2. Academic Validation
  3. Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway

Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway

  • J Cell Mol Med. 2020 Sep;24(18):10468-10477. doi: 10.1111/jcmm.15659.
Chaoliang Tang 1,  Yida Hu 2,  Haiyan Lyu 3,  Jie Gao 4,  Jiazhen Jiang 5,  Xiude Qin 6,  Yuanbo Wu 7,  Jiawu Wang 1,  Xiaoqing Chai 1
Affiliations

Affiliations

  • 1 Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
  • 2 Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
  • 3 Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
  • 4 Department of Anesthesia, Critical Care & Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
  • 5 Department of Emergency, Huashan Hospital North, Fudan University, Shanghai, China.
  • 6 Department of Neurology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, China.
  • 7 Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
PMID: 32677362 DOI: 10.1111/jcmm.15659
Abstract

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.

Keywords

1-O-Hexyl-2,3,5-trimethylhydroquinone; HO-1; Nrf2; PC12 cells; cerebral ischaemic/reperfusion.

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