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Qingkailing Suppresses the Activation of BV2 Microglial Cells by Inhibiting Hypoxia/Reoxygenation-Induced Inflammatory Responses.

Mana L, Wang S, Zhu H, Xing Y, Lou L, Wu A, Dong B, Sun Y, Yang S, Wang L, Gao Y - Evid Based Complement Alternat Med (2014)

Bottom Line: Our previous experiments confirmed that QKL exerts an inhibitory effect on cerebral ischemia-induced inflammatory responses.In this study, BV2 microglial cells were used to validate the protective effects of QKL treatment following ischemia-reperfusion injury simulated via hypoxia/reoxygenation in vitro.However, QKL treatment also displayed dose-dependent differences in its inhibitory effects on p38 phosphorylation and inflammatory factor expression.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

ABSTRACT
Qingkailing (QKL) is a well-known composite extract used in traditional Chinese medicine. This extract has been extensively administered to treat the acute phase of cerebrovascular disease. Our previous experiments confirmed that QKL exerts an inhibitory effect on cerebral ischemia-induced inflammatory responses. However, whether QKL suppresses the activation of microglia, the primary resident immune cells in the brain, has yet to be determined. In this study, BV2 microglial cells were used to validate the protective effects of QKL treatment following ischemia-reperfusion injury simulated via hypoxia/reoxygenation in vitro. Under these conditions, high expression levels of ROS, COX-2, iNOS, and p-p38 protein were detected. Following ischemia/reperfusion injury, QKL significantly increased the activity of BV2 cells to approximately the basal level by modulating microglial activation via inhibition of inflammatory factors, including TNF- α , COX-2, iNOS, and p-p38. However, QKL treatment also displayed dose-dependent differences in its inhibitory effects on p38 phosphorylation and inflammatory factor expression.

No MeSH data available.


Related in: MedlinePlus

Effects of different dosages of QKL on the viability of BV2 microglial cells in the hypoxia/reoxygenation model. The cells were treated with 0.0625%, 0.125%, or 0.25% QKL or 200 μM minocycline before hypoxia. The MTT method was performed, and the results are expressed as the means ± SD; n = 6.  ##P < 0.01 compared to the control group; **P < 0.01 compared to the model group.
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fig2: Effects of different dosages of QKL on the viability of BV2 microglial cells in the hypoxia/reoxygenation model. The cells were treated with 0.0625%, 0.125%, or 0.25% QKL or 200 μM minocycline before hypoxia. The MTT method was performed, and the results are expressed as the means ± SD; n = 6.  ##P < 0.01 compared to the control group; **P < 0.01 compared to the model group.

Mentions: Based on the model establishment above, according to the results of pilot experiments, the nontoxic dose range of QKL treatment was chosen to be 0.0625%, 0.125%, and 0.25% (Figure 2). Alternatively, 200 nmol/L minocycline, the specific inhibitor of microglia, was applied prior to hypoxia. The results revealed that the A value of the cells treated with any of the three concentrations of QKL or minocycline, which were exposed to hypoxia for 12 h and reoxygenation for 12 h, was significantly higher than the model group. This result confirmed that QKL remarkably increases BV2 cell survival and activation under ischemia-reperfusion conditions, reverting them to control levels, preventing both the activation and injury of BV2 cells.


Qingkailing Suppresses the Activation of BV2 Microglial Cells by Inhibiting Hypoxia/Reoxygenation-Induced Inflammatory Responses.

Mana L, Wang S, Zhu H, Xing Y, Lou L, Wu A, Dong B, Sun Y, Yang S, Wang L, Gao Y - Evid Based Complement Alternat Med (2014)

Effects of different dosages of QKL on the viability of BV2 microglial cells in the hypoxia/reoxygenation model. The cells were treated with 0.0625%, 0.125%, or 0.25% QKL or 200 μM minocycline before hypoxia. The MTT method was performed, and the results are expressed as the means ± SD; n = 6.  ##P < 0.01 compared to the control group; **P < 0.01 compared to the model group.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020462&req=5

fig2: Effects of different dosages of QKL on the viability of BV2 microglial cells in the hypoxia/reoxygenation model. The cells were treated with 0.0625%, 0.125%, or 0.25% QKL or 200 μM minocycline before hypoxia. The MTT method was performed, and the results are expressed as the means ± SD; n = 6.  ##P < 0.01 compared to the control group; **P < 0.01 compared to the model group.
Mentions: Based on the model establishment above, according to the results of pilot experiments, the nontoxic dose range of QKL treatment was chosen to be 0.0625%, 0.125%, and 0.25% (Figure 2). Alternatively, 200 nmol/L minocycline, the specific inhibitor of microglia, was applied prior to hypoxia. The results revealed that the A value of the cells treated with any of the three concentrations of QKL or minocycline, which were exposed to hypoxia for 12 h and reoxygenation for 12 h, was significantly higher than the model group. This result confirmed that QKL remarkably increases BV2 cell survival and activation under ischemia-reperfusion conditions, reverting them to control levels, preventing both the activation and injury of BV2 cells.

Bottom Line: Our previous experiments confirmed that QKL exerts an inhibitory effect on cerebral ischemia-induced inflammatory responses.In this study, BV2 microglial cells were used to validate the protective effects of QKL treatment following ischemia-reperfusion injury simulated via hypoxia/reoxygenation in vitro.However, QKL treatment also displayed dose-dependent differences in its inhibitory effects on p38 phosphorylation and inflammatory factor expression.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Chinese Internal Medicine of Ministry of Education and Beijing, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100700, China.

ABSTRACT
Qingkailing (QKL) is a well-known composite extract used in traditional Chinese medicine. This extract has been extensively administered to treat the acute phase of cerebrovascular disease. Our previous experiments confirmed that QKL exerts an inhibitory effect on cerebral ischemia-induced inflammatory responses. However, whether QKL suppresses the activation of microglia, the primary resident immune cells in the brain, has yet to be determined. In this study, BV2 microglial cells were used to validate the protective effects of QKL treatment following ischemia-reperfusion injury simulated via hypoxia/reoxygenation in vitro. Under these conditions, high expression levels of ROS, COX-2, iNOS, and p-p38 protein were detected. Following ischemia/reperfusion injury, QKL significantly increased the activity of BV2 cells to approximately the basal level by modulating microglial activation via inhibition of inflammatory factors, including TNF- α , COX-2, iNOS, and p-p38. However, QKL treatment also displayed dose-dependent differences in its inhibitory effects on p38 phosphorylation and inflammatory factor expression.

No MeSH data available.


Related in: MedlinePlus