长治医学院学报
長治醫學院學報
장치의학원학보
JOURNAL OF CHANGZHI MEDICAL COLLEGE
2014年
3期
161-164
,共4页
李旭炯%张慧英%张丽丽%王黎敏%范毅敏%刘燕%张翠英
李旭炯%張慧英%張麗麗%王黎敏%範毅敏%劉燕%張翠英
리욱형%장혜영%장려려%왕려민%범의민%류연%장취영
甜菜碱%肝纤维化%内毒素%肺损伤%氧化应激
甜菜堿%肝纖維化%內毒素%肺損傷%氧化應激
첨채감%간섬유화%내독소%폐손상%양화응격
betaine%hepatic fibrosis%endotoxin%lung injury%oxidative stress
目的:观察甜菜碱对肝纤维化大鼠肺组织氧化应激的影响。方法:复合致病因素诱导复制肝纤维化大鼠模型,给予甜菜碱[500 mg/(kg·d)]进行干预。4周末,测定大鼠血浆内毒素、白蛋白、总胆固醇、甘油三酯、透明质酸含量及碱性磷酸酶活性;观察肝组织及肺组织的病理学改变;检测肺组织匀浆中TNF-α、ONOO-、NO、MDA的变化。结果:肝纤维化组动物血浆内毒素、白蛋白、总胆固醇、甘油三酯、透明质酸含量明显增高、碱性磷酸酶活性增加,肺组织 TNF-α、NO、ONOO-、MDA 含量均升高;给予甜菜碱后大鼠血浆内毒素及其余各项指标水平均降低,肺组织中 TNF-α、ONOO-、NO、MDA明显降低,尤以TNF-α和MDA的变化更为显著,肺组织的病理学改变也减轻。结论:(1)肝损伤及肝纤维化可导致肺部损伤。(2)甜菜碱可能通过某种机制降低肠源性内毒素水平,进而降低炎性因子水平、减轻肺组织的氧化应激反应,减轻肺损伤。
目的:觀察甜菜堿對肝纖維化大鼠肺組織氧化應激的影響。方法:複閤緻病因素誘導複製肝纖維化大鼠模型,給予甜菜堿[500 mg/(kg·d)]進行榦預。4週末,測定大鼠血漿內毒素、白蛋白、總膽固醇、甘油三酯、透明質痠含量及堿性燐痠酶活性;觀察肝組織及肺組織的病理學改變;檢測肺組織勻漿中TNF-α、ONOO-、NO、MDA的變化。結果:肝纖維化組動物血漿內毒素、白蛋白、總膽固醇、甘油三酯、透明質痠含量明顯增高、堿性燐痠酶活性增加,肺組織 TNF-α、NO、ONOO-、MDA 含量均升高;給予甜菜堿後大鼠血漿內毒素及其餘各項指標水平均降低,肺組織中 TNF-α、ONOO-、NO、MDA明顯降低,尤以TNF-α和MDA的變化更為顯著,肺組織的病理學改變也減輕。結論:(1)肝損傷及肝纖維化可導緻肺部損傷。(2)甜菜堿可能通過某種機製降低腸源性內毒素水平,進而降低炎性因子水平、減輕肺組織的氧化應激反應,減輕肺損傷。
목적:관찰첨채감대간섬유화대서폐조직양화응격적영향。방법:복합치병인소유도복제간섬유화대서모형,급여첨채감[500 mg/(kg·d)]진행간예。4주말,측정대서혈장내독소、백단백、총담고순、감유삼지、투명질산함량급감성린산매활성;관찰간조직급폐조직적병이학개변;검측폐조직균장중TNF-α、ONOO-、NO、MDA적변화。결과:간섬유화조동물혈장내독소、백단백、총담고순、감유삼지、투명질산함량명현증고、감성린산매활성증가,폐조직 TNF-α、NO、ONOO-、MDA 함량균승고;급여첨채감후대서혈장내독소급기여각항지표수평균강저,폐조직중 TNF-α、ONOO-、NO、MDA명현강저,우이TNF-α화MDA적변화경위현저,폐조직적병이학개변야감경。결론:(1)간손상급간섬유화가도치폐부손상。(2)첨채감가능통과모충궤제강저장원성내독소수평,진이강저염성인자수평、감경폐조직적양화응격반응,감경폐손상。
Obj ective:To explore the protective effects of betaine on the pulmonary oxidative stress in hepatic fibrosis induced by multiple pathogenic factors in rat.Methods:The Sprague Dawley rats were randomly divided into normal control group,liver fibrosis group and betaine group.Liver fibrosis was induced by multiple pathogenic factors.The rats in betaine group were gavage administration with betaine [500 mg/(kg·d)].On the end of 4th week,blood samples were collected to assay endotoxin,alkaline phosphatase,albumin,triglyceride,total cholesterol,hyaluronic acid in plasma.And TNF-α,NO, ONOO-,MDA were detected in pulmonary tissue.The histopathological change of the liver and lung were observed with light microscopy.Results:The hepatic fibrosis model was successfully established in rats.The levels of endotoxin,albumin, triglyceride,total cholesterol,hyaluronic acid and alkaline phosphatase activities in plasma were significantly increased in rats with hepatic fibrosis.After betaine administration,the levels of endotoxin in plasma,and TNF-α,NO and ONOO- and MDA in lung tissue were markedly decreased,and the pathological features of lung tissue were alleviated.Conclusion:Liver fibrosis can lead to pulmonary inj ury.Betaine may exert a protecting role by reducing intestinal endotoxin,reducing inflammation factors,antagonizing pulmonary oxidative stress.