ArticleJournal of molecular histology2026
Modulatory effects of Withania somnifera supplementation on p38 MAPK/NF-κB/COX-2 and TRPC1/CHOP signaling pathways in methotrexate-induced parotid and submandibular salivary gland toxicity in rats.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Methotrexate (MTX), a chemotherapeutic and immunosuppressive drug, is well known to cause salivary gland (SG) toxicity. Although Withania somnifera (WS) exhibits strong antioxidant and cytoprotective properties, its potential to counteract MTX-induced SG injury remains poorly explored. The current study aimed to assess the protective effect of WS supplementation against MTX-induced toxicity in rat parotid and submandibular glands and to explore the underlying mechanisms. Forty adult male albino rats, each weighing ~ 200 g, were randomly allocated into four groups (n = 10): Control (distilled water orally/8 days), WS (300 mg/kg orally/8 days), MTX (single intraperitoneal injection of 60 mg/kg on day 4), and WS + MTX (WS/8 days with MTX on day 4). Glandular injury was assessed histologically using hematoxylin and eosin staining and immunohistochemically for cyclooxygenase-2 (COX-2) and cleaved caspase-3. Biochemical assays measured malondialdehyde (MDA) and total antioxidant capacity (TAC). p38 mitogen-activated protein kinase (p38 MAPK) and transient receptor potential canonical channel 1 (TRPC1) were quantified using ELISA. Gene expression of nuclear factor-κB (NF-κB) and C/EBP homologous protein (CHOP) was analyzed by qPCR. MTX induced acinar and ductal degeneration, cytoplasmic vacuolization, and nuclear pyknosis; increased MDA; reduced TAC; activated the p38 MAPK/NF-κB/COX-2 inflammatory axis; ER stress through the TRPC1/CHOP pathway; and elevated cleaved caspase-3 expression. Co-treatment with WS preserved glandular architecture, restored antioxidant balance, attenuated oxidative, inflammatory, and ER-stress responses, and suppressed the apoptosis. This demonstrates that WS supplementation provided protection against MTX-induced toxicity in both the parotid and submandibular glands largely through modulation of p38 MAPK/NF-κB/COX-2 and TRPC1/CHOP pathways.
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