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Sertoli cells play crucial roles in spermatogenesis and are impaired by aging. Icariin, a flavonoid from Epimedium , has been reported to exhibit anti-aging effects and improve testicular dysfunction in the clinical setting. However, whether icariin improves age-related degeneration of testicular function via protection from Sertoli cell injury remains unclear. In the present study, we evaluated the protective effect of icariin on Sertoli cell injury and explored the possible mechanism(s) in vivo and in vitro. Dietary administration of icariin for 4 months significantly ameliorated the age-related decline in testicular function by increasing testicular and epididymal weights and indices, sperm count and sperm viability, testicular testosterone and estradiol concentrations, and seminiferous tubule diameters and heights. In addition, icariin protected age-related Sertoli cells from injury as evidenced by an analysis of Sertoli cell number, ultrastructure, and function. Such changes were accompanied by upregulation of ER α and Nrf2 signaling in Sertoli cells. Parallel in vitro studies also demonstrated that icariin inhibited untoward effects on the TM4 mouse Sertoli cell line with concomitant upregulation of ER α and Nrf2 signaling. Conversely, ER α siRNA reversed icariin-mediated protection of Sertoli cell injury. Our data suggest that icariin effectively ameliorates age-related degeneration of testicular function by alleviating Sertoli cell injury via the ER α /Nrf2 signal-transduction pathway. Thus, mitigating Sertoli cell damage via the ER α /Nrf2 signaling pathway likely represents a promising strategy for the prevention of age-related testicular dysfunction. [ABSTRACT FROM AUTHOR]

Objective: Lower genital tract microbiome dysbiosis has been associated with several gynecological diseases. However, the differences in microbiome composition among patients with several gynecological diseases, such as endometrial polyps and uterine myoma, are poorly understood. Studying the lower genital tract microbiome composition in patients with benign gynecological diseases could provide new insights for interpreting the complex interplay between the microbiome and pathogenesis and finding new targets for preventive measures., Methods: A total of 16 patients with endometrial polyps (EPs), 11 patients with uterine myoma (UM), 6 patients with ovarian cysts (OC) and 36 healthy women (HWs) were recruited for this study. Samples were obtained from vaginal secretions. The DNA was isolated from the samples, and the V3-V4 regions were amplified. The sequencing libraries were generated and sequenced on an Illumina NovaSeq 6000 platform., Results: Firmicutes, Actinobacteria and Bacteroidota were the most common phyla in all four groups, whereas OC presented the highest abundance of Firmicutes and the lowest abundance of Bacteroidota. At the genus level, Lactobacillus in the OC group was significantly greater than that in the HW group, and Atopobium in the UM group was significantly lower than that in the HW group. The abundance of Gardnerella was greater in the UM group than in the EP group, and the abundance of Streptococcus was greater in the EP group. The richness and evenness of the microbiome were generally consistent among the HW, EP, UM, and OC groups. Principal component analysis (PCA), principal coordinate analysis (PCoA) and nonmetric multidimensional scaling (NMDS) revealed no distinct separation trends among the four groups. According to ANOSIM, there was no significant difference in community structure among the four groups., Conclusions: A nonsignificant result was obtained from the microbiome diversity comparison among the different groups. However, we demonstrated that the OC group had a greater abundance of Lactobacillus and that the UM group had a lower abundance of Atopobium, which might contribute to the occurrence of diseases, providing new clues for preventive measures., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2025 Shi, Li, Xie, Yang, Ma, Chen and Guo.)

Objective To establish a model of decline in secretion of senescent TM4 cells in vitro induced by D-galactose (D-gal). Methods Different concentrations of D-Gal (25, 50, 100, 150, 200 and 250 mmol/L) were used to induce TM4 cell senescence. The viability of TM4 cells was detected by MTT assay. The cell cycle was analyzed by flow cytometry. The cell morphology was observed by light microscopy and the percentage of senescent cells was observed by senescence-associated β-galactosidase (SA-β-Gal) staining. The mRNA expression levels of P21, P16, glial-derived neurotrophic factor (GDNF) and stem cell factor (SCF) were detected by reverse transcription PCR. The protein expression levels of GDNF, SCF, nuclear factor erythroid 2 like 2 (NRF2), NAD(P)H dehydrogenase [quinone] 1 (NQO-1) and heme oxygenase-1 (HO-1) were detected by Western blot analysis. Results Compared with normal control group, D-Gal stimulation significantly decreased the cell viability in a concentration-dependent manner. The arrest of D-Gal-treated cells in G1 phase of cell cycle significantly increased, while it significantly decreased in S phase, and D-Gal induced cell cycle arrest at G0/G1 phase in TM4 cells. The percentages of SA-β-Gal positive cells increased significantly. The expression levels of P21 and P16 mRNAs were significantly up-regulated. The mRNA and protein levels of GDNF and SCF-1 were significantly down-regulated. Furthermore, the expression levels of oxidative stress-related protein NRF2, HO-1 and NQO-1 were significantly reduced. Conclusion The model of declined secretion function of senescent TM4 cells induced by D-Gal we established is stable and reliable. Its mechanism may be related to the down-regulation of NRF2 signaling pathway.