PurposeTo investigate whether autologous platelet-rich plasma (PRP) treatment can improve regeneration of the endometrium in an experimental model of ethanol-induced damage.Materials and MethodsSixty female Sprague-Dawley rats were randomly assigned into three groups: control group, ethanol group, and PRP-treated group (administration of 0.25 mL of PRP into both uterine cavities 72 hours after ethanol injection). After 15 days of endometrial damage, all the animals were sacrificed during the estrous cycle, and samples were taken from the mid-uterine horn. Functional and structural recovery of the endometrium was analyzed by hematoxylin-eosin (H&E) and Masson trichrome (MT) staining, real-time polymerase chain reaction (PCR) assay, and immuno-histochemical (IHC) analyses.ResultsH&E and MT staining confirmed significantly decreased fibrosis and increased cellular proliferation in the PRP-treated group, compared to the ethanol group. The endometrial areas in the ethanol and PRP-treated groups were 212.83±15.84 µm2 and 262.34±12.33 µm2 (p=0.065). Significantly stronger IHC expression of cytokeratin, homeobox A10 (HOXA10), vascular endothelial growth factor (VEGF), and Ki-67 was found in the PRP-treated group, compared to the ethanol group. In real-time PCR analyses, interleukin-1β mRNA was down-regulated, while c-Kit mRNA was up-regulated, in the PRP-treated group, compared to the ethanol group.ConclusionIntrauterine administration of autologous PRP stimulated and accelerated regeneration of the endometrium and also decreased fibrosis in a murine model of damaged endometrium.

Background: IL-4 can directly inhibit growth of several tumor cell types, but the molecular mechanism is not known. Results: IL-4 induces senescence by increasing p21 WAF1/CIP1 expression through STAT6 and p38 MAPK. Conclusion: STAT6 and p38 MAPK play important roles in senescence induction by IL-4. Significance: This is the first report of cellular senescence induction by IL-4 and the responsible mechanism.

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