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作 者:楚秉泉[1,2] 李云虹 李交杰 张英[1] CHU Bing-quan;LI Yun-hong;LI Jiao-jie;ZHANG Ying(College of Biosystems Engineering and Food Science,Zhejiang Key Laboratory for Agro-Food Processing,Zhejiang Engineering Center for Food Technology and Equipment,Zhejiang University,Hangzhou 310058,China;School of Biological and Chemical Engineering/School of Light Industry,Zhefiang University of Science and Technology,Zhejiang Provincial Key Laboratory of Chemical and Biological Processing Technology of Farm Products,Zhejiang Provincial Collaborative Innovation Center of Agricultural Biological Resources Biochemical Manufacturing,Hangzhou 310023,China;Aviation Medicine Training Center of Hangzhou,Hangzhou 310007,China)
机构地区:[1]浙江大学生物系统工程与食品科学学院、浙江省农产品加工技术研究重点实验室、浙江省食品加工技术与装备工程研究中心,杭州310058 [2]浙江科技学院生物与化学工程学院/轻工学院,浙江省农产品化学与生物加工技术重点试验室,浙江省农业生物资源生化制造协同创新中心,杭州310023 [3]空军杭州航空医学鉴定训练中心,杭州310007
出 处:《中国药学杂志》2018年第17期1463-1469,共7页Chinese Pharmaceutical Journal
基 金:国家自然科学基金面上项目资助(31371754)
摘 要:目的采用动物试验研究对香豆酸(p-coumaric acid,p-CA)对急性缺氧性肺水肿的预防作用。方法建立急性缺氧小鼠模型,以红景天苷为阳性对照,连续灌胃给药7 d,通过检测急性缺氧处理后小鼠肺组织的含水量、炎症因子、抗氧化酶活性和Na^+,K^+-ATP酶活力,观察苏木素伊红(hematoxylin-eosin,HE)染色切片结果,对p-CA预防急性缺氧性肺水肿的效果及其可能的作用机制进行研究。结果与正常组相比,急性缺氧(9.5%O_2)6 h使小鼠肺组织含水量显著增加了3.56%(P<0.01),而25和100 mg·kg^(-1)·d^(-1)剂量的p-CA均能有效抑制其升高趋势(P<0.05),与红景天苷的效果相当。其作用机制可能与p-CA提高小鼠肺组织Na^+,K^+-ATP酶活力与抗氧化能力[超氧化物歧化酶(SOD)升高、过氧化氢酶(CAT)升高和丙二醛(MDA)下降]及降低炎症因子[白细胞介素(IL)-1β和IL-6]水平有关。结论p-CA对急性缺氧导致的肺水肿具有较好的预防作用。OBJECTIVE To study the preventing effects of p-coumaric acid(p-CA) on acute hypoxia-induced pulmonary edema by mice experiments. METHODS Acute-hypoxia model was established using a normobaric hypoxia chamber in vivo. Salidroside was set as a positive control drug. And the test period was 7 d using a method of intragastric administration. The measurements including pulmonary water content, HE staining, inflammatory factors, anti-oxidative indexes and Na+ , K + -ATPase were performed to determine the efficacies and mechanisms of p-CA on preventive against acute hypoxia-induced pulmonary edema. RESULTS As compared with the normal group, pulmonary water contents increased significantly by 3.56% in the mice treated with acute hypoxia (9.5% 02) for 6 h ( control group) ( P 〈 0.01 ), and administration with p-CA (25, 100 mg· kg-1 d-l ) for 7 d could significantly reduce this index (P 〈 0.05) , which was as effective as the positive group. The action mecha- nisms of p-CA could be due to its abilities of improving the activity of Na + , K +-ATPase, enhancing antioxidant capacity (SOD ↑ , CAT ↑ and MDA ↓, ) and inhibiting inflammatory factors ( IL-1 β and IL-6). CONCLUSION p-CA has greater preventive effects on acute hypoxia-induced pulmonary edema in mice.
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