Cordycepin alleviates endometrial hyperplasia in rats via alteration of PTEN/PI3K/Akt axis

This is the authors' abstract. We don't add key points for this paper.

• Cordycepin from Cordyceps militaris reduces endometrial hyperplasia by decreasing uterine lining thickness. • Cordycepin lowers proliferation markers Ki-67 and PCNA, showing reduced cell proliferation in the uterus. • Cordycepin demonstrates antioxidant capabilities through the reduction of lipid peroxidation and the improvement of catalase and superoxide dismutase activities. • Cordycepin exhibits immunomodulatory properties by reducing inflammatory markers IL-6 and NF-κB in uterine tissues. • Cordycepin modulates PTEN/PI3K/Akt pathway, offering potential as a non-invasive treatment for endometrial hyperplasia. Endometrial hyperplasia (EH) is a reproductive health concern distinguished by unusual thickening of the uterine lining. Cordycepin (COR) is a bioactive substance with favorable antioxidant and anti-inflammatory properties. This study sought to explore the therapeutic benefits of COR in an estradiol (E2) induced EH. Thirty female Wistar rats were allocated into five groups and treated with different interventions, including COR, E2, or their combinations. The outcomes demonstrated a significant decrease in endometrial thickening and reduced expressions of the proliferation markers, antigen Kiel 67 (Ki-67) and proliferating cell nuclear antigen (PCNA), in the uterine tissue with COR treatment. COR showcased antioxidant properties, and downregulated key proteins involved in inflammation, including interleukin 6 (IL-6) and nuclear factor kappa B (NF-κB) in uterine tissues. Further analysis revealed that COR increased phosphatase and tensin homologue (PTEN) expression and down-regulated phosphorylated AKT serine/threonine kinase 1 (p-Akt) and phosphoinositide 3-kinase (PI3K) expressions. Overall, COR holds promise as a non-invasive treatment for EH, exerting its protective effects by enhancing antioxidant defenses, reducing inflammation, and modulating the PTEN/PI3K/Akt axis.