中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2014年
49期
8007-8014
,共8页
马红%郭春花%杨香玖%鲁华东%陈立刚%黄延玲%张文强
馬紅%郭春花%楊香玖%魯華東%陳立剛%黃延玲%張文彊
마홍%곽춘화%양향구%로화동%진립강%황연령%장문강
实验动物%组织工程%非酒精性脂肪性肝病%视黄醇结合蛋白4%饮食干预%二甲双胍%肝组织病理
實驗動物%組織工程%非酒精性脂肪性肝病%視黃醇結閤蛋白4%飲食榦預%二甲雙胍%肝組織病理
실험동물%조직공정%비주정성지방성간병%시황순결합단백4%음식간예%이갑쌍고%간조직병리
rat%fatty liver%retinol-binding proteins
背景:目前关于血清视黄醇结合蛋白4在非酒精性脂肪性肝病中的表达水平仍存在争议。目的:研究饮食或二甲双胍干预对非酒精性脂肪性肝病大鼠肝脏视黄醇结合蛋白4表达的影响。方法:将50只SD大鼠随机分为6组,8周对照组,正常饮食8周后处死;8周高脂组,高脂饮食8周制作非酒精性脂肪性肝病模型,随后处死;16周对照组,正常饮食16周后处死;16周高脂组,高脂饮食16周后处死;饮食干预组,8周高脂饮食后再正常饮食8周,随后处死;二甲双胍治疗组,8周高脂饮食后,继续8周高脂饮食,同时给予二甲双胍灌胃治疗,随后处死。采用ELISA法检测血清视黄醇结合蛋白4水平及生化指标,免疫组织化学法、Western blotting法、RT-PCR法检测肝脏组织视黄醇结合蛋白4表达。结果与结论:高脂饮食成功建立非酒精性脂肪性肝病大鼠模型,随造模时间延长,大鼠肝脏由单纯性脂肪肝逐渐进展成为脂肪性肝炎。饮食干预可改善高脂饮食引发的肝组织视黄醇结合蛋白4表达下降、肝功能异常、脂代谢紊乱和胰岛素抵抗,二甲双胍治疗仅改善了高脂饮食引发的肝脂肪变。结果表明肝组织视黄醇结合蛋白4表达的改变可能在非酒精性脂肪性肝病发病中起一定作用,饮食干预应作为防治非酒精性脂肪性肝病的基本措施,二甲双胍可以改善非酒精性脂肪性肝病的肝脂肪变。
揹景:目前關于血清視黃醇結閤蛋白4在非酒精性脂肪性肝病中的錶達水平仍存在爭議。目的:研究飲食或二甲雙胍榦預對非酒精性脂肪性肝病大鼠肝髒視黃醇結閤蛋白4錶達的影響。方法:將50隻SD大鼠隨機分為6組,8週對照組,正常飲食8週後處死;8週高脂組,高脂飲食8週製作非酒精性脂肪性肝病模型,隨後處死;16週對照組,正常飲食16週後處死;16週高脂組,高脂飲食16週後處死;飲食榦預組,8週高脂飲食後再正常飲食8週,隨後處死;二甲雙胍治療組,8週高脂飲食後,繼續8週高脂飲食,同時給予二甲雙胍灌胃治療,隨後處死。採用ELISA法檢測血清視黃醇結閤蛋白4水平及生化指標,免疫組織化學法、Western blotting法、RT-PCR法檢測肝髒組織視黃醇結閤蛋白4錶達。結果與結論:高脂飲食成功建立非酒精性脂肪性肝病大鼠模型,隨造模時間延長,大鼠肝髒由單純性脂肪肝逐漸進展成為脂肪性肝炎。飲食榦預可改善高脂飲食引髮的肝組織視黃醇結閤蛋白4錶達下降、肝功能異常、脂代謝紊亂和胰島素牴抗,二甲雙胍治療僅改善瞭高脂飲食引髮的肝脂肪變。結果錶明肝組織視黃醇結閤蛋白4錶達的改變可能在非酒精性脂肪性肝病髮病中起一定作用,飲食榦預應作為防治非酒精性脂肪性肝病的基本措施,二甲雙胍可以改善非酒精性脂肪性肝病的肝脂肪變。
배경:목전관우혈청시황순결합단백4재비주정성지방성간병중적표체수평잉존재쟁의。목적:연구음식혹이갑쌍고간예대비주정성지방성간병대서간장시황순결합단백4표체적영향。방법:장50지SD대서수궤분위6조,8주대조조,정상음식8주후처사;8주고지조,고지음식8주제작비주정성지방성간병모형,수후처사;16주대조조,정상음식16주후처사;16주고지조,고지음식16주후처사;음식간예조,8주고지음식후재정상음식8주,수후처사;이갑쌍고치료조,8주고지음식후,계속8주고지음식,동시급여이갑쌍고관위치료,수후처사。채용ELISA법검측혈청시황순결합단백4수평급생화지표,면역조직화학법、Western blotting법、RT-PCR법검측간장조직시황순결합단백4표체。결과여결론:고지음식성공건립비주정성지방성간병대서모형,수조모시간연장,대서간장유단순성지방간축점진전성위지방성간염。음식간예가개선고지음식인발적간조직시황순결합단백4표체하강、간공능이상、지대사문란화이도소저항,이갑쌍고치료부개선료고지음식인발적간지방변。결과표명간조직시황순결합단백4표체적개변가능재비주정성지방성간병발병중기일정작용,음식간예응작위방치비주정성지방성간병적기본조시,이갑쌍고가이개선비주정성지방성간병적간지방변。
BACKGROUND:Conflicting data have been reported regarding the expression of retinol-binding protein 4 in non-alcoholic fatty liver disease. OBJECTIVE:To evaluate the impact of dietary interventionversus metformin treatment on expression of retinol-binding protein 4 in rats with non-alcoholic fatty liver disease. METHODS: Fifty male Sprague-Dawley rats were randomized to six groups, including two normal control groups (rats were kiled after 8 and 16 weeks of normal diet), two HFD groups (rats were kiled after 8 and 16 weeks of high-fat diet), one dietary intervention group (rats were kiled after 8 weeks of high-fat diet and 8 weeks of normal diet) and one metformin treatment group (rats were kiled after 8 weeks of high-fat diet and 8 weeks of high-fat diet and metformin treatment). The levels of retinol-binding protein 4 in serum and biochemical indexes were detected through enzyme-linked immunosorbent assay. The expression of retinol-binding protein 4 mRNA in liver tissues was measuredvia western blot analysis, immunohistochemistry and RT-PCR. RESULTS AND CONCLUSION:Non-alcoholic fatty liver disease models were successfuly established by high-fat diet. Liver tissues of high-fat diet fed rats showed progressing non-alcoholic fatty liver disease histology, from non-alcoholic fatty liver to non-alcoholic steatohepatitis. Dietary intervention increased retinol-binding protein 4 expression in liver tissue as wel as improving liver enzyme, dyslipidemia and insulin resistance, and aleviated impaired liver histology. Metformin treatment only aleviated hepatic steatosis caused by high-fat diet. The results indicated that retinol-binding protein 4 expression might play a role in the pathogenesis of non-alcoholic fatty liver disease. Metformin treatment can aleviate non-alcoholic fatty liver disease histology,dietary intervention should be the fundamental treatment.