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Arjunolic acid counteracts fluoxetine-inducedreproductive neuroendocrine dysfunction through inhibitionof chromosomal derangements and hypercortisolism |
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| รหัสดีโอไอ | |
| Creator | 1. Edozie Ojochem Lynda 2. Nwangwa E. Kingsley 3. Oyovwi O. Mega 4. Ben-Azu Benneth 5. Emojevvwe Victor 6. Onome B. Oghenetega 7. Ejime Agbonifo-Chijiokwu 8. Ovuakporaye I. Simon 9. Tesi P. Edesiri |
| Title | Arjunolic acid counteracts fluoxetine-inducedreproductive neuroendocrine dysfunction through inhibitionof chromosomal derangements and hypercortisolism |
| Publisher | Research and Development Office, Prince of Songkla University |
| Publication Year | 2565 |
| Journal Title | Songklanakarin Journal of Science an Technology (SJST) |
| Journal Vol. | 44 |
| Journal No. | 6 |
| Page no. | 1473-1480 |
| Keyword | fluoxetine, arjunolic acid, spermatogenesis, hypercortisolism, reproductive hormone |
| URL Website | https://sjst.psu.ac.th/ |
| ISSN | 0125-3395 |
| Abstract | Antidepression-related HPA-HPG alteration is gaining more attention in stress research on humans and animals withdepression. Therefore, the search for therapeutic drugs such as Arjunolic acid (AA) might be a core value in the management ofreproductive neuro-endocrine dysfuction in rats treated with FXT. In this context, this study aimed to determine the effects of AAon reproductive neuro-endocrine functions in fluoxetine (FXT)-induced HPA-HPG axis dysfunction in rats. The subjects wererandomly divided into 6 groups with six (6) rats each after 14 days of acclimatization. Rats in group 1 received normal saline (10mL/kg); groups 2 & 3 were respectively given AA (1.0 mg/100gm body weight) and AA (2.0 mg/100gm body weight), whereasrats in group 4 were given FXT (10 mg/kg/p.o./day), and groups 5 & 6 were respectively given a combination of FXT (10 mg/kg)+ AA (1.0 mg/100g body weight) and of FXT (10 mg/kg) + AA (2.0 mg/100g body weight). The results revealed that FXTaltered reproductive neuro-endocrine function as evidenced by increased corticosterone, tDFI, tCSA, and abnormal spermmorphology; with corresponding decreases in Kisspeptin, GnRH, LH, FSH, testosterone, HOST value, TP, Sialic acid, Johnsonscore, sperm count, motility, and viability. However, AA dose dependently significantly counteracted the FXT-elicited changesin corticosterone, tDFI, tCSA and abnormal sperm morphology as well as Kisspeptin, GnRH, LH, FSH, testosterone, HOSTvalue, TP, Sialic acid, Johnson score, sperm count, motility, and viability; and improved the body and testicular weight in rats. Inconclusion, AA attenuates fluoxetine-induced reproductive neuroendocrine dysfunction through inhibition of chromosomalderangements and hypercortisolism. However, co-administration of FXT with AA could be a better therapeutic option in themanagement of FXT-induced altered HPA-HPG-axis. |
