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作 者:段斐[1] 耿德海[2] 许文杰[1] 唐志远[1] 史建红[1]
机构地区:[1]河北大学医学部,河北保定071000 [2]河北省保定市第四医院,071051
出 处:《时珍国医国药》2008年第5期1054-1055,共2页Lishizhen Medicine and Materia Medica Research
基 金:河北省科技攻关课题(No.20042761459);河北省保定市科技局资助课题〔No.04F001(4)〕
摘 要:目的通过观察细胞凋亡,探讨复方鳖甲软肝方防治肺纤维化的机理和疗效。方法选SD雄性大鼠180只,随机分为假手术组,模型组,阳性药物对照组,复方鳖甲软肝方高、中、低剂量组,共6组,每组30只。博莱霉素常规造模的同时给药,假手术组和模型组每天灌胃生理盐水,其余4组灌药进行防治。各组分别于7,14,28 d随机抽取10只大鼠,8只制成光镜标本,2只麻醉后快速开胸取肺组织,进行电镜标本的制作。免疫组化载玻片用DEPC处理后备用。结果Ⅰ型和Ⅱ型肺泡上皮细胞以及成纤维细胞均有凋亡。bax在肺泡Ⅰ型和Ⅱ型上皮细胞,肺泡巨嗜细胞胞质和胞膜均表达。假手术组和高、中剂量组呈弱阳性表达,模型组强阳性表达。Bc l-2在核膜和线粒体表达,模型组强阳性表达,药物组弱表达。结论复方鳖甲软肝方通过调节细胞凋亡,上调Bax活性,抑制Bc l-2的活性,抑制Ⅱ型上皮细胞凋亡,减少纤维积聚和纤维化形成,对肺纤维化起到防治作用。Objective To study the preventive and therapeutic effect of compound prescription with turtle shell (CPTS) on rats with IPF (Idiopathic pulmonary interstitial fibrosis) caused by Bleomycin AS. Methods 180 SD rats were randomly divided into six groups : sham operation group, model group, positive medicine group, high - dosage group, medium - dosage group and low - medium group. After they were given the medicine, ten rats in each group each time were killed respectively on the 7th,14th and 28th day. 8 of them were made for light microscope specimen. 2 rats were operated to open thorax and get lung tissue speedily. Immunohistochemical glass covers were dealt with DEPC for use. Results AT Ⅰ , AT Ⅱ and fibroblast all showed apoptosis, Bax expression in AT Ⅰ , AT Ⅱ and alveolus macrophage cytoplasm, cytolemma expression was less positive in sham operation group, high CPTS and medium CPTS groups and remarkably positive in model group, which showed CPTS could restrain apoptosis of AT and macrophage. Bcl -2 was expressed in chondriosome and on karyotheca. Expression in model group was less positive and remarkably positive in CPTS groups, which showed CPTS could restrain formation of IPF. Conclusion CPTS has obvious treating effect through reducing fiber piling and restraining forming of fbrosis on rats with IPF caused by Bleomyein AS, CPTS can regulate the alveolar apoptosis by inhibiting the Bcl -2 expression, enhancing the Bax expression and inhibiting the apoptosis of AT Ⅱ .
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