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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 exhibits antimigratory property in BV2 microglial cells. ((a), (b)) The wound scratch assay was carried out to analyze motility of LPS-activated BV2 cells. Representative phase contrast images show the width of scratch captured at 12 h after scraping. The cell migration distances were determined with the ratios of wound closure. ((c), (d)) Determination of BV2 cell migration by transwell migration assay. Cells were fixed, stained, and examined microscopically in five random fields at 100x magnification after 24 h treatment and then were harvested and read with microplate reader. Absorbance correlating with the number of cells invaded expressed as mean ± SD (n = 3). #P < 0.05 versus the control group; *P < 0.05 versus LPS group.
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fig2: Salidroside exhibits antimigratory property in BV2 microglial cells. ((a), (b)) The wound scratch assay was carried out to analyze motility of LPS-activated BV2 cells. Representative phase contrast images show the width of scratch captured at 12 h after scraping. The cell migration distances were determined with the ratios of wound closure. ((c), (d)) Determination of BV2 cell migration by transwell migration assay. Cells were fixed, stained, and examined microscopically in five random fields at 100x magnification after 24 h treatment and then were harvested and read with microplate reader. Absorbance correlating with the number of cells invaded expressed as mean ± SD (n = 3). #P < 0.05 versus the control group; *P < 0.05 versus LPS group.

Mentions: Scratch wounds were inflicted on cells treated by LPS alone or with salidroside for 12 h. In this study, we set out to deserve closure of the wound which depends on cell migration from the scratched edge to determine whether salidroside affects the migration potential in LPS-induced BV2 cell line. The difference of surface area generated by the wound between the groups was observed after 12 h of treatment (Figure 2(a)). We observed that there were few cell migrations in the control group, which made no influence on microglial migration, while LPS group exhibited highly BV2 cell migratory potential, which was significantly reduced by salidroside (150 μM) (Figure 2(b)).


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 exhibits antimigratory property in BV2 microglial cells. ((a), (b)) The wound scratch assay was carried out to analyze motility of LPS-activated BV2 cells. Representative phase contrast images show the width of scratch captured at 12 h after scraping. The cell migration distances were determined with the ratios of wound closure. ((c), (d)) Determination of BV2 cell migration by transwell migration assay. Cells were fixed, stained, and examined microscopically in five random fields at 100x magnification after 24 h treatment and then were harvested and read with microplate reader. Absorbance correlating with the number of cells invaded expressed as mean ± SD (n = 3). #P < 0.05 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

fig2: Salidroside exhibits antimigratory property in BV2 microglial cells. ((a), (b)) The wound scratch assay was carried out to analyze motility of LPS-activated BV2 cells. Representative phase contrast images show the width of scratch captured at 12 h after scraping. The cell migration distances were determined with the ratios of wound closure. ((c), (d)) Determination of BV2 cell migration by transwell migration assay. Cells were fixed, stained, and examined microscopically in five random fields at 100x magnification after 24 h treatment and then were harvested and read with microplate reader. Absorbance correlating with the number of cells invaded expressed as mean ± SD (n = 3). #P < 0.05 versus the control group; *P < 0.05 versus LPS group.
Mentions: Scratch wounds were inflicted on cells treated by LPS alone or with salidroside for 12 h. In this study, we set out to deserve closure of the wound which depends on cell migration from the scratched edge to determine whether salidroside affects the migration potential in LPS-induced BV2 cell line. The difference of surface area generated by the wound between the groups was observed after 12 h of treatment (Figure 2(a)). We observed that there were few cell migrations in the control group, which made no influence on microglial migration, while LPS group exhibited highly BV2 cell migratory potential, which was significantly reduced by salidroside (150 μM) (Figure 2(b)).

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