Neuroprotective Effects of Taraxacum officinale Wigg. Extract on Glutamate-Induced Oxidative Stress in HT22 Cells via HO-1/Nrf2 Pathways
Department of Pharmacy, Qingdao University of Science & Technology, Qingdao 266042, China
The College of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China
The Breeding Base of State Key Laboratory of Resources systems Research and Development Utilization of Chinese Herbal Medicines Constructioned by The Ministry of Science and Technology of the PRC and Sichuan Province, Chengdu 611137, China
Author to whom correspondence should be addressed.
Nutrients 2018, 10(7), 926; https://doi.org/10.3390/nu10070926
Received: 16 June 2018 / Revised: 7 July 2018 / Accepted: 16 July 2018 / Published: 19 July 2018
Oxidative stress-mediated neuron damage is considered an important contributor to the pathogenesis and development of neurodegenerative diseases. Taraxacum officinale has been reported to possess antioxidant activities. However, whether it can protect neurons against oxidative damage and the underlying molecular mechanisms have not been fully determined. In the present study, we examined the neuroprotective effects of ethanol extracts of this plant (ETOW) on glutamate-induced oxidative stress in HT22 cells. Both cell viability and reactive oxygen species (ROS) assays showed that ETOW effectively attenuated glutamate-induced cytotoxicity and ROS generation. Furthermore, our results revealed that ETOW increased the expression of heme oxygenase-1 (HO-1) and promoted the nuclear translocation of nuclear factor erythroid 2-related factor-2 (Nrf2). The inhibitory effects of ETOW on glutamate-stimulated cell toxicity and ROS production were partially reversed by tin protoporphyrin (SnPP), an HO activity inhibitor. Taken together, these results demonstrate that ETOW can protect HT22 cells against glutamate-induced oxidative damage by inducing the Nrf2/HO-1 pathways. Our study supports the idea that Taraxacum officinale Wigg. is a promising agent for preventing neurodegenerative diseases.