Steroids · 2026
Carnosic acid ameliorates methotrexate-induced male infertility: targeting testicular redox imbalance and nitric oxide/CGMP signaling.
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Ajibare Ayodeji Johnson, Adejumo Miracle Oyaname, Akanbioluwa Ewaoluwa Faith, Adelokiki Ibukunoluwa, Akinfe Oluwadamilola, Aransi-Ola Kafilat Temidayo, Akintoye Olabode Oluwadare
Аннотация
PURPOSE: Methotrexate (MTX), a folate antagonist used in the treatment of cancer and autoimmune disorders, unfortunately, induces testicular toxicity and impairs male fertility. Although the tissue-protective properties of Carnosic acid (CAR) are known, its effectiveness in mitigating MTX-induced reproductive toxicity has not been adequately studied. This study explores the protective role of CAR against the toxicity of MTX in rat testes.
METHODS: Forty male Wistar rats were divided into four groups: control, MTX (20 mg/kg i.p., day 7), MTX + low-dose CAR (20 mg/kg p.o., 14 days), and MTX + high-dose CAR (40 mg/kg p.o., 14 days). On day 15, testicular tissue and serum were analyzed for oxidative stress markers (GSH, GPx, MDA), NO/cGMP pathway components (iNOS, NO, cGMP), inflammatory markers (NF- κB, IL-6), steroidogenesis parameters (total cholesterol, 3β-HSD, 17β-HSD), and hormonal levels (GnRH, FSH, LH, testosterone, estradiol). Histopathological examinations were conducted on testicular sections.
RESULTS: MTX significantly reduced antioxidant levels, increased lipid peroxidation, disrupted NO/cGMP signaling, elevated inflammation, impaired steroidogenesis, and altered hormone levels, with evidence of histological changes. CAR, especially at higher doses, mitigated these effects, restoring antioxidant status, normalizing NO/cGMP signaling, reducing inflammation, enhancing steroidogenesis, and improving testicular morphology.
CONCLUSION: CAR ameliorates MTX-induced adverse effects in the testes of rats via controlling redox balance, NO/cGMP signaling, inflammation, and steroidogenesis, with the potential of CAR to be used as a treatment to protect male reproductive function during therapy with MTX.
METHODS: Forty male Wistar rats were divided into four groups: control, MTX (20 mg/kg i.p., day 7), MTX + low-dose CAR (20 mg/kg p.o., 14 days), and MTX + high-dose CAR (40 mg/kg p.o., 14 days). On day 15, testicular tissue and serum were analyzed for oxidative stress markers (GSH, GPx, MDA), NO/cGMP pathway components (iNOS, NO, cGMP), inflammatory markers (NF- κB, IL-6), steroidogenesis parameters (total cholesterol, 3β-HSD, 17β-HSD), and hormonal levels (GnRH, FSH, LH, testosterone, estradiol). Histopathological examinations were conducted on testicular sections.
RESULTS: MTX significantly reduced antioxidant levels, increased lipid peroxidation, disrupted NO/cGMP signaling, elevated inflammation, impaired steroidogenesis, and altered hormone levels, with evidence of histological changes. CAR, especially at higher doses, mitigated these effects, restoring antioxidant status, normalizing NO/cGMP signaling, reducing inflammation, enhancing steroidogenesis, and improving testicular morphology.
CONCLUSION: CAR ameliorates MTX-induced adverse effects in the testes of rats via controlling redox balance, NO/cGMP signaling, inflammation, and steroidogenesis, with the potential of CAR to be used as a treatment to protect male reproductive function during therapy with MTX.