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Resveratrol induces the expression of interleukin-10 and brain-derived neurotrophic factor in BV2 microglia under hypoxia.

Song J, Cheon SY, Jung W, Lee WT, Lee JE - Int J Mol Sci (2014)

Bottom Line: However, overactivation of microglia leads to neuronal death that is associated with CNS disorders.In the present study, we investigated the beneficial effect of resveratrol, a natural phenol with antioxidant effects, in the microglial cell line, BV2, in a model of hypoxia injury.Overall, resveratrol may promote the beneficial function of microglia in ischemic brain injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea. sjh1008@yuhs.ac.

ABSTRACT
Microglia are the resident macrophages of the central nervous system (CNS) and play an important role in neuronal recovery by scavenging damaged neurons. However, overactivation of microglia leads to neuronal death that is associated with CNS disorders. Therefore, regulation of microglial activation has been suggested to be an important target for treatment of CNS diseases. In the present study, we investigated the beneficial effect of resveratrol, a natural phenol with antioxidant effects, in the microglial cell line, BV2, in a model of hypoxia injury. Resveratrol suppressed the mRNA expression of the pro-inflammatory molecule, tumor necrosis factor-α, and promoted the mRNA expression of the anti-inflammatory molecule, interleukin-10, in BV2 microglia under hypoxic conditions. In addition, resveratrol inhibited the activation of the transcription factor, nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB), which is upstream in the control of inflammatory reactions in hypoxia-injured BV2 microglia. Moreover, resveratrol promoted the expression of brain-derived neurotrophic factor (BDNF) in BV2 microglia under hypoxic stress. Overall, resveratrol may promote the beneficial function of microglia in ischemic brain injury.

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The expression of Iba-1in hypoxia-injured BV2 microglia. (A) The level of Iba-1 (a marker of activated microglia) was evaluated by immunocytochemistry. This image shows that the expression of Iba-1 in the hypoxia group exposed to hypoxia was increased compared to the control group (no hypoxia). The resveratrol (25 μM) pre-treatment group (Hypoxia + Resv) showed a decreaseof Iba-1 expression compared with the hypoxia group. Resveratrol (25 μM) decreased the activation of microglia under hypoxic conditions; (B) Western blotting data showed that the protein level of Iba-1 was increased in the hypoxia group compared to the control group. Resveratrol (25 μM) decreased the protein level of Iba-1 in BV2 microglia under hypoxic conditions. β-actin was used as an internal, loading control (mean ± S.E.M., n = 3).**p < 0.01 (compared to the hypoxia group). Control: normal control group, Hypoxia: hypoxia injury group for 4 h, Resv: resveratrol (25 μM) treatment group under normal condition, Hypoxia + Resv: resveratrol (25 μM) pre-treatment before 4 h hypoxia injury, Res (25 μM): 25 μM resveratrol pre-treatment for 3 h. 4',6-diamidino-2-phenylindole (DAPI): blue, Ionized calcium binding adaptor molecule 1 (Iba-1): green, Scale bar: 200 µm.
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ijms-15-15512-f002: The expression of Iba-1in hypoxia-injured BV2 microglia. (A) The level of Iba-1 (a marker of activated microglia) was evaluated by immunocytochemistry. This image shows that the expression of Iba-1 in the hypoxia group exposed to hypoxia was increased compared to the control group (no hypoxia). The resveratrol (25 μM) pre-treatment group (Hypoxia + Resv) showed a decreaseof Iba-1 expression compared with the hypoxia group. Resveratrol (25 μM) decreased the activation of microglia under hypoxic conditions; (B) Western blotting data showed that the protein level of Iba-1 was increased in the hypoxia group compared to the control group. Resveratrol (25 μM) decreased the protein level of Iba-1 in BV2 microglia under hypoxic conditions. β-actin was used as an internal, loading control (mean ± S.E.M., n = 3).**p < 0.01 (compared to the hypoxia group). Control: normal control group, Hypoxia: hypoxia injury group for 4 h, Resv: resveratrol (25 μM) treatment group under normal condition, Hypoxia + Resv: resveratrol (25 μM) pre-treatment before 4 h hypoxia injury, Res (25 μM): 25 μM resveratrol pre-treatment for 3 h. 4',6-diamidino-2-phenylindole (DAPI): blue, Ionized calcium binding adaptor molecule 1 (Iba-1): green, Scale bar: 200 µm.

Mentions: To examine the activation of microglia, we conducted immunochemical analysis using a marker of activated microglia (ionized calcium binding adaptor molecule 1 (Iba-1)) in all groups. The expression of Iba-1 was increased in the hypoxia group compared to the control group (no hypoxia) (Figure 2A). Resveratrol (25 μM) reduced the activation of microglia compared to the hypoxia group in spite of hypoxic injury (Figure 2A). In addition, to confirm the protein level of Iba-1, we performed western blotting in all groups. The protein level of Iba-1 was greatly increased in the hypoxia injury group compared with the control group (Figure 2B). In hypoxic stress, resveratrol (25 μM) attenuated the protein levels of Iba-1 in BV2 microglia compared to the hypoxia group (Figure 2B).


Resveratrol induces the expression of interleukin-10 and brain-derived neurotrophic factor in BV2 microglia under hypoxia.

Song J, Cheon SY, Jung W, Lee WT, Lee JE - Int J Mol Sci (2014)

The expression of Iba-1in hypoxia-injured BV2 microglia. (A) The level of Iba-1 (a marker of activated microglia) was evaluated by immunocytochemistry. This image shows that the expression of Iba-1 in the hypoxia group exposed to hypoxia was increased compared to the control group (no hypoxia). The resveratrol (25 μM) pre-treatment group (Hypoxia + Resv) showed a decreaseof Iba-1 expression compared with the hypoxia group. Resveratrol (25 μM) decreased the activation of microglia under hypoxic conditions; (B) Western blotting data showed that the protein level of Iba-1 was increased in the hypoxia group compared to the control group. Resveratrol (25 μM) decreased the protein level of Iba-1 in BV2 microglia under hypoxic conditions. β-actin was used as an internal, loading control (mean ± S.E.M., n = 3).**p < 0.01 (compared to the hypoxia group). Control: normal control group, Hypoxia: hypoxia injury group for 4 h, Resv: resveratrol (25 μM) treatment group under normal condition, Hypoxia + Resv: resveratrol (25 μM) pre-treatment before 4 h hypoxia injury, Res (25 μM): 25 μM resveratrol pre-treatment for 3 h. 4',6-diamidino-2-phenylindole (DAPI): blue, Ionized calcium binding adaptor molecule 1 (Iba-1): green, Scale bar: 200 µm.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4200860&req=5

ijms-15-15512-f002: The expression of Iba-1in hypoxia-injured BV2 microglia. (A) The level of Iba-1 (a marker of activated microglia) was evaluated by immunocytochemistry. This image shows that the expression of Iba-1 in the hypoxia group exposed to hypoxia was increased compared to the control group (no hypoxia). The resveratrol (25 μM) pre-treatment group (Hypoxia + Resv) showed a decreaseof Iba-1 expression compared with the hypoxia group. Resveratrol (25 μM) decreased the activation of microglia under hypoxic conditions; (B) Western blotting data showed that the protein level of Iba-1 was increased in the hypoxia group compared to the control group. Resveratrol (25 μM) decreased the protein level of Iba-1 in BV2 microglia under hypoxic conditions. β-actin was used as an internal, loading control (mean ± S.E.M., n = 3).**p < 0.01 (compared to the hypoxia group). Control: normal control group, Hypoxia: hypoxia injury group for 4 h, Resv: resveratrol (25 μM) treatment group under normal condition, Hypoxia + Resv: resveratrol (25 μM) pre-treatment before 4 h hypoxia injury, Res (25 μM): 25 μM resveratrol pre-treatment for 3 h. 4',6-diamidino-2-phenylindole (DAPI): blue, Ionized calcium binding adaptor molecule 1 (Iba-1): green, Scale bar: 200 µm.
Mentions: To examine the activation of microglia, we conducted immunochemical analysis using a marker of activated microglia (ionized calcium binding adaptor molecule 1 (Iba-1)) in all groups. The expression of Iba-1 was increased in the hypoxia group compared to the control group (no hypoxia) (Figure 2A). Resveratrol (25 μM) reduced the activation of microglia compared to the hypoxia group in spite of hypoxic injury (Figure 2A). In addition, to confirm the protein level of Iba-1, we performed western blotting in all groups. The protein level of Iba-1 was greatly increased in the hypoxia injury group compared with the control group (Figure 2B). In hypoxic stress, resveratrol (25 μM) attenuated the protein levels of Iba-1 in BV2 microglia compared to the hypoxia group (Figure 2B).

Bottom Line: However, overactivation of microglia leads to neuronal death that is associated with CNS disorders.In the present study, we investigated the beneficial effect of resveratrol, a natural phenol with antioxidant effects, in the microglial cell line, BV2, in a model of hypoxia injury.Overall, resveratrol may promote the beneficial function of microglia in ischemic brain injury.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy, Yonsei University College of Medicine, Seoul 120-752, Korea. sjh1008@yuhs.ac.

ABSTRACT
Microglia are the resident macrophages of the central nervous system (CNS) and play an important role in neuronal recovery by scavenging damaged neurons. However, overactivation of microglia leads to neuronal death that is associated with CNS disorders. Therefore, regulation of microglial activation has been suggested to be an important target for treatment of CNS diseases. In the present study, we investigated the beneficial effect of resveratrol, a natural phenol with antioxidant effects, in the microglial cell line, BV2, in a model of hypoxia injury. Resveratrol suppressed the mRNA expression of the pro-inflammatory molecule, tumor necrosis factor-α, and promoted the mRNA expression of the anti-inflammatory molecule, interleukin-10, in BV2 microglia under hypoxic conditions. In addition, resveratrol inhibited the activation of the transcription factor, nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB), which is upstream in the control of inflammatory reactions in hypoxia-injured BV2 microglia. Moreover, resveratrol promoted the expression of brain-derived neurotrophic factor (BDNF) in BV2 microglia under hypoxic stress. Overall, resveratrol may promote the beneficial function of microglia in ischemic brain injury.

Show MeSH
Related in: MedlinePlus