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Salidroside Reduces Cell Mobility via NF- κ B and MAPK Signaling in LPS-Induced BV2 Microglial Cells.

Hu H, Li Z, Zhu X, Lin R, Chen L - Evid Based Complement Alternat Med (2014)

Bottom Line: Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells.Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF- κ B) by blocking degradation of I κ B α and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression.These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

View Article: PubMed Central - PubMed

Affiliation: Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China ; Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China.

ABSTRACT
The unregulated activation of microglia following stroke results in the production of toxic factors that propagate secondary neuronal injury. Salidroside has been shown to exhibit protective effects against neuronal death induced by different insults. However, the molecular mechanisms responsible for the anti-inflammatory activity of salidroside have not been elucidated clearly in microglia. In the present study, we investigated the molecular mechanism underlying inhibiting LPS-stimulated BV2 microglial cell mobility of salidroside. The protective effect of salidroside was investigated in microglial BV2 cell, subjected to stretch injury. Moreover, transwell migration assay demonstrated that salidroside significantly reduced cell motility. Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells. Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF- κ B) by blocking degradation of I κ B α and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression. These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

No MeSH data available.


Related in: MedlinePlus

Salidroside does not affect cell viability of BV2 microglial cells. Cytotoxic effect of salidroside on cultured BV2 cell exposure to LPS. BV2 cells were treated with LPS in the presence and absence of salidroside at the concentration of 75, 150, and 300 μM for 24 h. The cell viability was expressed as the percentage of surviving cells compared with control cells by using MTT assay. The data are presented as means ± SD of three independent experiments (n = 3).
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fig1: Salidroside does not affect cell viability of BV2 microglial cells. Cytotoxic effect of salidroside on cultured BV2 cell exposure to LPS. BV2 cells were treated with LPS in the presence and absence of salidroside at the concentration of 75, 150, and 300 μM for 24 h. The cell viability was expressed as the percentage of surviving cells compared with control cells by using MTT assay. The data are presented as means ± SD of three independent experiments (n = 3).

Mentions: MTT assay was used to determine the cytotoxic potential of salidroside on the viability of BV2 microglial cells. After treatment with LPS (1 μg/mL) in the presence or absence of salidroside at various concentrations (75–300 μM) for 24 h, salidroside at different concentrations alone caused no apparent cytotoxicity on cultured BV2 cells. Furthermore, salidroside in the presence of LPS also indicated no cytotoxic effects on BV2 cells (Figure 1). Therefore, salidroside levels at the concentration of 75, 150, and 300 μM were chosen for protecting BV2 cells in all subsequent experiments unless otherwise stated.


Salidroside Reduces Cell Mobility via NF- κ B and MAPK Signaling in LPS-Induced BV2 Microglial Cells.

Hu H, Li Z, Zhu X, Lin R, Chen L - Evid Based Complement Alternat Med (2014)

Salidroside does not affect cell viability of BV2 microglial cells. Cytotoxic effect of salidroside on cultured BV2 cell exposure to LPS. BV2 cells were treated with LPS in the presence and absence of salidroside at the concentration of 75, 150, and 300 μM for 24 h. The cell viability was expressed as the percentage of surviving cells compared with control cells by using MTT assay. The data are presented as means ± SD of three independent experiments (n = 3).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4016849&req=5

fig1: Salidroside does not affect cell viability of BV2 microglial cells. Cytotoxic effect of salidroside on cultured BV2 cell exposure to LPS. BV2 cells were treated with LPS in the presence and absence of salidroside at the concentration of 75, 150, and 300 μM for 24 h. The cell viability was expressed as the percentage of surviving cells compared with control cells by using MTT assay. The data are presented as means ± SD of three independent experiments (n = 3).
Mentions: MTT assay was used to determine the cytotoxic potential of salidroside on the viability of BV2 microglial cells. After treatment with LPS (1 μg/mL) in the presence or absence of salidroside at various concentrations (75–300 μM) for 24 h, salidroside at different concentrations alone caused no apparent cytotoxicity on cultured BV2 cells. Furthermore, salidroside in the presence of LPS also indicated no cytotoxic effects on BV2 cells (Figure 1). Therefore, salidroside levels at the concentration of 75, 150, and 300 μM were chosen for protecting BV2 cells in all subsequent experiments unless otherwise stated.

Bottom Line: Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells.Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF- κ B) by blocking degradation of I κ B α and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression.These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

View Article: PubMed Central - PubMed

Affiliation: Academy of Integrative Medicine Biomedical Research Center, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China ; Fujian Key Laboratory of Integrative Medicine on Geriatrics, Fujian University of Traditional Chinese Medicine, Huatuo Road, Minhou Shangjie, Fuzhou, Fujian 350108, China.

ABSTRACT
The unregulated activation of microglia following stroke results in the production of toxic factors that propagate secondary neuronal injury. Salidroside has been shown to exhibit protective effects against neuronal death induced by different insults. However, the molecular mechanisms responsible for the anti-inflammatory activity of salidroside have not been elucidated clearly in microglia. In the present study, we investigated the molecular mechanism underlying inhibiting LPS-stimulated BV2 microglial cell mobility of salidroside. The protective effect of salidroside was investigated in microglial BV2 cell, subjected to stretch injury. Moreover, transwell migration assay demonstrated that salidroside significantly reduced cell motility. Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells. Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF- κ B) by blocking degradation of I κ B α and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression. These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

No MeSH data available.


Related in: MedlinePlus