Activation of Nrf2/ARE signaling pathway attenuates lanthanum chloride induced injuries in primary rat astrocytes. Issue 8 (19th July 2017)

• Record Type: Journal Article
• Authors: Zhang, Lijin; Yang, Jinghua; Wu, Shengwen; Jin, Cuihong; Lu, Xiaobo; Hu, Xiaoyu; Sun, Yaling; Gao, Xiang; Cai, Yuan
• Is Part Of: Metallomics. Volume 9:Issue 8(2017
• Page Start: 1120
• Page End: 1131
• Publication Date: 2017-07-19
• Subjects: Metals -- Physiological effect -- Periodicals; 572.51
• DOI: 10.1039/c7mt00182g
• Languages: English
• ISSNs: 1756-5901

Abstract

Abstract : Lanthanum (La) exposure can lead to learning and memory disorder in animals; however, the underlying mechanism of La induced neurotoxicity is still unknown. Abstract : Lanthanum (La) exposure can lead to learning and memory disorder in animals; however, the underlying mechanism of La induced neurotoxicity is still unknown. It has been demonstrated that Nrf2 activation by tert -butylhydroquinone ( t BHQ) results in neuroprotection against brain injuries. However, little study has been done with respect to its effect on La induced neurotoxicity. Herein, experiments are undertaken to determine if there is a correlation between La damaged astrocytes and the Nrf2/ARE signalling pathway. Primary rat astrocytes are exposed to 0 mmol L −1, 0.125 mmol L −1, 0.25 mmol L −1 and 0.5 mmol L −1 lanthanum chloride (LaCl3 ) for 24 hours. The results reveal that LaCl3 increases the apoptosis/necrosis rate of astrocytes, decreases the glutathione (GSH) content, increases reactive oxygen species (ROS) levels and significantly down-regulates Nrf2 as well as the mRNA and protein expression of Nrf2-regulated genes, including NADP(H): dehydrogenase quinone 1 (NQO1), hemeoxygenase-1 (HO-1), superoxide dismutase 2 (SOD2 ), glutathione peroxidase 1 (GSH-Px1 ), glutathione- s -transferase (GST) and γ-glutamine cysteine synthase (γ-GCS) in astrocytes. In addition, it is found that t BHQ displays an antagonistic effect on astrocytes damaged by LaCl3 . Therefore, La damaged astrocytes are possibly related to the down-regulated Nrf2/ARE pathway, and treatment with t BHQ clearly activates the Nrf2/ARE signalling pathway, which exerts protection against oxidative stress.