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

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

  • Inflammopharmacology. 2019 Dec;27(6):1143-1153. doi: 10.1007/s10787-019-00592-7.
Xiaobo Zhu 1,  Jiankun Liu 2,  Ou Chen 1 3,  Jiang Xue 1,  Shanying Huang 4,  Weiwei Zhu 5 6,  Yibiao Wang 7 8
Affiliations

Affiliations

  • 1 Department of Pediatrics, The Second Hospital of Shandong University, Jinan, 250012, China.
  • 2 Department of Ophthalmology, The Second People's Hospital of Jinan City, Jinan, 250000, China.
  • 3 Nursing School, Shandong University, Jinan, 250012, China.
  • 4 The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University, Jinan, 250012, China.
  • 5 Department of Pediatrics, Jinan Central Hospital Affiliated To Shandong University, Jinan, 250000, China. drwwzhu@yahoo.com.
  • 6 Department of Pediatrics, The Second Hospital of Shandong University, No. 247 Beiyuan Street, Jinan, 250033, China. drwwzhu@yahoo.com.
  • 7 Department of Pediatrics, The Second Hospital of Shandong University, Jinan, 250012, China. wybsdey@hotmail.com.
  • 8 Department of Pediatrics, The Second Hospital of Shandong University, No. 247 Beiyuan Street, Jinan, 250033, China. wybsdey@hotmail.com.
PMID: 31037573 DOI: 10.1007/s10787-019-00592-7
Abstract

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 < 0.01, ηp2 = 0.94) and glial fibrillary acidic protein (GFAP)-positive astrocytes (F(3, 20) = 72.48, p < 0.01, ηp2 = 0.92), and the release of inflammatory mediators, such as TNF-α (F(3, 20) = 133.14, p < 0.01, ηp2 = 0.95), IL-1β, and C-C motif chemokine ligand 3 (CCL3). ISL pretreatment given before KA also significantly prevented apoptotic neuronal injury by upregulating the activities of superoxide dismutase and Glutathione Peroxidase. It also significantly suppressed the protein levels of Toll-like Receptor 4 (TLR4) (F(3, 20) = 63.23, p < 0.01, ηp2 = 0.91) and its downstream molecules, myeloid differentiation primary response 88 (MyD88), phosphorylated (p-)IκBα, and p-NF-κB. Blocking TLR4/MyD88 signaling also attenuated KA-induced neuroinflammation and neuronal damage in the hippocampus. Overall, our study demonstrates that ISL pretreatment plays neuroprotective and anti-inflammatory roles in KA-induced epileptogenesis, which may be mediated by the TLR4/MyD88 signaling pathway.

Keywords

Epileptogenesis; Isoliquiritigenin; Kainic acid; Neuroprotection; Rat; Toll-like receptor 4.

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