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自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =Autoph...

吳怡萱

自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model /

Record Type:	Language materials, printed : Monograph/item
Title/Author:	自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =/ 吳怡萱
Reminder of title:	Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model /
remainder title:	Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model
Author:	吳怡萱
Published:	[高雄市]: [撰者], : 民110,
Description:	66葉 :圖 ; : 30公分;
Notes:	指導教授: 阮雍順.
基督教聖經之智慧書導讀 :	推論自噬作用可能透過調控血管新生及發炎反應，影響K它命膀胱炎之修復及功能改善。建立K它命膀胱炎的動物疾病模式，分別給予雷帕黴素(Rapamycin)及渥曼青黴素(Wortmannin，磷酸肌醇-3激酶抑制劑)，總共將大鼠隨機分做四組: (1)對照組 (2) K它命組 (3) K它命+ 雷帕黴素 (4) K它命 + 渥曼青黴素。檢測大鼠膀胱功能、膀胱逼尿肌收縮活動、自噬小體及自噬溶酶體分佈、白血球總數及白血球分類、自噬作用相關蛋白質表現、血管新生相關生物標記及訊息傳導路徑。實驗結果發現 K它命膀胱炎之大鼠有明顯的逼尿肌過動，呈現間質纖維化及內皮細胞受損，嗜酸性發炎反應，粒線體及胞器腫脹及降解，並抑制血管生成作用及磷酸化蛋白質激酶。雷帕黴素治療會抑制血管生成，移除K它命代謝物，減緩嗜酸性發炎反應，減輕膀胱過動，改善膀胱功能; 渥曼青黴素治療會減緩嗜鹼性發炎反應，透過增加微血管密度及血管內皮生長因子表現改善膀胱血管生成作用。推論自噬作用改善K它命膀胱炎的膀胱功能可能是透過調節發炎反應及血管生成作用。.
Online resource:	電子資源
[NT 15000934]:	(平裝)

自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model /
吳怡萱

自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model /Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model吳怡萱 - [高雄市]: [撰者], 民110 - 66葉 :圖 ;30公分

指導教授: 阮雍順.

碩士論文--高雄醫學大學臨床醫學研究所.

參考書目：葉.

中文摘要 2

推論自噬作用可能透過調控血管新生及發炎反應，影響K它命膀胱炎之修復及功能改善。建立K它命膀胱炎的動物疾病模式，分別給予雷帕黴素(Rapamycin)及渥曼青黴素(Wortmannin，磷酸肌醇-3激酶抑制劑)，總共將大鼠隨機分做四組: (1)對照組 (2) K它命組 (3) K它命+ 雷帕黴素 (4) K它命 + 渥曼青黴素。檢測大鼠膀胱功能、膀胱逼尿肌收縮活動、自噬小體及自噬溶酶體分佈、白血球總數及白血球分類、自噬作用相關蛋白質表現、血管新生相關生物標記及訊息傳導路徑。實驗結果發現 K它命膀胱炎之大鼠有明顯的逼尿肌過動，呈現間質纖維化及內皮細胞受損，嗜酸性發炎反應，粒線體及胞器腫脹及降解，並抑制血管生成作用及磷酸化蛋白質激酶。雷帕黴素治療會抑制血管生成，移除K它命代謝物，減緩嗜酸性發炎反應，減輕膀胱過動，改善膀胱功能; 渥曼青黴素治療會減緩嗜鹼性發炎反應，透過增加微血管密度及血管內皮生長因子表現改善膀胱血管生成作用。推論自噬作用改善K它命膀胱炎的膀胱功能可能是透過調節發炎反應及血管生成作用。.

(平裝)Subjects--Index Terms:

自噬作用

自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 =Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model /
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100 1 $a 吳怡萱 $3 454628
245 1 0 $a 自噬作用影響K它命膀胱炎之血管新生作用且改善其膀胱過動症 = $b Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model / $c 吳怡萱
246 1 1 $a Autophagy alters bladder angiogenesis and improves bladder hyperactivity in the pathogenesis of ketamine-induced cystitis in a rat model
260 # $a [高雄市]: $b [撰者], $c 民110
300 $a 66葉 : $b 圖 ; $c 30公分
500 $a 指導教授: 阮雍順.
500 $a 學年度: 109.
502 $a 碩士論文--高雄醫學大學臨床醫學研究所.
504 $a 參考書目：葉.
505 0 # $a 中文摘要 2
520 3 $a 推論自噬作用可能透過調控血管新生及發炎反應，影響K它命膀胱炎之修復及功能改善。建立K它命膀胱炎的動物疾病模式，分別給予雷帕黴素(Rapamycin)及渥曼青黴素(Wortmannin，磷酸肌醇-3激酶抑制劑)，總共將大鼠隨機分做四組: (1)對照組 (2) K它命組 (3) K它命+ 雷帕黴素 (4) K它命 + 渥曼青黴素。檢測大鼠膀胱功能、膀胱逼尿肌收縮活動、自噬小體及自噬溶酶體分佈、白血球總數及白血球分類、自噬作用相關蛋白質表現、血管新生相關生物標記及訊息傳導路徑。實驗結果發現 K它命膀胱炎之大鼠有明顯的逼尿肌過動，呈現間質纖維化及內皮細胞受損，嗜酸性發炎反應，粒線體及胞器腫脹及降解，並抑制血管生成作用及磷酸化蛋白質激酶。雷帕黴素治療會抑制血管生成，移除K它命代謝物，減緩嗜酸性發炎反應，減輕膀胱過動，改善膀胱功能; 渥曼青黴素治療會減緩嗜鹼性發炎反應，透過增加微血管密度及血管內皮生長因子表現改善膀胱血管生成作用。推論自噬作用改善K它命膀胱炎的膀胱功能可能是透過調節發炎反應及血管生成作用。.
520 3 $a Background: The present study attempted to elucidate whether autophagy alters bladder angiogenesis, decreases inﬂammatory response and ameliorates bladder hyperactivity, influencing bladder function in ketamine-induced cystitis (KIC). Methods: Female Sprague-Dawley (S-D) rats were randomly divided into the control group, the ketamine group, the ketamine + rapamycin group, and the ketamine + wortmannin group. The bladder function, contractile activity of detrusor smooth muscle, distribution of autophagosome and autolysosome, total white blood cells (WBCs) and leukocyte differential counts, the expressions of autophagy-associated protein, angiogenesis markers and signaling pathway molecules involved in KIC were tested, respectively. Results: The data revealed that treatment with ketamine significantly resulted in bladder overactivity, enhanced interstitial fibrosis, impaired endothelium, induced eosinophil-mediated inflammation, swelling and degraded mitochondria and organelles, inhibited angiogenesis and elevated the phosphorylation of Akt. But, treatment with rapamycin caused an inhibitory effect on vascular formation, removed ketamine metabolites, decreased the eosinophil-mediated inﬂammation and ameliorated bladder hyperactivity, leading to improving bladder function in KIC. However, wortmannin treatment reduced basophil-mediated inﬂammatory response, improved bladder angiogenesis by increasing capillary density and VEGF expression, to reverse anti-angiogenic effect to repair KIC. Conclusions: These findings suggested that autophagy could modulate inflammatory responses and angiogenesis, which improve bladder function in KIC..
563 $a (平裝)
653 # # $a 自噬作用 $a K它命膀胱.
653 # # $a Autophagy $a Ketamine-induced cystitis.
856 7 # $u https://handle.ncl.edu.tw/11296/g9tgrg $z 電子資源 $2 http