Therapeutic effects of apilarnil, a bee product, on apoptosis and autophagy in cisplatin-induced rat ovarian toxicity
- PMID: 40541689
- DOI: 10.1016/j.fct.2025.115594
Therapeutic effects of apilarnil, a bee product, on apoptosis and autophagy in cisplatin-induced rat ovarian toxicity
Abstract
Objective: Cisplatin (CP) is a platinum derivative used to treat ovarian, breast, testicular, and bladder cancers. As one of the apitherapy products, apilarnil (API) contains androgenic hormones and is extremely chemically complex. CP alterations in rats' ovarian tissue were evaluated by API, a possible therapeutic medicine.
Methods: Each group of female rats consisted of seven rats. One dosage of 7.5 mg/kg/day CP was administered intraperitoneally to the CP group. The API group received 0.5 g/kg/day of apilarnil orally for ten days. Ovarian tissues were then examined histopathologically, immunohistochemically, and biochemically. Beclin-1, p62, and LC-3, along with Caspase-3 and AIF, were immunohistochemically determined. ELISA tests were performed on MDA, GSH-PX, SOD, CAT, AMH, FSH, and LH levels.
Results: The CP group had significantly fewer primordial follicles than the control group. This group also showed edema, vacuolization, and congested blood vessels. The findings were improved by the API therapy. Furthermore, API was shown to restore Beclin-1 and p62 levels, as well as Caspase-3 and AIF expression, which had all increased in the CP group. API reduced MDA, which had grown due to toxicity, whereas SOD and CAT levels improved. Furthermore, it greatly increased AMH levels, which are an indicator of ovarian reserve and decrease.
Conclusions: This study concluded that API, an organic chemical used in apitherapy, can restore damage to the female reproductive system caused by CP treatment. Apilarnil is a promising therapy for female gonadal failure.
Keywords: Apilarnil; Apitherapy; Cisplatin; Ovary; Rat.
Copyright © 2025 Elsevier Ltd. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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