| Title: | Role of IRE1α/XBP1/CHOP/NLRP3 Signalling Pathway in Neonicotinoid Imidacloprid-Induced Pancreatic Dysfunction in Rats and Antagonism of Lycopene: In Vivo and Molecular Docking Simulation Approaches |
| Authors: | Walaa Bayoumie El Gazzar, Heba Bayoumi, Heba S. Youssef, Tayseer A. Ibrahim, Reham M. Abdelfatah , Noha M. Gamil , Mervat K. Iskandar , Amal M. Abdel-Kareim , Shaymaa M. Abdelrahman , Mohammed A. Gebba , Mona Atya Mohamed , Maha M. Mokhtar |
| Year: | 2024 |
| Keywords: | Not Available |
| Journal: | Toxics |
| Volume: | 12 |
| Issue: | 445 |
| Pages: | Not Available |
| Publisher: | Not Available |
| Local/International: | International |
| Paper Link: | Not Available |
| Full paper | maha mahmoud_paper 6 - Copy.pdf |
| Supplementary materials | Not Available |
| Abstract: |
Background: Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. Aim of the work: Analyze both the adverse on the pancreas following oral consumption of imidacloprid neonicotinoids and the potential protective effects of lycopene (LYC) Material and methods: oral consumption of imidacloprid neonicotinoids (45 mg/kg daily for 30 days) and the potential protective effects of lycopene (LYC) administration (10 mg/kg/day for 30 days) with IMI exposure in male Sprague–Dawley rats. The apoptotic, pyroptotic, inflammatory, oxidative stress and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Results: Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, and inflammatory, pyroptotic, and apoptotic biomarkers were also observed following IMI administration. LYC effectively reversed these alterations by reducing oxidative stress markers (e.g., MDA) and enhancing antioxidant enzymes (SOD, CAT). It downregulated ER stress markers (IRE1α, XBP1, CHOP), decreased pro-inflammatory cytokines (TNF-α, IL-1β), and suppressed |
