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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.
J Cell Mol Med. 2020 Jul 17 [Online ahead of print]JC

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.

Authors+Show Affiliations

Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.Department of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.Department of Anesthesia, Critical Care & Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.Department of Emergency, Huashan Hospital North, Fudan University, Shanghai, China.Department of Neurology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, China.Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

32677362

Citation

Tang, Chaoliang, et al. "Neuroprotective Effects of 1-O-hexyl-2,3,5-trimethylhydroquinone On Ischaemia/reperfusion-induced Neuronal Injury By Activating the Nrf2/HO-1 Pathway." Journal of Cellular and Molecular Medicine, 2020.
Tang C, Hu Y, Lyu H, et al. 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.
Tang, C., Hu, Y., Lyu, H., Gao, J., Jiang, J., Qin, X., Wu, Y., Wang, J., & Chai, X. (2020). Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway. Journal of Cellular and Molecular Medicine. https://doi.org/10.1111/jcmm.15659
Tang C, et al. 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 Jul 17; PubMed PMID: 32677362.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway. AU - Tang,Chaoliang, AU - Hu,Yida, AU - Lyu,Haiyan, AU - Gao,Jie, AU - Jiang,Jiazhen, AU - Qin,Xiude, AU - Wu,Yuanbo, AU - Wang,Jiawu, AU - Chai,Xiaoqing, Y1 - 2020/07/17/ PY - 2019/09/18/received PY - 2020/04/29/revised PY - 2020/06/29/accepted PY - 2020/7/18/entrez KW - 1-O-Hexyl-2,3,5-trimethylhydroquinone KW - HO-1 KW - Nrf2 KW - PC12 cells KW - cerebral ischaemic/reperfusion JF - Journal of cellular and molecular medicine JO - J. Cell. Mol. Med. N2 - 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. SN - 1582-4934 UR - https://www.unboundmedicine.com/medline/citation/32677362/Neuroprotective_effects_of_1_O_hexyl_235_trimethylhydroquinone_on_ischaemia/reperfusion_induced_neuronal_injury_by_activating_the_Nrf2/HO_1_pathway_ L2 - https://doi.org/10.1111/jcmm.15659 DB - PRIME DP - Unbound Medicine ER -
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