ReferenceID 4987

GLP-1 mediates the neuroprotective action of crocin against cigarette smoking-induced cognitive disorders via suppressing HMGB1-RAGE/TLR4-NF-κB pathway

Int Immunopharmacol

Cigarette smoking (CS) has been associated with an increased risk of cognitive disorders. Although HMGB1 has been connected to various neurological ailments, its role in the pathogenesis of CS-induced cognitive impairmen

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Reference Id
4987
Evidence Id
21577
Core Evidence Id
21577
Source Reference Id
3222
Herb2 Reference Id
HBREF004019
Subject Paper Key
HBIN021714_35785730
Pubmed Id
35785730
Doi
10.1016/j.intimp.2022.108995
Paper Title
GLP-1 mediates the neuroprotective action of crocin against cigarette smoking-induced cognitive disorders via suppressing HMGB1-RAGE/TLR4-NF-κB pathway
Paper Abstract
Cigarette smoking (CS) has been associated with an increased risk of cognitive disorders. Although HMGB1 has been connected to various neurological ailments, its role in the pathogenesis of CS-induced cognitive impairments is undefined. With the ability of GLP-1 to lower HMGB1 expression and improve learning and memory performance, we sought to assess the potential neuroprotective efficacy of Crocin (Cro) as a GLP-1 stimulator against CS-induced cognitive impairments, with a focus on the HMGB1-RAGE/TLR4-NF-κB pathway. Fifty adult rats were specified into: Control; Cro (30 mg/kg); CS; Cro then CS and CS concurrently with Cro. Cognitive functions were assessed by MWM, EMP, and passive avoidance tests. Hippocampal levels of GLP-1, HMGB1, pro-inflammatory cytokines, and apoptotic markers were detected using ELISA, western blotting, and immunohistochemistry. Hippocampal oxidant/antioxidant status was evaluated via colorimetric determination of MDA and TAC. The results revealed that Cro either before or along with CS produced a significant improvement in learning and memory. Cro markedly hindered HMGB1-RAGE/TLR4-NF-κB pathway through enhancing GLP-1 level and expression, which in turn suppressed TNF-α and IL-1β levels and alleviated CS-induced neuroinflammation. Cro significantly counteracted CS-triggered oxidative stress as evidenced by reducing MDA level and raising TAC. Histopathologically, Cro lessened neuronal apoptosis by lowering Bax/Bcl-2 ratio at hippocampal CA2 region. These findings confirmed a GLP-1-dependent neuroprotective action of Cro against CS-induced cognitive disorders via suppressing HMGB1-RAGE/TLR4-NF-κB axis.
Journal
Int Immunopharmacol
Publish Year
2022
Experiment Subject
rat
Experiment Type
Animal Experiment
Phenotype Related
Cognitive Disorders; Cognitive Impairments; Cs-induced Cognitive Impairments
Paper Title Cn
Paper Title En
GLP-1 mediates the neuroprotective action of crocin against cigarette smoking-induced cognitive disorders via suppressing HMGB1-RAGE/TLR4-NF-κB pathway
Bilingual Status
semi_complete