本文選題：霍山石斛 + 多糖　； 參考：《合肥工業(yè)大學(xué)》2017年碩士論文

【摘要】：霍山石斛是我國傳統(tǒng)的可食用中草藥,具有增強(qiáng)機(jī)體免疫、抗氧化、抗腫瘤、改善肺功能等多種生物活性。本文主要開展了霍山石斛多糖(DHP)對香煙煙霧暴露致小鼠肺部炎癥的預(yù)防機(jī)制研究。取得的主要研究結(jié)果如下:(1)DHP對香煙煙霧暴露致小鼠的表觀現(xiàn)象和指標(biāo)的影響:小鼠體重變化及臟器指數(shù)結(jié)果表明,香煙煙霧暴露可明顯減輕小鼠體重,降低食物攝入量,造成肺組織、肝臟、脾臟和腎臟的損傷;DHP可有效恢復(fù)小鼠的體重和食物攝入量,抑制臟器的損傷。(2)DHP對香煙煙霧暴露致小鼠肺部炎癥的預(yù)防分子機(jī)制:小鼠肺組織HE染色研究顯示,DHP能顯著抑制香煙煙霧誘導(dǎo)的小鼠肺組織炎癥細(xì)胞浸潤,明顯降低平均內(nèi)襯間隔和肺泡破壞指數(shù),從而減輕小鼠肺泡破壞情況;巨噬細(xì)胞CD68免疫組化表明DHP能明顯減少巨噬細(xì)胞在肺組織氣管內(nèi)的聚集。ELISA實(shí)驗(yàn)表明,DHP能顯著抑制香煙煙霧暴露致小鼠血清和肺組織中促炎因子TNF-α和IL-1β的產(chǎn)生。當(dāng)DHP劑量為400 mg/kg·day時(shí),血清TNF-α和IL-1β的水平及肺組織中TNF-α和IL-1β的含量分別比模型組減小了13.6%、35.3%、20.2%和21.8%。Western Blot分析表明,DHP能顯著抑制香煙煙霧暴露致小鼠肺損傷中炎性通路MAPK和NF-κB信號通路特征性蛋白P65、P38和JNK的磷酸化程度及IκB的降解,且呈劑量效應(yīng)關(guān)系。EMSA結(jié)果表明,DHP可有效阻斷香煙煙霧暴露致小鼠肺損傷中NF-κB和AP-1的DNA結(jié)合活性,且結(jié)合活性隨著濃度的增大而逐漸降低。綜上所述,DHP通過改善表觀現(xiàn)象,調(diào)控炎性信號通路,從而抑制炎性因子的過度分泌,抑制肺部炎癥的發(fā)生。
[Abstract]:Dendrobium huoshanense is a traditional edible Chinese herbal medicine with many biological activities, such as enhancing immunity, anti-oxidation, anti-tumor, improving lung function and so on. The preventive mechanism of DHP on lung inflammation induced by cigarette smoke exposure in mice was studied. The main results were as follows: the effects of DHP on the apparent phenomena and indexes of mice exposed to cigarette smoke: the results of body weight change and viscera index showed that cigarette smoke exposure could significantly reduce the weight and food intake of mice. DHP can effectively recover the body weight and food intake of mice caused by damage to lung tissue, liver, spleen and kidney. The molecular mechanism of inhibiting the lung inflammation induced by cigarette smoke exposure: the study of HE staining in mouse lung tissue showed that DHP could significantly inhibit the infiltration of inflammatory cells in lung tissue induced by cigarette smoke. The average lining interval and alveolar destruction index were significantly decreased, so as to alleviate the alveolar destruction in mice. CD68 of macrophages showed that DHP could significantly reduce the aggregation of macrophages in the trachea of lung tissue. Elisa showed that DHP could significantly inhibit the production of TNF- 偽 and IL-1 尾 in serum and lung tissues of mice exposed to cigarette smoke. When the dose of DHP is 400 mg/kg day, The levels of TNF- 偽 and IL-1 尾 in serum and the contents of TNF- 偽 and IL-1 尾 in lung tissue in the model group were significantly decreased by 13.6% and 35.30.2% than those in the model group, respectively. 21.8%.Western Blot analysis showed that DHP could significantly inhibit the inflammatory pathway MAPK and NF- 魏 B signaling pathway characteristic eggs in lung injury induced by cigarette smoke exposure in mice. The phosphorylation degree of P65, P38 and JNK and the degradation of I 魏 B, The results showed that DHP could effectively block the DNA binding activity of NF- 魏 B and AP-1 in mice lung injury induced by cigarette smoke exposure, and the binding activity decreased with the increase of concentration. To sum up, DHP inhibits the excessive secretion of inflammatory factors and the occurrence of pulmonary inflammation by improving the apparent phenomenon and regulating the inflammatory signaling pathway.
【學(xué)位授予單位】：合肥工業(yè)大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R285.5

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