β-Caryophyllene Protects Against Foodborne Ochratoxin A–Induced Pancreatic Toxicity: Implications for Food Safety and Environmental Health

The increasing prevalence of mycotoxin contamination due to climate change and environmental stressors represents a growing global health concern, necessitating effective preventive and therapeutic strategies. Ochratoxin A (OTA) is a pervasive foodborne mycotoxin linked to multisystem toxicity; nonetheless, its harmful effects on pancreatic tissue and the underlying molecular processes are inadequately defined. Increasing evidence indicates that oxidative stress and sterile inflammation produced by OTA are pivotal in pancreatic damage. β-Caryophyllene (BCP), a natural sesquiterpene found in consumable flora, demonstrates significant antioxidant and anti-inflammatory effects. The objective of this study was to examine the protective effect of BCP against OTA-induced pancreatic toxicity, focusing on the modulation of the Nrf2/HO-1 antioxidant pathway and the NF-κB-mediated activation of the NLRP3 inflammasome. Experimental animals were subjected to OTA to elicit pancreatic toxicity and simultaneously administered BCP at both low and high dosages. Pancreatic damage was assessed via serum biochemical markers and histological analysis. Parameters of oxidative stress and inflammatory mediators were measured in pancreatic tissue. Protein expression levels of Nrf2, HO-1, NF-κB, and NLRP3 signaling components were examined to clarify the molecular foundation of BCP-induced protection. OTA exposure caused significant pancreatic damage, indicated by increased oxidative stress, activation of NF-κB and NLRP3 inflammasome signaling, and notable histoarchitectural disruption. BCP therapy markedly reduced OTA-induced pancreatic damage in a dose-dependent fashion. BCP augmented intrinsic antioxidant defenses through the activation of the Nrf2/HO-1 pathway while simultaneously inhibiting NF-κB activation and subsequent NLRP3 inflammasome signaling. BCP significantly alleviates OTA-induced pancreatic damage by reestablishing redox equilibrium and suppressing inflammatory signaling pathways. These findings offer new understanding of OTA-induced pancreatic damage and recognize BCP as a potential dietary strategy for mitigating mycotoxin-related pancreatic impairment, with possible implications for health hazards connected with environmental and food safety.