Silencing PDCD10 Protects the Uterus Against Ischemia/Reperfusion Injury by Inhibiting Fibrosis, Inflammation and Apoptosis in Rats

Abstract

Background: Programmed cell death 10 (PDCD10) is associated with cell apoptosis and inflammation, but its role in uterine ischemia/reperfusion injury (IRI) is unclear. The aim of this study was to evaluate the role of PDCD10 in uterine IRI in rats. Methods: A uterine IRI model was induced by using a microvascular clamp at the distal end of the abdominal aorta, followed by silencing smallinterfering (si) RNA-PDCD10 transfection. Histologic examinations including hematoxylin, eosin staining and Masson trichrome staining were performed. Enzyme-linked immunosorbent assays were used to determine the expression of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-a. The protein levels of PDCD10, Bcl-2, caspase-3, collagen 1, α-smooth muscle actin (α-SMA), fibroblast growth factor 2 (FGF2), IL-β, IL-6, and TNF-α were determined by western blot analysis. Results: The expression of PDCD10 was significantly increased in a time-dependent manner after induction of IRI, while siRNA-PDCD10 downregulated its expression. Silencing PDCD10 thickened the endometrium;thinned the myometrium;attenuated expression of collagen 1, α-SMA, and FGF2;repressed the expression of IL-1β, IL-6, and TNF-α;and suppressed apoptosis by activating Bcl-2 and inhibiting Bax and caspase-3 in the uterus following IRI. Conclusions: Silencing PDCD10 ameliorated uterine IRI through inhibition of fibrosis, inflammation and apoptosis, and may serve as a promising management tool for women with uterine IRI.