肝脏
肝髒
간장
CHINESE HEPATOLOGY
2014年
5期
323-328
,共6页
张明月%王冰%丁启龙%杨瑞宁%邱红
張明月%王冰%丁啟龍%楊瑞寧%邱紅
장명월%왕빙%정계룡%양서저%구홍
非酒精性脂肪肝%黄嘌呤氧化酶%对氧磷酶 1%氧化应激
非酒精性脂肪肝%黃嘌呤氧化酶%對氧燐酶 1%氧化應激
비주정성지방간%황표령양화매%대양린매 1%양화응격
Nonalcoholic fatty liver%Xanthine oxidase%Paraoxonase 1%Oxidative stress
目的:观察黄嘌呤氧化酶(XOD)和对氧磷酶1(PON1)活力在非酒精性脂肪性肝病(NAFLD)发生及发展过程中的变化并探讨其与 NAFLD 严重程度的关系。方法采用高脂饮食(HFD)喂养大鼠建立 NAFLD 模型,32只雄性SD 大鼠,随机均分4组:正常对照组、HFD 组、HFD +α-硫辛酸(α-LA)40 mg/kg 和20 mg/kg 干预组。测量大鼠体重、肝重,常规 HE 染色观察肝脏病理形态学改变,检测血清和肝组织 XOD 和 PON1活力、相关脂质指标和氧化应激指标。结果HFD 饲养12周可成功诱导大鼠 NAFLD 模型建立,表现为血脂紊乱、肝细胞脂质沉积及氧化应激。与正常对照组比较,HFD 组大鼠血清 XOD 活力从第4周末明显升高,12周末达最高(P <0.01);PON1活力从4周末开始呈梯度降低趋势(P <0.01)。与 HFD 组比较,α-LA 干预组能显著降低 TG 和升高的 XOD,同时使下降的 PON1有所恢复。肝组织的变化趋势与血清相同。结论XOD 和 PON1活力在 NAFLD 形成的不同时期存在显著差异,提示其在该病发生发展过程中起了重要作用,对二者活力的检测有助于判断 NAFLD 严重程度。α-LA 对 NAFLD 有一定的防治作用,作用机制可能与其抗氧化应激和抗脂质过氧化有关。
目的:觀察黃嘌呤氧化酶(XOD)和對氧燐酶1(PON1)活力在非酒精性脂肪性肝病(NAFLD)髮生及髮展過程中的變化併探討其與 NAFLD 嚴重程度的關繫。方法採用高脂飲食(HFD)餵養大鼠建立 NAFLD 模型,32隻雄性SD 大鼠,隨機均分4組:正常對照組、HFD 組、HFD +α-硫辛痠(α-LA)40 mg/kg 和20 mg/kg 榦預組。測量大鼠體重、肝重,常規 HE 染色觀察肝髒病理形態學改變,檢測血清和肝組織 XOD 和 PON1活力、相關脂質指標和氧化應激指標。結果HFD 飼養12週可成功誘導大鼠 NAFLD 模型建立,錶現為血脂紊亂、肝細胞脂質沉積及氧化應激。與正常對照組比較,HFD 組大鼠血清 XOD 活力從第4週末明顯升高,12週末達最高(P <0.01);PON1活力從4週末開始呈梯度降低趨勢(P <0.01)。與 HFD 組比較,α-LA 榦預組能顯著降低 TG 和升高的 XOD,同時使下降的 PON1有所恢複。肝組織的變化趨勢與血清相同。結論XOD 和 PON1活力在 NAFLD 形成的不同時期存在顯著差異,提示其在該病髮生髮展過程中起瞭重要作用,對二者活力的檢測有助于判斷 NAFLD 嚴重程度。α-LA 對 NAFLD 有一定的防治作用,作用機製可能與其抗氧化應激和抗脂質過氧化有關。
목적:관찰황표령양화매(XOD)화대양린매1(PON1)활력재비주정성지방성간병(NAFLD)발생급발전과정중적변화병탐토기여 NAFLD 엄중정도적관계。방법채용고지음식(HFD)위양대서건립 NAFLD 모형,32지웅성SD 대서,수궤균분4조:정상대조조、HFD 조、HFD +α-류신산(α-LA)40 mg/kg 화20 mg/kg 간예조。측량대서체중、간중,상규 HE 염색관찰간장병리형태학개변,검측혈청화간조직 XOD 화 PON1활력、상관지질지표화양화응격지표。결과HFD 사양12주가성공유도대서 NAFLD 모형건립,표현위혈지문란、간세포지질침적급양화응격。여정상대조조비교,HFD 조대서혈청 XOD 활력종제4주말명현승고,12주말체최고(P <0.01);PON1활력종4주말개시정제도강저추세(P <0.01)。여 HFD 조비교,α-LA 간예조능현저강저 TG 화승고적 XOD,동시사하강적 PON1유소회복。간조직적변화추세여혈청상동。결론XOD 화 PON1활력재 NAFLD 형성적불동시기존재현저차이,제시기재해병발생발전과정중기료중요작용,대이자활력적검측유조우판단 NAFLD 엄중정도。α-LA 대 NAFLD 유일정적방치작용,작용궤제가능여기항양화응격화항지질과양화유관。
Objective To observe changes of xanthine oxidase (XOD)and paraoxonase-1 (PON1 )in nonalcoholic fatty liver disease (NAFLD)in rats,and study the relevance of activity of XOD and PON1 with the severity of NAFLD. Methods A model of NAFLD in rats was established by intaking high fat diet (HFD).Thirty-two rats were randomly assigned to normal group,NAFLD model group,NAFLD with different dosage ofα-LA (α-LA:20 or 40mg/kg)groups, 8 rats for each group.Body weight and liver weight of rats were measured.Histological changes were observed by HE staining.Xanthine oxidase (XOD)and paraoxon-1 (PON1 )were detected in blood serum and liver tissue.Related lipid content and redox indicators were also determined.Results Rat model of NAFLD was induced successfully by HFD for 12 weeks,with obvious NAFLD-associated symptoms,namely blood lipid disorders,hepatic fat deposition and oxidative stress damage.XOD in serum increased significantly from the 4th week,remarkably higher than the normal group and reached the pinnacle at the 12th week (P <0.01 ).In addition,a negative correlation between PON1 and XOD was observed.Compared with the model group,α-LA medication could obviously decrease TG and XOD activity,enhance PON1 activity.Similar results were also found in liver tissue.Conclusion There were significant differences of both XOD and PON1 activity in different periods of NAFLD,indicating their important role in the occurrence and development of NAFLD.Furthermore,the detection of XOD and PON1 activity might be noninvasive approaches for identifying the severity of NAFLD in clinical practice.Besides,α-LA showed a protective effect on NAFLD rats.The potential mechanism may be related to the inhibition of oxidative stress and anti-lipid peroxidation.