Phoenixin Attenuates Monosodium Glutamate-Induced Testicular Toxicity in Rats: A Potential Protective Approach | ||
| Bulletin of Egyptian Society for Physiological Sciences | ||
| Volume 45, Issue 4, October 2025, Pages 502-518 PDF (1019.32 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/besps.2025.374725.1210 | ||
| Authors | ||
| islam hegab1; mayada mohamed azab* 2; heba shoeib3; asmaa mohamed3; nancy Abed El-Hady4; nesren mohamed aboadra2 | ||
| 1Department of Bio-Physiology, Ibn Sina National College for Medical Studies, Jeddah 22413, Saudi Arabia | ||
| 2Physiology Department, Faculty of Medicine, Tanta University, Egypt | ||
| 3medical biochemistry & molecular biology department, Faculty of Medicine, Tanta University, Egypt. | ||
| 4Anatomy and Embryology Department Faculty of Medicine, Tanta University | ||
| Abstract | ||
| Background: Monosodium glutamate (MSG), a widely utilized food additive, has been implicated in the provocation of testicular toxicity through oxidative stress and hormonal dysregulation. Aim: This study explores the potential role of phoenixin in ameliorating MSG-persuaded testicular toxicity. Methods: The Experimental design involved allocating male Wistar rats into four distinct groups: Control, Phoenixin, MSG, and Phoenixin+ MSG. Semen samples were analyzed for sperm count, motility, and viability. Gonadotropin-releasing hormone.(GnRH). In serum, luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and kisspeptin were quantitatively assessed. The activity of the testicular steroidogenic enzymes 3β-hydroxysteroid dehydrogenase (3β-HSD) and 17β-HSD, together with markers of testicular oxidative stress and tumor necrosis factor-alpha (TNF-α), were assessed. Additionally, the testicular levels of silent information.regulator.of/transcription.1(SIRT1), phosphorylated AMP-activated protein kinase (p-AMPK), and caspase3 immunoreactivity were estimated. Results: MSG exposure significantly impaired sperm parameters, disrupted hormonal balance, and triggered oxidative stress and inflammatory responses. Meanwhile, co-administration of phoenixin restored sperm function, improved serum GnRH, LH, FSH, testosterone, and kisspeptin levels, and enhanced testicular antioxidant defense. Moreover, phoenixin upregulated p-AMPK and SIRT1 while attenuating TNF-α expression and caspase3 immunoreactivity, elucidating its beneficial role in mitigating testicular function and steroidogenesis. Conclusion: Phoenixin effectively protected against MSG-provoked testicular toxicity through the restoration of the hypothalamic-pituitary-gonadal(HPG), enhancement of steroidogenesis, attenuation of oxidative stress, inflammation, and apoptotic cascade, which was enforced by its upregulation to the SIRT1/AMPK signaling. These results imply a beneficial role of phoenixin in mitigating the reproductive dysfunction associated with MSG testicular toxicity. Keywords: Phoenixin, Monosodium Glutamate, Testicular Toxicity. | ||
| Keywords | ||
| Keywords: Phoenixin; Monosodium Glutamate; Testicular Toxicity | ||
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