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Objective: To examine the effects of deltamethrin(DM) and tBHQ on the activation of Nrf2 and expression of GCS-HS in primary astrocytes. Methods: Rat primary astrocytes were treated with DM (10 μmol/L) and tBHQ (40 μmol/L), for 1 and 6 h respectively. Results: Analysis using immunofluorescent confocal microscopy revealed that tBHQ treatment led to a dramatic increase in the level of Nrf2. The ratio of cytoplasmic Nrf2 protein to nuclear Nrf2 protein was markedly reduced in astrocytes by either tBHQ or DM treatment. The level of Nrf2 was reduced by combined tBHQ with DM treatment for 1 h, but treatment the ratio of cytoplasmic Nrf2 protein to nuclear Nrf2 protein was increased compared with that of the tBHQ only. The expression of GCS-HS in astrocytes was not altered by DM or tBHQ or both in astrocytes. Conclusion: These findings demonstrated for the first time that Nrf2 was activated by pesticides and antioxidants in astrocytes, implicating a role of Nrf2 in response to pesticide neurotoxicity ingla.
Methods: Rat primary astrocytes were treated with DM (10 μmol / L) and tBHQ (40 μmol / L) for the effects of deltamethrin (DM) and tBHQ on the activation of Nrf2 and expression of GCS-HS in primary astrocytes ) for 1 and 6 h respectively. Results: Analysis using immunofluorescent confocal microscopy revealed that tBHQ treatment led to a dramatic increase in the level of Nrf2. The ratio of cytoplasmic Nrf2 protein to nuclear Nrf2 protein was markedly reduced in astrocytes by either tBHQ or The level of Nrf2 was reduced by combined tBHQ with DM treatment for 1 h, but treatment of the ratio of cytoplasmic Nrf2 protein to nuclear Nrf2 protein was increased compared with that of the tBHQ only. The expression of GCS-HS in astrocytes was not altered by DM or tBHQ or both in astrocytes. Conclusion: These findings demonstrated for the first time that Nrf2 was activated by pesticides and antioxidants in astrocytes, implicating a role of Nrf2 in response to pesticide neu rotoxicity ingla.