2014
DOI: 10.1016/j.neuint.2014.06.003
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Gastrodin protects against MPP+-induced oxidative stress by up regulates heme oxygenase-1 expression through p38 MAPK/Nrf2 pathway in human dopaminergic cells

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Cited by 103 publications
(65 citation statements)
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“…RNAi-mediated Nrf2 knockdown diminished the cytoprotective effects of 20C, which strongly suggests that the Nrf2/ HO-1/NQO1 pathway was activated. These results are similar to previous studies demonstrating that Nrf2 plays a key role in protecting cells against oxida tive stress [34][35][36] . However, in the MTT assay, 1 μmol/L 20C had a beneficial effect against rotenone-induced apoptosis in Nrf2-knockdown PC12 cells, which indicated that, 20C might activate other targets, in addition to Nrf2/ARE/HO-1 signaling pathway, to exert its cytoprotective effect.…”
Section: Discussionsupporting
confidence: 92%
“…RNAi-mediated Nrf2 knockdown diminished the cytoprotective effects of 20C, which strongly suggests that the Nrf2/ HO-1/NQO1 pathway was activated. These results are similar to previous studies demonstrating that Nrf2 plays a key role in protecting cells against oxida tive stress [34][35][36] . However, in the MTT assay, 1 μmol/L 20C had a beneficial effect against rotenone-induced apoptosis in Nrf2-knockdown PC12 cells, which indicated that, 20C might activate other targets, in addition to Nrf2/ARE/HO-1 signaling pathway, to exert its cytoprotective effect.…”
Section: Discussionsupporting
confidence: 92%
“…In physiological conditions, p38 MAPK is at a static status by binding with its inhibitor, Keap1 14. Various pathological stimuli and intracellular responses activate p38 MAPK by phosphorylation, which facilitates disassociation of Nrf2/Keap1 complex and nuclear translocation of Nrf2 38.…”
Section: Discussionmentioning
confidence: 99%
“…The activation of Nrf2/ARE signaling is regulated by the upstream kinases. Theses kinases are referred to as mitogen‐activated protein kinases (MAPKs) 14. As a member of the MAPKs family, p38 MAPK is a key signaling transducer in response to harmful stimuli, including ROS 15.…”
Section: Introductionmentioning
confidence: 99%
“…Therefore, EEEP, EEBGP and EECP could stimulate Nrf2 to translocate into the nucleus to bind to DNA to regulate the expression of HO-1, GCLM and TrxR1. Moreover, numerous studies have confirmed that the activation of p38 and Erk kinases was required to activate Nrf2 in regulating the expression of antioxidant genes (HO-1, TrxR1 and GCLM) (Zipper & Mulcahy 2000Jiang et al 2014). Thus, we inferred that EEBGP regulated the expression of HO-1, TrxR1 To determine the inhibition effects of the inhibitors on p38 and Erk, RAW264.7 cells were pre-treated with SB203580 or PD98059 for 0.5 h and then cultured in the presence or absence of EEEP, EEBGP and EECP for 1 h. (F-I) To confirm that the expression of HO-1, GCLM and TrxR1 was regulated by p38/p-p38 kinase or Erk/p-Erk kinase, RAW264.7 cells were pre-treated with SB203580 or PD98059 for 0.5 h and cultured in the presence or absence of EEEP, EEBGP and EECP for 5 h, then the medium was removed, and the cells were cultured with new medium for an additional 4 h. All the genes expressed at protein level were detected by western blot and -tubulin was used as an internal reference.…”
Section: The Effects Of Eeep Eebgp and Eecp On The Nuclear Translocamentioning
confidence: 99%