Mervat Kamal Abdo iskandar
Lecturer
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
Toxics • 2024
Publication Information
Authors
El Gazzar, W.B.; Bayoumi, H.; Youssef, H.S.; Ibrahim, T.A.; Abdelfatah, R.M.; Gamil, N.M.; Iskandar, M.K.; Abdel-Kareim, A.M.; Abdelrahman, S.M.; Gebba, M.A.; et al.
Keywords
imidacloprid; lycopene; endoplasmic reticulum stress; apoptosis; pyroptosis; pancreas.
Journal
Toxics
Publisher
mdpi
Volume
12
Issue
7
Pages
445
publication.type
International
Paper Link
Open Link
Supplementary Materials
Not Available
Abstract
Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse
effects on the pancreas following 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. Upon IMI administration, noticeable changes were observed in
pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress
biomarkers, 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 pyroptotic
(NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the
histopathological and ultrastructure alterations brought on by IMI toxicity
Abstract
Citation: El Gazzar, W.B.; Bayoumi, H.; Youssef, H.S.; Ibrahim, T.A.; Abdelfatah, R.M.; Gamil, N.M.; Iskandar, M.K.; Abdel-Kareim, A.M.; Abdelrahman, S.M.; Gebba, M.A.; et al. 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. Toxics 2024, 12, 445. Abstract: Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following 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, inflam-matory, oxidative stress, and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, 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 pyroptotic (NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the histopathological and ultrastructure alterations brought on by IMI toxicity.
effects on the pancreas following 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. Upon IMI administration, noticeable changes were observed in
pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress
biomarkers, 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 pyroptotic
(NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the
histopathological and ultrastructure alterations brought on by IMI toxicity
Abstract
Citation: El Gazzar, W.B.; Bayoumi, H.; Youssef, H.S.; Ibrahim, T.A.; Abdelfatah, R.M.; Gamil, N.M.; Iskandar, M.K.; Abdel-Kareim, A.M.; Abdelrahman, S.M.; Gebba, M.A.; et al. 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. Toxics 2024, 12, 445. Abstract: Imidacloprid (IMI) is a commonly used new-generation pesticide that has numerous harmful effects on non-targeted organisms, including animals. This study analysed both the adverse effects on the pancreas following 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, inflam-matory, oxidative stress, and endoplasmic reticulum stress biomarkers were evaluated, along with the histopathological alterations. Upon IMI administration, noticeable changes were observed in pancreatic histopathology. Additionally, elevated oxidative/endoplasmic reticulum-associated stress biomarkers, 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 pyroptotic (NLRP3, caspase-1) along with apoptotic markers (Bax, cleaved caspase-3). It also improved the histopathological and ultrastructure alterations brought on by IMI toxicity.