Chrysin Counteracts Sodium Hydroxide-Induced Alkali Esophageal Burn by Regulating Beclin-1/HO-1/NQO1, PERK/IRE1-α/ATF-6, Oxidative Stress, Inflammation, Apoptosis Signaling Pathways and Ki-67, EGF Expressions in Rats

Aim Alkali-esophageal burn due to ingestion of corrosive substances is an important clinical entity that can be seen in all age groups, especially children. Chrysin is a natural favonoid compound with a wide range of biological activities, including antioxidant, anti-infammatory, antiapoptotic, and anticancer efects. This study aimed to ascertain the preventive efcacy of chrysin in the treatment of alkali-esophageal burns. Materials and Methods Rats were administered 0.2 ml of 25% NaOH orally and CHR at 25 and 50 mg/kg intraperitoneally for four days. The levels of oxidative stress, ER stress, infammation, damage, and apoptotic and autophagic cell death in esophageal tissues were analyzed using biochemical and molecular methods. Additionally, esophageal tissue structure and function were examined using histological methods. Results Chrysin alleviated NaOH-induced increased oxidative stress by decreasing MDA and increasing antioxidants. Chrysin alleviated infammation damage by inhibiting the NF-κB signaling pathway. Chrysin decreased apoptotic Caspase-3, and Bax and increased antiapoptotic Bcl-2. Moreover, Chrysin reduced autophagic death damage and ER stress damage. Chrysin facilitated the restoration of impaired structural integrity of esophageal tissue and increased Ki-67 and EGF levels, contributing to the healing process. Conclusion Chrysin exhibited antioxidant, antiapoptotic, anti-autophagic, anti-infammatory, and anti-oxidant properties in alkali esophageal burns, as well as an efect on reducing ER stress injury. Additionally, chrysin facilitates esophageal tissue healing and maintains tissue integrity.