Abstract：
OBJECTIVE: We investigated, the effects of aprepitant (APRE) on the lung tissues of rats with an experimental polymicrobial sepsis model (CLP: cecal ligation and puncture) biochemically, molecularly and histopathologically.
METHODS: A total of 40 rats were divided into 5 groups with 8 animals in each group. Group 1 (SHAM), control group; Group 2 (CLP), cecal ligation and puncture; Group 3 (CLP + APRE10), rats were administered CLP + 10 mg/kg aprepitant; Group 4 (CLP + APRE20), rats were administered CLP + 20 mg/kg aprepitant; and Group 5 (CLP + APRE40), rats were administered CLP + 40 mg/kg aprepitant. A polymicrobial sepsis model was induced with CLP. After 16 h, lung tissues were taken for examination. Tumour necrosis factor α (TNF-α) and nuclear factor-kappa b (NFK-b) messenger ribonucleic acid (mRNA) expressions were analysed by real-time PCR (RT-PCR), biochemically antioxidant parameters such as superoxide dismutase (SOD) and glutathione (GSH) and oxidant parameters such as malondialdehyde (MDA) and lung damage histopathologically.
CONCLUSIONS: The GSH level and SOD activity increased while the MDA level and the expressions of TNF-α and NFK-b were reduced in the groups treated with APRE, especially in the CLP + APRE40 group. The histopathology results supported the molecular and biochemical results.
METHODS: A total of 40 rats were divided into 5 groups with 8 animals in each group. Group 1 (SHAM), control group; Group 2 (CLP), cecal ligation and puncture; Group 3 (CLP + APRE10), rats were administered CLP + 10 mg/kg aprepitant; Group 4 (CLP + APRE20), rats were administered CLP + 20 mg/kg aprepitant; and Group 5 (CLP + APRE40), rats were administered CLP + 40 mg/kg aprepitant. A polymicrobial sepsis model was induced with CLP. After 16 h, lung tissues were taken for examination. Tumour necrosis factor α (TNF-α) and nuclear factor-kappa b (NFK-b) messenger ribonucleic acid (mRNA) expressions were analysed by real-time PCR (RT-PCR), biochemically antioxidant parameters such as superoxide dismutase (SOD) and glutathione (GSH) and oxidant parameters such as malondialdehyde (MDA) and lung damage histopathologically.
CONCLUSIONS: The GSH level and SOD activity increased while the MDA level and the expressions of TNF-α and NFK-b were reduced in the groups treated with APRE, especially in the CLP + APRE40 group. The histopathology results supported the molecular and biochemical results.
摘要：
目标：我们调查了，阿瑞吡坦（APRE）对实验性多微生物败血症模型（CLP：盲肠结扎穿孔）大鼠肺组织的影响，分子和组织病理学。
方法：将40只大鼠分为5组，每组8只。第1组(SHAM),对照组；第2组（CLP），盲肠结扎和穿刺；第3组（CLP+APRE10），大鼠给予CLP+10mg/kg阿瑞吡坦;第4组(CLP+APRE20),大鼠给予CLP+20mg/kg阿瑞吡坦;和第5组(CLP+APRE40),给大鼠施用CLP+40mg/kg阿瑞吡坦。用CLP诱导多微生物败血症模型。16小时后，取肺组织检查。实时荧光定量PCR(RT-PCR)检测肿瘤坏死因子α(TNF-α)和核因子-κB(NFK-b)信使核糖核酸(mRNA)表达,生化抗氧化参数如超氧化物歧化酶（SOD）和谷胱甘肽（GSH）和氧化剂参数如丙二醛（MDA）和肺损伤的组织病理学。
■在APRE治疗组中，GSH水平和SOD活性升高，而MDA水平和TNF-α和NFK-b的表达降低，尤其是CLP+APRE40组。组织病理学结果支持分子和生化结果。
方法：将40只大鼠分为5组，每组8只。第1组(SHAM),对照组；第2组（CLP），盲肠结扎和穿刺；第3组（CLP+APRE10），大鼠给予CLP+10mg/kg阿瑞吡坦;第4组(CLP+APRE20),大鼠给予CLP+20mg/kg阿瑞吡坦;和第5组(CLP+APRE40),给大鼠施用CLP+40mg/kg阿瑞吡坦。用CLP诱导多微生物败血症模型。16小时后，取肺组织检查。实时荧光定量PCR(RT-PCR)检测肿瘤坏死因子α(TNF-α)和核因子-κB(NFK-b)信使核糖核酸(mRNA)表达,生化抗氧化参数如超氧化物歧化酶（SOD）和谷胱甘肽（GSH）和氧化剂参数如丙二醛（MDA）和肺损伤的组织病理学。
■在APRE治疗组中，GSH水平和SOD活性升高，而MDA水平和TNF-α和NFK-b的表达降低，尤其是CLP+APRE40组。组织病理学结果支持分子和生化结果。
