缺氧誘發的Akt2可能參與果糖飼養老鼠的良性前列腺增生
陳奕宏、唐一清1、林永明1、鄭瑞棠2
成大醫院斗六分院 外科部 泌尿科；1成大醫院 泌尿部；2奇美醫院 醫學研究部
Hypoxia induced Akt2 could Mediate Development of Benign Prostatic Hyperplasia in Fructose-fed Rats
I-Hung Chen, Yat-Ching Tong1, Yung-Ming Lin1, Juei-Tang Cheng2
Division of Urology, Department of Surgery, National Cheng Kung University Hospital Dou-Liou Branch, Yunlin, Taiwan; 1Department of Urology, National Cheng Kung University Hospital, Tainan, Taiwan; 2Department of Medical Research, Chi-Mei Medical Center, Tainan, Taiwan,
Purpose: We studied the relation between hypoxia and Akt2 in pathogenesis of benign prostatic hyperplasia (BPH) in fructose-fed rats.
Materials and Methods: Dorsolateral lobe of prostate was harvested from fructose-fed rats and normal rats. The expression of HIF-1α and AKT2 was investigated in rat prostate. Hypoxic treatment was conducted in normal rat prostate cell line (YPEN-1) and rat prostatic tumor cell line (AT3B-1) to study the level of Hif-1α and Akt2. The expression of Akt2 in both cell lines was indentified via gain and loss of Hif-1α function. Cell proliferation was explored in both cell lines under normoxia and hypoxia, as well as overexpression and knockdown of Akt2.
Results: High protein expression of HIF-1α and AKT2 was found in prostate was harvested from fructose-fed rats. Expression of Hif-1α and Akt2 were elevated in YPEN-1 and AT3B-1 under hypoxia. Expression level of Akt2 increased in YPEN-1 with overexpression of Hif-1α under normoxia. Promotion of cell proliferation developed in YPEN-1 under hypoxia, as well as overexpression of Akt2 under normoxia. Reduction of cell proliferation was identified in AT3B-1 with knockdown of Akt2 under hypoxia.
Conclusions: Hypoxia induced Akt2 could mediate development of BPH in fructose-fed rats.