安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
5期
603-605,606
,共4页
龚文辉%张成鑫%华天凤%汪裕琪%黄大可%赵强
龔文輝%張成鑫%華天鳳%汪裕琪%黃大可%趙彊
공문휘%장성흠%화천봉%왕유기%황대가%조강
瘦素%肺损伤%肺保护%缺血再灌注
瘦素%肺損傷%肺保護%缺血再灌註
수소%폐손상%폐보호%결혈재관주
Leptin%lung injury%lung protection%ischemia-reperfusion
目的研究大鼠肺缺血再灌注损伤后血清炎症因子及肺组织相关酶活性的变化,并探讨外源性瘦素( Leptin)在肺缺血损伤中的作用及可能机制。方法建立大鼠肺缺血再灌注损伤模型,并用外源性Leptin干预治疗,对各组术后肺组织匀浆中丙二醛( MDA)、髓过氧化物酶( MPO)、超氧化物歧化酶( SOD)的活性、血清C反应蛋白( CRP)、肿瘤坏死因子-α( TNF-α)和核因子-资B ( NF-资B )浓度进行分析和比较,并观察各组肺组织病理学改变。结果缺血再灌注组血清炎症指标CRP、TNF-α、NF-资B浓度较假手术组明显升高,用外源性Leptin预处理后的炎症指标浓度较缺血再灌注组有显著下降( P<0.05)。肺组织匀浆MPO、MDA水平测定结果同样显示Leptin预处理组的肺组织匀浆酶学指标较缺血再灌注组有显著下降( P<0.05)。组织学病理显示缺血再灌注组肺损伤严重;Leptin预处理组肺泡结构较完整,炎症改变相对较轻,水肿及出血较再灌注组明显减少。结论运用外源性Leptin后肺缺血再灌注损伤明显减轻;外源性Leptin对肺缺血再灌注损伤有保护作用,可能与减轻脂质过氧化反应及炎性细胞浸润有关。
目的研究大鼠肺缺血再灌註損傷後血清炎癥因子及肺組織相關酶活性的變化,併探討外源性瘦素( Leptin)在肺缺血損傷中的作用及可能機製。方法建立大鼠肺缺血再灌註損傷模型,併用外源性Leptin榦預治療,對各組術後肺組織勻漿中丙二醛( MDA)、髓過氧化物酶( MPO)、超氧化物歧化酶( SOD)的活性、血清C反應蛋白( CRP)、腫瘤壞死因子-α( TNF-α)和覈因子-資B ( NF-資B )濃度進行分析和比較,併觀察各組肺組織病理學改變。結果缺血再灌註組血清炎癥指標CRP、TNF-α、NF-資B濃度較假手術組明顯升高,用外源性Leptin預處理後的炎癥指標濃度較缺血再灌註組有顯著下降( P<0.05)。肺組織勻漿MPO、MDA水平測定結果同樣顯示Leptin預處理組的肺組織勻漿酶學指標較缺血再灌註組有顯著下降( P<0.05)。組織學病理顯示缺血再灌註組肺損傷嚴重;Leptin預處理組肺泡結構較完整,炎癥改變相對較輕,水腫及齣血較再灌註組明顯減少。結論運用外源性Leptin後肺缺血再灌註損傷明顯減輕;外源性Leptin對肺缺血再灌註損傷有保護作用,可能與減輕脂質過氧化反應及炎性細胞浸潤有關。
목적연구대서폐결혈재관주손상후혈청염증인자급폐조직상관매활성적변화,병탐토외원성수소( Leptin)재폐결혈손상중적작용급가능궤제。방법건립대서폐결혈재관주손상모형,병용외원성Leptin간예치료,대각조술후폐조직균장중병이철( MDA)、수과양화물매( MPO)、초양화물기화매( SOD)적활성、혈청C반응단백( CRP)、종류배사인자-α( TNF-α)화핵인자-자B ( NF-자B )농도진행분석화비교,병관찰각조폐조직병이학개변。결과결혈재관주조혈청염증지표CRP、TNF-α、NF-자B농도교가수술조명현승고,용외원성Leptin예처리후적염증지표농도교결혈재관주조유현저하강( P<0.05)。폐조직균장MPO、MDA수평측정결과동양현시Leptin예처리조적폐조직균장매학지표교결혈재관주조유현저하강( P<0.05)。조직학병리현시결혈재관주조폐손상엄중;Leptin예처리조폐포결구교완정,염증개변상대교경,수종급출혈교재관주조명현감소。결론운용외원성Leptin후폐결혈재관주손상명현감경;외원성Leptin대폐결혈재관주손상유보호작용,가능여감경지질과양화반응급염성세포침윤유관。
Objective Rats serum inflammatory factors and enzyme activities of lung tissue were measured to inves-tigate the protective role and mechanisms of exogenous Leptin alleviating rat lung ischemia-reperfusion injury. Methods Rats lung ischemia-reperfusion injury models were established and one group was treated with exogenous Leptin. Plasma concentrations of C-reactive protein ( CRP) , tumor necrosis factor-α ( TNF-α) and nuclear factor-κB ( NF-κB) were measured by ELISA. The activity of malondialdehyde ( MDA) , myeloperoxidase ( MPO) , su-peroxide dismutase ( SOD) of lung homogenates were measured using colorimetric assay, and the morphological changes were observed under a microscope. Results In ischemia-reperfusion group, CRP, TNF-α, NF-κB con-centration were significantly higher than that of the sham group, and the concentration of exogenous Leptin group was significantly decreased compared with the value of ischemia-reperfusion group ( P<0.05 ) . The lung tissue enzymatic indicators examination also showed that the MPO, MDA levels of exogenous Leptin pretreatment had sig-nificantly decreased ( P<0.05 ) compared with ischemia-reperfusion group ( P<0.05 ) . Histological study showed relatively mild inflammation, edema and bleeding in exogenous Leptin treatment group with alveolar structure intact compared with ischemia-reperfusion injury group. Conclusion Lung ischemia-reperfusion injury was significantly alleviated after application of exogenous Leptin. The exogenous Leptin may play a protective role in lung ischemia-reperfusion injury through reducing lipid peroxidation and inflammatory cell infiltration.