ArticleNaunyn-Schmiedeberg's archives of pharmacology2025
Piperazine ferulate impact on diabetes-induced testicular dysfunction: unveiling genetic insights, MAPK/ERK/JNK pathways, and TGF-β signaling.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The hepatoprotective role of piperazine ferulate against cisplatin-induced hepatotoxicity in rats: insights into the Keap1/Nrf-2/HO-1 signaling and inflammatory pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Mechanism of the traditional Chinese medicine SMBJ alleviates diabetes mellitus-induced Leydig cell dysfunction in rats testes.Scientific reports · 2025Article
- Understanding the impact of streptozotocin on diabetic male infertility: perspectives from rodent models and pharmacological networking.BMC pharmacology & toxicology · 2025Review
- Diabetic testicular dysfunction and spermatogenesis impairment: mechanisms and therapeutic prospects.Frontiers in endocrinology · 2025Review
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Authors and funding
6 authors.
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Abstract
Diabetic testicular dysfunction (DTD) poses a significant threat to male reproductive health. This study delves into the potential of piperazine ferulate (PF), a natural phenolic compound, in alleviating DTD and sheds light on its underlying mechanisms in rats. Animals were divided into the control, PF, diabetic, and diabetic plus PF groups. Diabetes was induced in rats with a single intraperitoneal (i.p.) injection of streptozotocin (STZ) at 50 mg/kg. PF was administered at 50 mg/kg/day via i.p. injection for four weeks. Significant changes in sexual behavior were observed in diabetic rats, which additionally revealed lower serum levels of testosterone, FSH, and LH. The abnormalities in sperm count, viability, motility, and morphology occurred along with the demonstrated suppression of genes and protein expression related to spermatogenesis. Atrophy of the seminiferous tubules and extensive degeneration and necrosis of the germ and Leydig cells were highlighted by histopathological examination. The testicular function of diabetic rats was significantly improved after PF administration, evidenced by normalized testicular histology, increased testosterone levels, and enhanced sperm quality. In addition to reducing inflammatory cytokines, COX2, and NF-κB expression, pf administration elevated the antioxidant levels and Nrf2/HO-1 expression. Furthermore, key signaling pathways involved in testicular degeneration are regulated by PF. It promoted cell survival and tissue repair by activating the protective TGF-β signaling pathway and attenuating the MAPK/ERK/JNK signaling cascade, which in turn reduced inflammation and apoptosis. PF suppressed the expression of INSL3, SPHK1, CD62E, ANGPTL2, and miR-148a-5p, while increasing the expression of testicular genes like HSD17B1, DAZL, and S1P, addressing DTD. This study highlights the potential of PF to restore testicular function and fertility in diabetic males by modulating genetic and signaling pathways.
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