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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

The NF-κB and MAPK pathway were involved in the cell motility suppression of salidroside in LPS-induced BV2 cells. Cells were treated with LPS and salidroside at indicated concentrations and time. The protein level relating to NF-κB and MAPK pathway was measured by Western-blotting analysis. The representative image was from one of three repeated experiments. Expression of all proteins was quantified by densitometry analysis. Data were shown as the mean ± SD. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05 versus LPS group.
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fig5: The NF-κB and MAPK pathway were involved in the cell motility suppression of salidroside in LPS-induced BV2 cells. Cells were treated with LPS and salidroside at indicated concentrations and time. The protein level relating to NF-κB and MAPK pathway was measured by Western-blotting analysis. The representative image was from one of three repeated experiments. Expression of all proteins was quantified by densitometry analysis. Data were shown as the mean ± SD. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05 versus LPS group.

Mentions: In order to investigate the mechanism underlying the inhibitory effect of salidroside, we used LPS to activate NF-κB and MAPK pathway measured by Western-blotting assay. The results showed significant increases in the degradation of IκBα and phosphorylation of p65, IκBα, P38, JNK, and ERK1/2 in the LPS-treated group as compared to the control group, whereas treatment with salidroside at indicated concentrations exhibited significant reduction of IκBα degradation and all the phosphorylated protein expression in a dose-dependent pattern (Figure 5). The measurement revealed that salidroside attenuates the LPS-induced BV2 cell activation, perhaps partly, by blocking the NF-κB and MAPK signaling simultaneously.


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)

The NF-κB and MAPK pathway were involved in the cell motility suppression of salidroside in LPS-induced BV2 cells. Cells were treated with LPS and salidroside at indicated concentrations and time. The protein level relating to NF-κB and MAPK pathway was measured by Western-blotting analysis. The representative image was from one of three repeated experiments. Expression of all proteins was quantified by densitometry analysis. Data were shown as the mean ± SD. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05 versus LPS group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig5: The NF-κB and MAPK pathway were involved in the cell motility suppression of salidroside in LPS-induced BV2 cells. Cells were treated with LPS and salidroside at indicated concentrations and time. The protein level relating to NF-κB and MAPK pathway was measured by Western-blotting analysis. The representative image was from one of three repeated experiments. Expression of all proteins was quantified by densitometry analysis. Data were shown as the mean ± SD. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05 versus LPS group.
Mentions: In order to investigate the mechanism underlying the inhibitory effect of salidroside, we used LPS to activate NF-κB and MAPK pathway measured by Western-blotting assay. The results showed significant increases in the degradation of IκBα and phosphorylation of p65, IκBα, P38, JNK, and ERK1/2 in the LPS-treated group as compared to the control group, whereas treatment with salidroside at indicated concentrations exhibited significant reduction of IκBα degradation and all the phosphorylated protein expression in a dose-dependent pattern (Figure 5). The measurement revealed that salidroside attenuates the LPS-induced BV2 cell activation, perhaps partly, by blocking the NF-κB and MAPK signaling simultaneously.

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