Ischemic/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.
No takes yet. Share an insight, caveat, or question.
Wu et al. (2016) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: