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Apigenin, a common dietary flavonoid abundantly present in a variety of fruits and vegetables, has promising anticancer properties. As an effector of apigenin in myoblasts, protein arginine methyltransferase 7 ( Prmt7 ) is required for male germ cell development. However, whether apigenin may influence male reproductive health through  Prmt7  is still unclear. To this end, mouse spermatogonia were treated with different concentrations (2.5 to 50 μM) of apigenin for 48 h, which showed that apigenin could cause reduced cell proliferation in conjunction with longer S phase and G2/M phase (with concentrations of 10 and 20 μM, respectively), and increased apoptosis of spermatogonia (with concentration of 20 μM). Reduced  Prmt7  expression was found in 20 μM apigenin-treated spermatogonia. Moreover, siRNA-induced  Prmt7  knockdown exhibited similar influence on spermatogonia as that of apigenin treatment. In mechanistic terms, transcriptome analysis revealed 287 differentially expressed genes between  Prmt7 -downregulated and control spermatogonia. Furthermore, rescue experiments suggested that the effects of apigenin on spermatogonia might be mediated through the  Prmt7 / Akt3  pathway. Overall, our study supports that apigenin can interfere with mouse spermatogonial proliferation by way of the downregulated  Prmt7 / Akt3  pathway, which demonstrates that the concentration should be taken into account in future applications of apigenin for cancer therapy of men.

The Effects of Flavonoid Apigenin on Male Reproductive Health: Inhibition of Spermatogonial Proliferation through Downregulation of Prmt7/Akt3 Pathway