药学与临床研究
藥學與臨床研究
약학여림상연구
PHARMACEUTICAL AND CLINICAL RESEARCH
2014年
2期
101-104
,共4页
吡非尼酮%百草枯%氧化应激%炎症反应%转化生长因子%结缔组织生长因子
吡非尼酮%百草枯%氧化應激%炎癥反應%轉化生長因子%結締組織生長因子
필비니동%백초고%양화응격%염증반응%전화생장인자%결체조직생장인자
Pirfenidone%Paraquat%Oxidative stress%Inflammatory reaction%Transforming growth factor%Connective tissue growth factor
目的：研究吡非尼酮（pirfenidone，PF）对百草枯（paraquat，PQ）诱导的大鼠急性肺损伤的保护作用及机制。方法：30只雄性成年SD大鼠随机分为对照组、PQ组、PF治疗低、中、高组，采用腹腔注射20% PQ溶液诱导大鼠成急性PQ中毒模型。测定各组大鼠肺组织中超氧化物歧化酶（SOD）活性、丙二醛（MDA）以及炎症因子白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）含量变化，同时以蛋白免疫印迹法测定转化生长因子（TGF-β）、结缔组织生长因子（CTGF）、smad3蛋白表达。HE染色观察大鼠肺组织病理改变。结果：与对照组大鼠相比，PQ组大鼠肺组织氧化应激和炎症反应水平明显升高，而给予PF可明显抑制中毒大鼠肺组织氧化应激和炎症反应。蛋白免疫印迹结果显示，中毒大鼠肺组织中TGF-β、CTGF、smad3蛋白表达显著升高，光镜观察显示中毒大鼠肺组织大量肺泡萎缩，部分过度膨胀，组织炎性浸润和纤维化明显。给予PF治疗后，大鼠肺组织TGF-β、CTGF和smad3蛋白表达以及组织损伤和纤维化显著降低。结论：PF可以减轻百草枯中毒大鼠肺组织损伤，其治疗作用可能与其抗炎、抗氧化、抑制TGF-β、CTGF和smad3表达有关。
目的：研究吡非尼酮（pirfenidone，PF）對百草枯（paraquat，PQ）誘導的大鼠急性肺損傷的保護作用及機製。方法：30隻雄性成年SD大鼠隨機分為對照組、PQ組、PF治療低、中、高組，採用腹腔註射20% PQ溶液誘導大鼠成急性PQ中毒模型。測定各組大鼠肺組織中超氧化物歧化酶（SOD）活性、丙二醛（MDA）以及炎癥因子白介素-6（IL-6）、腫瘤壞死因子-α（TNF-α）含量變化，同時以蛋白免疫印跡法測定轉化生長因子（TGF-β）、結締組織生長因子（CTGF）、smad3蛋白錶達。HE染色觀察大鼠肺組織病理改變。結果：與對照組大鼠相比，PQ組大鼠肺組織氧化應激和炎癥反應水平明顯升高，而給予PF可明顯抑製中毒大鼠肺組織氧化應激和炎癥反應。蛋白免疫印跡結果顯示，中毒大鼠肺組織中TGF-β、CTGF、smad3蛋白錶達顯著升高，光鏡觀察顯示中毒大鼠肺組織大量肺泡萎縮，部分過度膨脹，組織炎性浸潤和纖維化明顯。給予PF治療後，大鼠肺組織TGF-β、CTGF和smad3蛋白錶達以及組織損傷和纖維化顯著降低。結論：PF可以減輕百草枯中毒大鼠肺組織損傷，其治療作用可能與其抗炎、抗氧化、抑製TGF-β、CTGF和smad3錶達有關。
목적：연구필비니동（pirfenidone，PF）대백초고（paraquat，PQ）유도적대서급성폐손상적보호작용급궤제。방법：30지웅성성년SD대서수궤분위대조조、PQ조、PF치료저、중、고조，채용복강주사20% PQ용액유도대서성급성PQ중독모형。측정각조대서폐조직중초양화물기화매（SOD）활성、병이철（MDA）이급염증인자백개소-6（IL-6）、종류배사인자-α（TNF-α）함량변화，동시이단백면역인적법측정전화생장인자（TGF-β）、결체조직생장인자（CTGF）、smad3단백표체。HE염색관찰대서폐조직병리개변。결과：여대조조대서상비，PQ조대서폐조직양화응격화염증반응수평명현승고，이급여PF가명현억제중독대서폐조직양화응격화염증반응。단백면역인적결과현시，중독대서폐조직중TGF-β、CTGF、smad3단백표체현저승고，광경관찰현시중독대서폐조직대량폐포위축，부분과도팽창，조직염성침윤화섬유화명현。급여PF치료후，대서폐조직TGF-β、CTGF화smad3단백표체이급조직손상화섬유화현저강저。결론：PF가이감경백초고중독대서폐조직손상，기치료작용가능여기항염、항양화、억제TGF-β、CTGF화smad3표체유관。
Objective: To study the protective effect of Pirfenidone (PF) against Paraquat (PQ)-induced lung damage in rats and its underlying mechanisms. Methods: Thirty rats were randomly divided into five groups: control group, PQ group, PF low-, middle- and high-dose treatment groups. The activties of super-oxide dismutase (SOD), the contents of malondialdehyde (MDA), IL-6 and TNF-α in the lung tissues were examined. Also, the expression of TGF-β, CTGF and smad3 in lung tissues w measured by Western-blot-ting. The lung coefficient was calculated and pathological changes of lung tissues were observed by HE staining. Results: Compared with the control group rats, the levels of oxidative stress and inflammation were increased in the lung tissues of PQ group rats, while the PF group rats exhibited significant decrease in oxidative stress and inflammation. The expression of TGF-β, CTGF and smad3 were increased in PQ group rats. The sections showed that the lung tissue damage was obvious in PQ group rats with alveolar a-trophy, overinflation, inflammatory cell infiltration and pulmonary fibrosis. However, the administration of PF significantly decreased the damage. Conclusion: The results indicated that PF had a protective effect a-gainst PQ-induced lung damage in rats. It is considered that this protective effect may be related to its free radical scavenging activity, inhibition of inflammation and inhibition of the expression of TGF-β, CTGF and smad3.
