Tissue & cell · 2026
Targeting oxidative stress, inflammation, and apoptosis: The protective role of desloratadine against vancomycin-induced testicular toxicity via the SIRT1/Nrf2/NF-κB axis.
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Alshehre Sallwa M, Qusty Naeem F, Bokhari Bayan T, Rajab Bodour S, Alghamdi Saad, Khan Anmar, Saati Abdullah A, Taha Medhat
Аннотация
BACKGROUND: Vancomycin (VCM), a glycopeptide antibiotic frequently employed against methicillin-resistant Staphylococcus aureus (MRSA), has been linked to testicular toxicity and impaired male fertility. This study explores the protective effects of desloratadine (DES), a non-sedating antihistamine, against VCM-induced testicular damage in rats.
METHODS: Adult male albino rats were allocated into four groups: control, DES-only, VCM-only, and combined VCM+DES. Hormonal assays, sperm analysis, histological scoring, and molecular evaluations were conducted to assess reproductive function, oxidative stress, inflammation, and apoptosis.
RESULTS: VCM administration led to a significant decline in serum testosterone and a marked elevation in FSH and LH, indicating disruption of the pituitary-gonadal axis. Sperm motility decreased, while the number of abnormal and dead sperm forms increased. Histological analysis revealed degeneration of seminiferous tubules and reduced PCNA expression, reflecting impaired spermatogenesis. VCM additionally elevated malondialdehyde (MDA) levels and suppressed antioxidant enzymes, including SOD, CAT, GPx, and glutathione (GSH). This was accompanied by downregulation of Nrf2 and HO-1. Inflammatory markers (NF-κB, TNF-α, IL-6, IL-1β) were elevated. Apoptotic proteins, including P53, Bax, and caspase-3, were upregulated, while Bcl-2 was reduced. Notably, DES co-treatment reversed these effects, restoring hormonal balance, improving sperm quality, and enhancing testicular architecture. DES similarly was associated with upregulation of the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/PGC-1α signaling pathway, which correlated with Nrf2/HO-1 activation and suppression of NF-κB-mediated inflammation and P53-driven apoptosis.
CONCLUSION: DES exerts multifaceted protection against VCM-induced testicular damage by modulating oxidative stress, inflammation, and apoptosis, with SIRT1 pathway activation playing a central role, regulating mitochondrial biogenesis, enhances antioxidant defenses, and modulates inflammatory and apoptotic signaling. These findings highlight DES as a promising therapeutic agent for preserving male reproductive function during antibiotic therapy.
METHODS: Adult male albino rats were allocated into four groups: control, DES-only, VCM-only, and combined VCM+DES. Hormonal assays, sperm analysis, histological scoring, and molecular evaluations were conducted to assess reproductive function, oxidative stress, inflammation, and apoptosis.
RESULTS: VCM administration led to a significant decline in serum testosterone and a marked elevation in FSH and LH, indicating disruption of the pituitary-gonadal axis. Sperm motility decreased, while the number of abnormal and dead sperm forms increased. Histological analysis revealed degeneration of seminiferous tubules and reduced PCNA expression, reflecting impaired spermatogenesis. VCM additionally elevated malondialdehyde (MDA) levels and suppressed antioxidant enzymes, including SOD, CAT, GPx, and glutathione (GSH). This was accompanied by downregulation of Nrf2 and HO-1. Inflammatory markers (NF-κB, TNF-α, IL-6, IL-1β) were elevated. Apoptotic proteins, including P53, Bax, and caspase-3, were upregulated, while Bcl-2 was reduced. Notably, DES co-treatment reversed these effects, restoring hormonal balance, improving sperm quality, and enhancing testicular architecture. DES similarly was associated with upregulation of the AMP-activated protein kinase (AMPK)/sirtuin 1 (SIRT1)/PGC-1α signaling pathway, which correlated with Nrf2/HO-1 activation and suppression of NF-κB-mediated inflammation and P53-driven apoptosis.
CONCLUSION: DES exerts multifaceted protection against VCM-induced testicular damage by modulating oxidative stress, inflammation, and apoptosis, with SIRT1 pathway activation playing a central role, regulating mitochondrial biogenesis, enhances antioxidant defenses, and modulates inflammatory and apoptotic signaling. These findings highlight DES as a promising therapeutic agent for preserving male reproductive function during antibiotic therapy.