CAJ | 학술논문

目的：观察胰高血糖素样肽-1（GLP-1）对非酒精性脂肪肝大鼠肝氧化应激及肿瘤坏死因子α（TNF-α）、转换生长因子β1（TGF-β1）的影响。方法雄性SD大鼠30只，随机分为3组，分别予普通饮食10只（ND组）、高脂饮食10只（HFD组）、高脂饮食加利拉鲁肽腹腔注射10只（GLP-1组）。高脂饮食12周建立大鼠NAFLD模型，建模成功后GLP-1组予利拉鲁肽腹腔注射治疗4周。16周末处死各组大鼠，生物化学法检测血清ALT、血清和肝组织甘油三酯（TG）、总胆固醇（TC），分光光度计测定肝匀浆超氧化物歧化酶（SOD）、丙二醛（MAD）及FFAs，酶联免疫吸附法测定血清TGF-β1、肝匀浆TNF-α。结果与ND组比较，HFD组大鼠体质量、肝指数、血清ALT、TG、TC、TGF-β1及肝匀浆TG、TC、MAD、FFAs、TNF-α均明显升高（P>0.05），肝匀浆SOD活力明显降低（P<0.05），肝脏脂肪变性程度和炎症活动度显著增高（P<0.05）；而与HFD组比较，GLP-1组可促进上述指标恢复（P<0.05）。结论利拉鲁肽可以减轻高脂饮食诱导肝脂肪变，改善氧应激及脂质过氧化，降低TNF-α及TGF-β1的含量，有可能作为治疗非酒精性脂肪肝病的有效药物。
목적：관찰이고혈당소양태-1（GLP-1）대비주정성지방간대서간양화응격급종류배사인자α（TNF-α）、전환생장인자β1（TGF-β1）적영향。방법웅성SD대서30지，수궤분위3조，분별여보통음식10지（ND조）、고지음식10지（HFD조）、고지음식가리랍로태복강주사10지（GLP-1조）。고지음식12주건립대서NAFLD모형，건모성공후GLP-1조여리랍로태복강주사치료4주。16주말처사각조대서，생물화학법검측혈청ALT、혈청화간조직감유삼지（TG）、총담고순（TC），분광광도계측정간균장초양화물기화매（SOD）、병이철（MAD）급FFAs，매련면역흡부법측정혈청TGF-β1、간균장TNF-α。결과여ND조비교，HFD조대서체질량、간지수、혈청ALT、TG、TC、TGF-β1급간균장TG、TC、MAD、FFAs、TNF-α균명현승고（P>0.05），간균장SOD활력명현강저（P<0.05），간장지방변성정도화염증활동도현저증고（P<0.05）；이여HFD조비교，GLP-1조가촉진상술지표회복（P<0.05）。결론리랍로태가이감경고지음식유도간지방변，개선양응격급지질과양화，강저TNF-α급TGF-β1적함량，유가능작위치료비주정성지방간병적유효약물。
Objective To investigate the effects of glucagon-like peptide-1 (GLP-1) on liver oxidative stress, TNF-αand TGF-β1 in rats with diet-induced non-alcoholic fatty liver disease (NAFLD). Methods Thirty male rats were randomly divided into 3 equal groups and fed for 16 weeks with normal diet (ND), high-fat diet (HFD), or high-fat diet with intraperitoneal injection of liraglutide (GLP-1, administered in the later 4 weeks). The rats were then sacrificed to obtain blood samples and liver tissues for analyzing the levels of blood aminotransferase (ALT), triglyceride (TG), and total-cholesterol (TC) using an automatic biochemical analyzer and the levels of superoxide dismutase (SOD), malondial-dehyde (MAD), free fatty acid (FFAs), TNF-αin the liver homogenates and TGF-β1 in serum by radioimmunoassay or ELISA. Results Compared with ND group, HFD group showed significantly increased body weight, liver index, serum levels of ALT, TG, TC, and TGF-β1, and TG, TC, MAD, FFAs, and TNF-a in the liver homogenates, with also significantly increased degree of hepatic steatosis and inflammation activity (P<0.05) and lowered level of SOD. All these changes were markedly ameliorated in GLP-1 group (P<0.05). Conclusion Liraglutide can reduce high-fat diet-induced hepatic steatosis, improve oxidative stress and lipid peroxidation, and decrease TGF-β1 and TNF-a levels in serum and liver homogenates, suggesting its potential as a therapeutic agent for NAFLD.