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Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway.
Tang, Chaoliang; Hu, Yida; Lyu, Haiyan; Gao, Jie; Jiang, Jiazhen; Qin, Xiude; Wu, Yuanbo; Wang, Jiawu; Chai, Xiaoqing.
Afiliação
  • Tang C; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
  • Hu Y; Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
  • Lyu H; Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
  • Gao J; Department of Anesthesia, Critical Care & Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • Jiang J; Department of Emergency, Huashan Hospital North, Fudan University, Shanghai, China.
  • Qin X; Department of Neurology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, China.
  • Wu Y; Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
  • Wang J; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
  • Chai X; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
J Cell Mol Med ; 24(18): 10468-10477, 2020 09.
Article em En | MEDLINE | ID: mdl-32677362
1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ), a lipophilic phenolic agent, has an antioxidant activity and reactive oxygen species (ROS) scavenging property. However, the role of HTHQ on cerebral ischaemic/reperfusion (I/R) injury and the underlying mechanisms remain poorly understood. In the present study, we demonstrated that HTHQ treatment ameliorated cerebral I/R injury in vivo, as demonstrated by the decreased infarct volume ration, neurological deficits, oxidative stress and neuronal apoptosis. HTHQ treatment increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant protein, haeme oxygenase-1 (HO-1). In addition, HTHQ treatment decreases oxidative stress and neuronal apoptosis of PC12 cells following hypoxia and reperfusion (H/R) in vitro. Moreover, we provided evidence that PC12 cells were more vulnerable to H/R-induced oxidative stress after si-Nrf2 transfection, and the HTHQ-mediated protection was lost in PC12 cells transfected with siNrf2. In conclusion, these results suggested that HTHQ possesses neuroprotective effects against oxidative stress and apoptosis after cerebral I/R injury via activation of the Nrf2/HO-1 pathway.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Traumatismo por Reperfusão / Transdução de Sinais / Fármacos Neuroprotetores / Heme Oxigenase-1 / Fator 2 Relacionado a NF-E2 / Hidroquinonas / Neurônios Limite: Animals Idioma: En Revista: J Cell Mol Med Assunto da revista: BIOLOGIA MOLECULAR Ano de publicação: 2020 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Traumatismo por Reperfusão / Transdução de Sinais / Fármacos Neuroprotetores / Heme Oxigenase-1 / Fator 2 Relacionado a NF-E2 / Hidroquinonas / Neurônios Limite: Animals Idioma: En Revista: J Cell Mol Med Assunto da revista: BIOLOGIA MOLECULAR Ano de publicação: 2020 Tipo de documento: Article País de afiliação: China