染色低于對照組(t=3.47,P<0.01).結論 PPARγ配體能夠抑製大鼠纖維化肝髒的膠原產生,在體內具有一定的抗肝纖維化作用.
목적 연구과양화물매체증식물격활수체γ(peroxisome proliferator activated receptorgamma,PPARγ)배체대대서간섬유화적작용.방법 장Wistar대서40지수궤분위량조,대조조(20지)화라격렬동조(20지).소유동물사용음수중가인질량비0.3‰류대을선알적방법 제작간섬유화모형.대조조위사보통과립사료.라격렬동조위사함200 ppm라격렬동적과립사료.위사6개월후,용RT-PCR방법 검측간섬유화대서간장PPARγ、TGF-β 1 급Ⅰ형전효원mRNA표체,용Westernblot법검측PPARγ、TGF-β 1 、Ⅰ형효원급α평활기기동단백(α-SMA)표체,용Van Gieson(VG)염색적방법 검측간조직절편적효원표체정황.결과 라격렬동조여대조조상비,PPARγmRNA표체현저증강(t=6.93,P<0.01),TGF-β 1 mRNA(t=3.89,P<0.01)화Ⅰ형전효원mRNA표체현저강저(t=5.67,P<0.01).PPARγ、TGF-β 1 급Ⅰ형효원단백표체소득결과 여RT-PCR결과 상일치.라격렬동조여대조조상비,α-SMA표체현저강저(t=3.12,P<0.01).라격렬동조간조직절편적효원염색저우대조조(t=3.47,P<0.01).결론 PPARγ배체능구억제대서섬유화간장적효원산생,재체내구유일정적항간섬유화작용.
Objective To study the effect of peroxisome proliferator-activated receptor garama (PPARγ) ligand on hepatic fibrosis in rats. Methods Forty Wistar rats were randomly divided into two groups: the control group(20 rats) ,in which liver cirrhosis was induced by adding 0. 3‰ thioacetamide in the fodder for 6 months, and rosiglitazone group(20 rats) in which 200 ppm of rosiglitazone in combination with 0. 3‰ thioacetamide was added in the fodder. Liver tissue's mRNA expression of PPARγ, TGF-β1 ,type Ⅰ pro-collagen and α-smooth muscle actin(α-SMA) was detected by RT-PCR. The protein expression of PPARγ, TGF-β1 ,type Ⅰ collagen and α-SMA was detected by Western blot. The expression of collagenof liver histological section was evaluated by Van Gieson (VG) staining. Results The expression ofPPARγ at mRNA level significantly increased in rosiglitazone group compared with those in the control group ( t = 6. 93, P < 0. 01 ), while the expression of TGF-β1 ( t = 3. 89, P < 0. 01 ) and type Ⅰ pro-collagen ( t =5.67,P <0. 01 ) were lower than that in the control group. The protein expression of PPARγ, TGF-β1 and type Ⅰ collagen was in similar tendence with that of mRNA expression. The expression of α-SMA decreased significantly in rosiglitazone group compared with that in the control group (t = 3. 12,P < 0.01 ). The collagen stainings of liver histological section in rosiglitazone group was lower than those in the control group (t = 3.47, P < 0. 01 ). Conclusion PPARγ ligand inhibits the production of collagen in fibrofic livers in rats and prevents hepatic fibrosis in vivo.
