Echinacoside Protects Against Dysfunction of Spermatogenesis Through the MAPK Signaling Pathway

Abstract

AbstractDysfunction at various levels of spermatogenesis (SD) is one of the important causes of infertility in men of reproductive age and requires advanced treatment strategies. Increasing evidence suggests that the therapeutic effects of echinacoside (ECH) mainly depend on their capacity to inhibit cell death. This study aimed to explore the therapeutic potential of ECH in SD rat models. Treatment with ECH reverted the morphological changes observed in testes with spermatogenesis dysfunction. It improved total sperm number, decreased the sperm deformity rate, and increased the sperm forward motility rate. The level of glutathione (GSH) was significantly higher in ECH-treated mice, whereas the lactate dehydrogenase (LDH) and SOD activities were improved compared with those in the spermatogenesis dysfunction model. Moreover, the increased expression of p38 and JNK was partially reversed by ECH. The number of normal TM3 cells increased gradually in an Echinacea dosage-dependent manner, suggesting that ECH promoted the proliferation of TM3 cells. In addition, treatment with ECH partially reversed the increased expression of p38 and JNK in TM3 cells. ECH protects against oxidative stress damage by activating antioxidant enzymes and MAPK signaling-related factors (p38 and JNK). It suggested that treatment with ECH alleviated spermatogenetic dysfunction of testes in male mice and it could be a promising strategy for patients suffering severe SD.