ABSTRACT
Objective To observe the changes of rat microglial inflammation and migration after exposure to sodium metavanadate(NaVO3·2H2O), and to analyze the possible mechanisms of vanadium neurotoxicity. Methods Primary cultured rat microglial cells were incubated with NaVO3·2H2 O. Morphological changes and the Iba1 expression of microglia were tested by immunofluorescence assay. iNOS, Cox-2, ERK and p-ERK protein expressions were determined by western blotting. The levels of TNF-α and IL-1β in the culture medium were tested by enzyme-linked immunosorbent assay. The migration of microglia was tested by immunofluorescence staining using wound-healing assay. Results Microglia changed from resting state with ramous shape to round shape in activated state after NaVO3·2H2 O exposure, and the expression of Iba1 increased obviously. The protein expressions of iNOS and COX-2 increased significantly compared with the control. The levels of TNF-αand IL-1βwere also increased significantly. NaVO3·2H2 O promotes the migration of microglia through ERK pathway. Conclusions Exposure to NaVO3·2H2 O promotes primary cultured rat microglial inflammation and migration. These results suggest that the inflammatory reaction of microglia may be one of the possible mechanisms of neurotoxicity caused by vanadium exposure.
ABSTRACT
Objective To observe the changes of rat microglial inflammation and migration after exposure to sodium metavanadate(NaVO3·2H2O), and to analyze the possible mechanisms of vanadium neurotoxicity. Methods Primary cultured rat microglial cells were incubated with NaVO3·2H2 O. Morphological changes and the Iba1 expression of microglia were tested by immunofluorescence assay. iNOS, Cox-2, ERK and p-ERK protein expressions were determined by western blotting. The levels of TNF-α and IL-1β in the culture medium were tested by enzyme-linked immunosorbent assay. The migration of microglia was tested by immunofluorescence staining using wound-healing assay. Results Microglia changed from resting state with ramous shape to round shape in activated state after NaVO3·2H2 O exposure, and the expression of Iba1 increased obviously. The protein expressions of iNOS and COX-2 increased significantly compared with the control. The levels of TNF-αand IL-1βwere also increased significantly. NaVO3·2H2 O promotes the migration of microglia through ERK pathway. Conclusions Exposure to NaVO3·2H2 O promotes primary cultured rat microglial inflammation and migration. These results suggest that the inflammatory reaction of microglia may be one of the possible mechanisms of neurotoxicity caused by vanadium exposure.