<dfn id="w48us"></dfn><ul id="w48us"></ul>
  • <ul id="w48us"></ul>
  • <del id="w48us"></del>
    <ul id="w48us"></ul>
  • 重癥急性胰腺炎大鼠DDFA對肺損傷細胞凋亡及Bax, Bcl

    時間:2024-07-26 14:46:54 藥學畢業(yè)論文 我要投稿
    • 相關推薦

    重癥急性胰腺炎大鼠DDFA對肺損傷細胞凋亡及Bax, Bcl

    作者:史學深,方馳華,朱明德,何鄒駿,陳鐵軍

    【關鍵詞】 危重病;急性;胰腺炎;肺/損傷;細胞凋亡;DDFA
    【Abstract】 AIM: To explore the effects of DDFA on cell apoptosis and expressions of Bax and Bcl2 in lung tissue of rats with severe acute pancreatitis(SAP). METHODS: 45 rats weighting 200250 g were randomized into 3 groups: control group (n=15), SAP group (n=15) and DDFA group (n=15). The models of SAP were established by the injection of 200 g/L arginine solution ip(once a hour for 2 h) into the rats. At the 24, 48 and 72 h after establishment of models, serum amylase, TNFa and calcium were determined. The left lungs were taken for light and electron microscopic observation. Cell apoptosis in lung tissue was determined by TUNEL method. Expressions of Bax and Bcl2 were detected by immunohistochemical staining of SABC. RESULTS: In the SAP group, serum amylase, TNFa, apoptotic index, expressions of Bax and Bcl2 markedly increased. Lung tissue injuries were significant under a light microscope. As compared with SAP group at the same phase, serum amylase, TNFa, apoptotic index and expressions of Bax in DDFA group decreased significantly. While the expression of Bcl2 increased significantly. The injury of lung tissue was relieved by DDFA. CONCLUSION: The apoptosis and the expressions of Bax and Bcl2 in lung tissue might be involved in pathogenesis of SAP. DDFA administration in the early stage is helpful for diminishing lung injury induced by SAP.
    【Keywords】 critical illness; acute disease; pancreatitis; lung/injuries; apoptosis; DDFA
    【摘要】 目的: 探討DDFA對重癥急性胰腺炎(SAP)大鼠肺組織內細胞凋亡及Bax,Bcl2基因表達的影響. 方法: 大鼠45只隨機分為對照組(CG), SAP組和DDFA治療組,每組15只. 大鼠SAP模型采用分2次ip 200 g/L精氨酸溶液方法建立,建模后24, 48和72 h時測定血清TNFa,淀粉酶. 血鈣及光鏡觀察肺組織病理變化,細胞凋亡原位檢測(TUNEL)法測定肺組織內細胞凋亡,SABC免疫組化染色法測定肺組織Bax, Bcl2基因表達. 結果: SAP組血清淀粉酶, TNFa和肺組織內細胞凋亡指數, Bax, Bcl2基因表達較CG組升高,光鏡下見肺組織損害明顯;經DDFA治療后,血清淀粉酶, TNFa和肺組織內細胞凋亡指數, Bax基因表達下降,而Bcl2基因表達增強,光鏡下見肺組織損害減輕. 結論: 肺組織細胞凋亡, Bax, Bcl2基因表達參與SAP發(fā)病機制,在SAP早期給予DDFA治療對減輕肺臟損害是有益的.
    【關鍵詞】 危重病;急性。灰认傺;肺/損傷;細胞凋亡;DDFA
    0引言
    重癥急性胰腺炎(severe acute pancreatitis, SAP)常并發(fā)多器官功能障礙,其胰外器官損傷中肺損傷最為常見,稱之為: 急性胰腺炎相關性肺損傷[1],其發(fā)病機制尚不完全清楚. 1997年方馳華等[2]應用DDFA方案(D: dexamethasone; D: dextran; F: 5Fluorouracil; A: Appotininum)治療SAP取得明顯效果. 我們利用SAP肺臟損害大鼠模型,探討細胞凋亡和Bax, Bcl2基因表達在SAP肺臟損害發(fā)病機制中的作用以及應用DDFA治療后的影響.
    1材料和方法
    1.1材料SD大鼠45只,雌雄不限,體質量2

    【重癥急性胰腺炎大鼠DDFA對肺損傷細胞凋亡及Bax, Bcl】相關文章:

    急性重癥胰腺炎非手術治療的護理體會03-02

    重癥急性胰腺炎胃腸動力障礙的研究進展03-08

    血必凈對大鼠急性胰腺炎保護作用機制探討03-18

    重癥急性胰腺炎并發(fā)急性呼吸窘迫綜合征臨床研究03-19

    淺析早期腸內營養(yǎng)治療重癥急性胰腺炎的護理03-18

    矽肺模型大鼠肺間質成纖維細胞MMP03-02

    論Nogo受體拮抗劑對大鼠急性脊髓損傷的保護作用03-26

    探討梗阻性黃疸大鼠外周血中性粒細胞凋亡的改變12-06

    談連續(xù)性血液凈化在治療重癥急性胰腺炎中的應用03-28

    白三烯受體拮抗劑及急性肺損傷中的炎性因子11-23

    主站蜘蛛池模板: 国内精品伊人久久久久| 国产精品哟女在线观看| 北条麻妃国产九九九精品视频| 亚洲综合国产精品第一页 | 欧美国产成人精品一区二区三区 | 99久久免费国产精精品| 亚洲精品成人网久久久久久| 北岛玲日韩精品一区二区三区| freesexvideos精品老师毛多| 在线观看自拍少妇精品| 精品综合久久久久久88小说| 老司机99精品99| 500av导航大全精品| 色偷偷88888欧美精品久久久| 毛片a精品**国产| 国产精品你懂的在线播放| 精品综合久久久久久97超人| 国产精品无码一区二区三级| 无码人妻精品一区二区三区久久| 日韩精品无码人妻一区二区三区| 国产va免费精品| 久久福利青草精品资源站免费| 国产精品丝袜黑色高跟鞋| 色欲国产麻豆一精品一AV一免费 | 国产精品污视频| 99精品国产在热久久无毒不卡| 久久精品国产亚洲av影院| 亚洲精品二区国产综合野狼| 亚洲精品二三区| 日韩精品成人亚洲专区| 久久国产精品免费一区| 国产亚洲精品精品国产亚洲综合| 国产精品龙口护士门在线观看| 亚洲精品电影网| 亚洲欧美日韩精品久久| 99久久99久久精品国产| 97久视频精品视频在线老司机| 91av国产精品| 国产精品无码不卡一区二区三区| 国产精品 日韩欧美| 国产精品免费久久|