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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

Effect of QKL on p38 phosphorylation in BV2 microglial cells exposed to hypoxia/reoxygenation. (a) Western blot was performed on the cell lysates using anti-p-p38 and anti-p38 antibodies. (b) The differences in the protein expression levels between the groups were analyzed using Image J software. ##P < 0.01 compared to the control group. **P < 0.01 compared to the model group.
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fig5: Effect of QKL on p38 phosphorylation in BV2 microglial cells exposed to hypoxia/reoxygenation. (a) Western blot was performed on the cell lysates using anti-p-p38 and anti-p38 antibodies. (b) The differences in the protein expression levels between the groups were analyzed using Image J software. ##P < 0.01 compared to the control group. **P < 0.01 compared to the model group.

Mentions: To further elucidate whether the p38 signaling pathway affects the expression of iNOS and COX2 in BV2 cells, we measured the expression of phosphorylated p38 protein and analyzed the ratio of p-p38 to p38. As shown in Figure 5, the control group expressed a small amount of p-p38 protein, and p-38 expression was significantly increased in the model group. Treatment with 0.0625% QKL or 200 nmol/L minocycline significantly decreased p-p38 protein expression in BV2 cells subjected to hypoxia/reoxygenation compared to the model group (P < 0.01).


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)

Effect of QKL on p38 phosphorylation in BV2 microglial cells exposed to hypoxia/reoxygenation. (a) Western blot was performed on the cell lysates using anti-p-p38 and anti-p38 antibodies. (b) The differences in the protein expression levels between the groups were analyzed using Image J software. ##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

fig5: Effect of QKL on p38 phosphorylation in BV2 microglial cells exposed to hypoxia/reoxygenation. (a) Western blot was performed on the cell lysates using anti-p-p38 and anti-p38 antibodies. (b) The differences in the protein expression levels between the groups were analyzed using Image J software. ##P < 0.01 compared to the control group. **P < 0.01 compared to the model group.
Mentions: To further elucidate whether the p38 signaling pathway affects the expression of iNOS and COX2 in BV2 cells, we measured the expression of phosphorylated p38 protein and analyzed the ratio of p-p38 to p38. As shown in Figure 5, the control group expressed a small amount of p-p38 protein, and p-38 expression was significantly increased in the model group. Treatment with 0.0625% QKL or 200 nmol/L minocycline significantly decreased p-p38 protein expression in BV2 cells subjected to hypoxia/reoxygenation compared to the model group (P < 0.01).

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