• Chia-Chun Wu, Chia-Yu Chang, Sheng-Tsung Chang, and Sheng-Hsien Chen.
• *Department of Nephrology, Chi Mei Medical Center, Tainan, Taiwan †Department of Pharmacy, Chia Nan University of Pharmacy and Science, Tainan, Taiwan ‡Department of Neurology, Chi Mei Medical Center, Tainan, Taiwan §Department of Pathology, Chi Mei Medical Center, Tainan, Taiwan ||Da-An Women and Children's Hospital, Tainan, Taiwan ¶Department of Biotechnology, Southern Taiwan University of Science and Technology, Tainan, Taiwan.
• Shock. 2016 Aug 1; 46 (2): 158-63.

AbstractIschemic/reperfusion injury (IRI) is the most common cause of acute kidney injury (AKI). Murine studies report that pretreatment with 17β-estradiol protects against AKI using multiple mechanisms, but how 17β-estradiol is involved in regenerating tubular cells is unknown. To visualize the kidney injury and repair, we used 17β-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 17β-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 17β-estradiol had less kidney injury than did vehicle-treated rats post-IRI day 1. The number of PCNA-positive (PCNA) cells was significantly higher in post-IRI kidneys on day 1 in 17β-estradiol-treated rats. Moreover, vimentin and E-cadherin cells, which were interpreted as regeneration markers, were expressed earlier and significantly more copiously in 17β-estradiol-treated rats. We hypothesize that 17β-estradiol attenuates IRI-induced AKI by reducing inflammation and accelerating injured tubular cell regeneration.

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