Neuroprotective and anti-inflammatory effects of isoliquiritigenin in kainic acid-induced epileptic rats via the TLR4/MYD88 signaling pathway

Epileptogenesis is a complex pathological process that occurs after an initial brain injury and involves a series of molecular events. Isoliquiritigenin (ISL), a flavonoid in licorice, is reported to have anti-inflammatory and antioxidant effects in various experimental models, but its specific role...

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Veröffentlicht in:	Inflammopharmacology 2019-12, Vol.27 (6), p.1143-1153
Hauptverfasser:	Zhu, Xiaobo, Liu, Jiankun, Chen, Ou, Xue, Jiang, Huang, Shanying, Zhu, Weiwei, Wang, Yibiao
Format:	Artikel
Sprache:	eng
Schlagworte:	Allergology Animals Anti-Inflammatory Agents - pharmacology bcl-2-Associated X Protein - analysis Biomedical and Life Sciences Biomedicine Chalcones - pharmacology Cytokines - analysis Dermatology Epilepsy - drug therapy Epilepsy - physiopathology Gastroenterology Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Immunology Kainic Acid - pharmacology Microglia - drug effects Microglia - physiology Myeloid Differentiation Factor 88 - antagonists & inhibitors Myeloid Differentiation Factor 88 - physiology Neuroprotective Agents - pharmacology Original Article Pharmacology/Toxicology Rats Rats, Wistar Rheumatology Signal Transduction - physiology Toll-Like Receptor 4 - antagonists & inhibitors Toll-Like Receptor 4 - physiology
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Zusammenfassung:	Epileptogenesis is a complex pathological process that occurs after an initial brain injury and involves a series of molecular events. Isoliquiritigenin (ISL), a flavonoid in licorice, is reported to have anti-inflammatory and antioxidant effects in various experimental models, but its specific roles and molecular mechanisms in the epileptogenic process following kainic acid (KA) treatment remain unclear. The purpose of this study was to explore the effects of ISL pretreatment in KA-induced epileptic rats and the underlying mechanisms. Our findings show that ISL pretreatment significantly attenuated the KA-induced expression of ionized calcium‐binding adapter molecule 1 (IBα1)-labeled microglia ( F (3, 20) = 97.29, p
ISSN:	0925-4692 1568-5608
DOI:	10.1007/s10787-019-00592-7