河北北方学院学报：自然科学版
河北北方學院學報：自然科學版
하북북방학원학보：자연과학판
Journa of Hebei North University:Natural Science Edition
2012年
3期
62-65
,共4页
王松柏%姜龙%齐绍鸿%张河
王鬆柏%薑龍%齊紹鴻%張河
왕송백%강룡%제소홍%장하
丝裂原活化蛋白激酶%肿瘤坏死因子-α%大鼠%休克
絲裂原活化蛋白激酶%腫瘤壞死因子-α%大鼠%休剋
사렬원활화단백격매%종류배사인자-α%대서%휴극
tumor necrosis factor-α%sepsis%rat%mitogen-activated protein kinase
目的探讨丝裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）活化与脓毒症大鼠肺组织和血浆肿瘤坏死因子-α（TNF-α）表达及组织炎症反应的关系。方法采用盲肠结扎穿孔术（CLP）模型制造大鼠腹腔感染。随机将56只大鼠分为正常对照组、CLP组和CLP＋MAPK抑制剂（SB203580）处理组，各组又分不同时间点亚组。采用反转录多聚酶链式反应和酶联免疫吸附试验检测试剂盒分别测定血浆和肺TNF-α mRNA和蛋白水平；同时测定肺髓过氧化酶（MPO）活性、HE染色病理切片检测肺组织炎症反应程度。结果与正常大鼠相比，CLP后各时间点肺血浆和肺组织TNF-α mRNA、蛋白含量均升高明显；同时肺MPO和组织病理学评分升高明显。MAPK抑制剂处理后，与CLP组相应时间点相比，MPO和病理学评分均显著下降；TNF-α mRNA表达和蛋白含量同时显著降低。结论抑制MAPK活化可缓和脓毒症所致大鼠肺组织炎症反应，减轻肺组织损伤。
目的探討絲裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）活化與膿毒癥大鼠肺組織和血漿腫瘤壞死因子-α（TNF-α）錶達及組織炎癥反應的關繫。方法採用盲腸結扎穿孔術（CLP）模型製造大鼠腹腔感染。隨機將56隻大鼠分為正常對照組、CLP組和CLP＋MAPK抑製劑（SB203580）處理組，各組又分不同時間點亞組。採用反轉錄多聚酶鏈式反應和酶聯免疫吸附試驗檢測試劑盒分彆測定血漿和肺TNF-α mRNA和蛋白水平；同時測定肺髓過氧化酶（MPO）活性、HE染色病理切片檢測肺組織炎癥反應程度。結果與正常大鼠相比，CLP後各時間點肺血漿和肺組織TNF-α mRNA、蛋白含量均升高明顯；同時肺MPO和組織病理學評分升高明顯。MAPK抑製劑處理後，與CLP組相應時間點相比，MPO和病理學評分均顯著下降；TNF-α mRNA錶達和蛋白含量同時顯著降低。結論抑製MAPK活化可緩和膿毒癥所緻大鼠肺組織炎癥反應，減輕肺組織損傷。
목적탐토사렬원활화단백격매（mitogen-activated protein kinase，MAPK）활화여농독증대서폐조직화혈장종류배사인자-α（TNF-α）표체급조직염증반응적관계。방법채용맹장결찰천공술（CLP）모형제조대서복강감염。수궤장56지대서분위정상대조조、CLP조화CLP＋MAPK억제제（SB203580）처리조，각조우분불동시간점아조。채용반전록다취매련식반응화매련면역흡부시험검측시제합분별측정혈장화폐TNF-α mRNA화단백수평；동시측정폐수과양화매（MPO）활성、HE염색병리절편검측폐조직염증반응정도。결과여정상대서상비，CLP후각시간점폐혈장화폐조직TNF-α mRNA、단백함량균승고명현；동시폐MPO화조직병이학평분승고명현。MAPK억제제처리후，여CLP조상응시간점상비，MPO화병이학평분균현저하강；TNF-α mRNA표체화단백함량동시현저강저。결론억제MAPK활화가완화농독증소치대서폐조직염증반응，감경폐조직손상。
Objective To investigate the effect of mitogen-activated protein kinase （MAPK） on ex- pression of tumor necrosis factor-α （TNF-α） and pulmonary injury induced by cecal ligation puncture （CLP） in septic rats. Methods Sepsis of rats was induced by CLP. 56 male SD rats were randomly di- vided into normal control, CLP group, and inhibitor （SB203580） of mitogen-activated protein kinase （MAPK） pre-treatment group. At serial time points in each group, animals were sacrificed. Then, pul- monary tissue and serum samples were harvested to determine TNF-α mRNA expression levels by reverse transcription polymerase chain reaction and its protein expression levels by enzyme-linked immunosorbent assay. Meanwhile, activity of myeloperoxidase and histopathology were also evaluated. Results Com- pared with that of normal control, pulmonary myeloperoxidase, histopathologic scoring as well as TNF-α mRNA and protein expression levels in lung or serum markedly increased respectively in CLP group. Fol- lowing pre-treatment with SB203580, MPO and histopathologic scoring reduced compared with that of CLP group, except for TNF-α mRNA and protein levels. Conclusion These data suggest that severe in- tra-abdoment infection could induce injury of remote lung and inhibiting the activation of MAPK could at- tenuate pulmonary tissue damage.
