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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/30934

    標題: 17-Estradiol Accelerated Renal Tubule Regeneration in Male Rats After Ischemia/Reperfusion-Induced Acute Kidney Injury
    作者: Wu, Chia-Chun
    Chang, Chia-Yu
    Chang, Sheng-Tsung
    Chen, Sheng-Hsien
    貢獻者: Chi Mei Med Ctr, Dept Nephrol
    Chia Nan Univ Pharm & Sci, Dept Pharm
    Chi Mei Med Ctr, Dept Neurol
    Chi Mei Med Ctr, Dept Pathol
    Da An Women & Childrens Hosp
    Southern Taiwan Univ Sci & Technol, Dept Biotechnol
    關鍵字: Acute tubular necrosis
    cell dedifferentiation
    renal proximal tubule
    日期: 2016-08
    上傳時間: 2018-01-18 11:38:14 (UTC+8)
    出版者: Lippincott Williams & Wilkins
    摘要: Ischemic/reperfusion injury (IRI) is the most common cause of acute kidney injury (AKI). Murine studies report that pretreatment with 17-estradiol protects against AKI using multiple mechanisms, but how 17-estradiol is involved in regenerating tubular cells is unknown. To visualize the kidney injury and repair, we used 17-estradiol to treat rats with postischemic acute kidney injury. AKI was induced by clamping the renal pedicle for 90 minutes 2 weeks after a unilateral nephrectomy. Rats were treated with an intravenous injection of 17-estradiol or vehicle immediately after reperfusion. Kidney injury was assessed by measuring biochemical and histopathological changes. Immunohistochemical staining of vimentin, proliferating cell nuclear antigen (PCNA), and E-cadherin were used to assess dedifferentiation, proliferation, and redifferentiation. Rats treated with 17-estradiol had less kidney injury than did vehicle-treated rats post-IRI day 1. The number of PCNA-positive (PCNA(Pos)) cells was significantly higher in post-IRI kidneys on day 1 in 17-estradiol-treated rats. Moreover, vimentin(Pos) and E-cadherin(Pos) cells, which were interpreted as regeneration markers, were expressed earlier and significantly more copiously in 17-estradiol-treated rats. We hypothesize that 17-estradiol attenuates IRI-induced AKI by reducing inflammation and accelerating injured tubular cell regeneration.
    關聯: Shock, v.46 n.2, pp.158-163
    Appears in Collections:[藥學系(所)] 期刊論文

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