17-Estradiol Accelerated Renal Tubule Regeneration in Male Rats After Ischemia/Reperfusion-Induced Acute Kidney Injury

doi:10.1097/SHK.0000000000000586

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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 estrogen renal proximal tubule vimentin failure
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
顯示於類別:	[藥學系(所)] 期刊論文

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