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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 suppresses LPS-induced chemokine production in BV2 microglial cells. Cells were incubated with salidroside at various concentrations and/or LPS for 12 h. The amounts of MCP-1, MIP-1α, and IL-8 production in the supernatant were measured using ELISA. The OD values are the mean ± SD of three separate experiments. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05, **P < 0.01 versus LPS group.
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fig3: Salidroside suppresses LPS-induced chemokine production in BV2 microglial cells. Cells were incubated with salidroside at various concentrations and/or LPS for 12 h. The amounts of MCP-1, MIP-1α, and IL-8 production in the supernatant were measured using ELISA. The OD values are the mean ± SD of three separate experiments. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05, **P < 0.01 versus LPS group.

Mentions: ELISA and RT-PCR assay was carried out to examine the effects of salidroside on protein and mRNA expressions of chemokines in LPS-induced BV2 cells after 12 h. We selected three chemokines that are associated with cell migration such as MCP-1, MIP-1α, and IL-8. As seen in Figure 3, BV2 cells subjected to LPS for 12 h at 1 μg/mL presented significant higher chemokine secretion than those in the control group; however, all concentrations of salidroside at 75, 150, and 300 μM treatments reduced the protein expression significantly in a dose-dependent manner, as assessed by ELISA technique.


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 suppresses LPS-induced chemokine production in BV2 microglial cells. Cells were incubated with salidroside at various concentrations and/or LPS for 12 h. The amounts of MCP-1, MIP-1α, and IL-8 production in the supernatant were measured using ELISA. The OD values are the mean ± SD of three separate experiments. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05, **P < 0.01 versus LPS group.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig3: Salidroside suppresses LPS-induced chemokine production in BV2 microglial cells. Cells were incubated with salidroside at various concentrations and/or LPS for 12 h. The amounts of MCP-1, MIP-1α, and IL-8 production in the supernatant were measured using ELISA. The OD values are the mean ± SD of three separate experiments. #P < 0.05, ##P < 0.01 versus the control group; *P < 0.05, **P < 0.01 versus LPS group.
Mentions: ELISA and RT-PCR assay was carried out to examine the effects of salidroside on protein and mRNA expressions of chemokines in LPS-induced BV2 cells after 12 h. We selected three chemokines that are associated with cell migration such as MCP-1, MIP-1α, and IL-8. As seen in Figure 3, BV2 cells subjected to LPS for 12 h at 1 μg/mL presented significant higher chemokine secretion than those in the control group; however, all concentrations of salidroside at 75, 150, and 300 μM treatments reduced the protein expression significantly in a dose-dependent manner, as assessed by ELISA technique.

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