1. Academic Validation
  2. Tyrosol attenuates pro-inflammatory cytokines from cultured astrocytes and NF-κB activation in in vitro oxygen glucose deprivation

Tyrosol attenuates pro-inflammatory cytokines from cultured astrocytes and NF-κB activation in in vitro oxygen glucose deprivation

  • Neurochem Int. 2018 Dec;121:140-145. doi: 10.1016/j.neuint.2018.10.006.
Gang Luo 1 Yinuo Huang 2 Dapeng Mo 3 Ning Ma 3 Feng Gao 3 Ligang Song 3 Xuan Sun 3 Xiaotong Xu 3 Lian Liu 3 Xiaochuan Huo 3 Bo Wang 3 Xiaoqing Li 3 Baixue Jia 3 Yiming Deng 3 Xuelei Zhang 3 Alejandro Fernandez-Escobar 4 Guangge Peng 3 Zhongrong Miao 5
Affiliations

Affiliations

  • 1 Department of Interventional Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Department of Neurology, First Affiliated Hospital, Henan University, Kaifeng, Henan, China.
  • 2 Department of Gastroenterology, First Affiliated Hospital, Henan University, Kaifeng, Henan, China.
  • 3 Department of Interventional Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
  • 4 Translational Research Program, University of Toronto, Toronto, ON, Canada.
  • 5 Department of Interventional Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China. Electronic address: zhongrongmiao@163.com.
Abstract

Subsequent inflammation in stroke plays an important role in the damage of neurons in the perilesional area. Therapeutic intervention targeting inflammation may be a promising complementary strategy to current treatments of stroke. Here, we explored the possible beneficial effects of tyrosol, a derivative of phenethyl alcohol and natural antioxidant, playing an anti-inflammatory role in astrocyte culture and in vitro oxygen glucose deprivation (OGD) model. MTT, western blot, ELISA and EMSA assays were carried out to investigate cell viability, protein expression level, cytokine expression and NF-κB activity. We found tyrosol protected cultured astrocytes against OGD-induced cell viability loss in MTT test. Meanwhile, tyrosol attenuated the released TNF-α and IL-6 level from astrocyte via regulating Janus N-terminal kinase (JNK). The reduction of cytokines from astrocyte might be due to its inhibition of astrocyte activation and regulation of STAT3 signaling pathway since tyrosol attenuated the expression level of GFAP (glial fibrillary acidic protein) and the phosphorylation of STAT3. Additionally, we demonstrated that tyrosol prevented the degradation of IκBα and the increase of IκBα phosphorylation in astrocytes exposed to OGD, which led to the suppression of NF-κB function during ischemia. Collectively, our results showed that tyrosol may be a promising complementary treatment compound for stroke via modulating the inflammatory response in astrocytes during ischemia.

Keywords

Astrocyte; IL-6; Oxygen glucose deprivation; STAT3; TNF-α.

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