Procyanidin B2 Activates PPARγ to Induce M2 Polarization in Mouse Macrophages

Tian, Ying; Yang, Chunmiao; Yao, Qinyu; Lei, Qian; Liu, Jia; Xie, Xinya; Ma, Wen; Nie, Xin; Lai, Baochang; Xiao, Lei; Wang, Nanping

doi:10.3389/fimmu.2019.01895

Cited by 49 publications

(32 citation statements)

References 52 publications

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“…Activation of PPAR-γ usually inhibits pro-inflammatory signaling pathways, such as TLR4/NF-κb, JAK/STAT1, etc., thereby inhibiting the gene transcriptional expression of pro-inflammatory cytokines ( Machado et al, 2019 ). On the other hand, activation of PPAR-γ increases the gene transcriptional expression of anti-inflammatory genes ( Lecca et al, 2018 , Tian et al, 2019 ). In this study, we found ASA VI promoted the transcriptional expression of PPAR-γ gene in LPS-treated microglia.…”

Section: Discussionmentioning

confidence: 99%

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

Zhang

Xiao

et al. 2020

Saudi Journal of Biological Sciences

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Microglia cells are the main mediators of neuroinflammation. Activation of microglia often aggravates the pathological process of various neurological diseases. Natural chemicals have unique advantages in inhibiting microglia-mediated neuroinflammation and improving neuronal function. Here, we examined the effects of asperosaponin VI (ASA VI) on LPS-activated primary microglia. Microglia were isolated from mice and pretreated with different doses of ASA VI, following lipopolysaccharide (LPS) administration. Activation and inflammatory response of microglia cells were evaluated by real-time fluorescence quantitative polymerase chain reaction (q-PCR), immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). Signaling pathways were detected by western blotting. We found that the ASA VI inhibited the morphological expansion of microglia cells, decreased the expression and release of proinflammatory cytokines, and promoted the expression of antiinflammatory cytokines in a dose-dependent manner. ASA VI also activated PPAR-γ signaling pathway in LPS-treated microglia. The anti-inflammatory effects of ASA VI in microglia were blocked by treating PPAR-γ antagonist (GW9662). These results showed that ASA VI promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-γ pathway.

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Section: Discussionmentioning

confidence: 99%

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

Zhang

Xiao

et al. 2020

Saudi Journal of Biological Sciences

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“…Meanwhile, the macrophage polarization from M1 phenotype confers protection against development of myocardial ischemia/reperfusion injury [10], though the function of M2 polarization in SCIRI pathology is not well investigated. M2 activation is also characterized by increased levels of M2 macrophage markers (Arg1, Ym1, and Fizz1) [11,12].…”

Section: Introductionmentioning

confidence: 99%

Bone marrow mesenchymal stem cell-derived exosomal microRNA-124-3p attenuates neurological damage in spinal cord ischemia-reperfusion injury by downregulating Ern1 and promoting M2 macrophage polarization

et al. 2020

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Background: Spinal cord ischemia-reperfusion injury (SCIRI) often leads to neurological damage and mortality. In this regard, understanding the pathology of SCIRI and preventing its development are of great clinic value. Methods: Herein, we analyzed the role of bone marrow mesenchymal stem cell (BMMSC)-derived exosomal microRNA (miR)-124-3p in SCIRI. A SCIRI rat model was established, and the expression of Ern1 and M2 macrophage polarization markers (Arg1, Ym1, and Fizz) was determined using immunohistochemistry, immunofluorescence assay, RT-qPCR, and western blot analysis. Targeting relationship between miR-124-3p and Ern1 was predicted using bioinformatic analysis and verified by dual-luciferase reporter assay. Macrophages were co-cultured with miR-124-3p-containing BMMSCderived exosomes. M2 macrophages were identified using flow cytometry, and the expression of Arg1, Ym1, and Fizz was determined. In addition, SCIRI rats were injected with miR-124-3p-containing exosomes, spinal cord cell apoptosis was observed using TUNEL assay, and the pathological condition was evaluated with H&E staining. Results: In SCIRI, Ern1 was highly expressed and M2 polarization markers were poorly expressed. Silencing Ern1 led to elevated expression of M2 polarization markers. MiR-124-3p targeted and negatively regulated Ern1. Exosomal miR-124-3p enhanced M2 polarization. Highly expressed exosomal miR-124-3p impeded cell apoptosis and attenuated SCIRIinduced tissue impairment and nerve injury. miR-124-3p from BMMSC-derived exosomes ameliorated SCIRI and its associated nerve injury through inhibiting Ern1 and promoting M2 polarization. Conclusion: In summary, exosomal miR-124-3p derived from BMMSCs attenuated nerve injury induced by SCIRI by regulating Ern1 and M2 macrophage polarization.

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“…Activation of PPAR-γ usually inhibits pro-inflammatory signaling pathways, such as TLR4/NF-ĸb, JAK/STAT1, etc., thereby inhibiting the gene transcriptional expression of pro-inflammatory cytokines (Machado et al, 2019). On the other hand, activation of PPAR-γ increases the gene transcriptional expression of anti-inflammatory genes (Lecca et al, 2018, Tian et al, 2019. In this study, we found ASA Ⅵ promoted the transcriptional expression of PPAR-γ gene in LPS-treated microglia.…”

Section: Discussionmentioning

confidence: 45%

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

Zhang

Xiao

et al. 2020

Preprint

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Microglia cells are the main mediators of neuroinflammation.Activation of microglia often aggravates the pathological process of various neurological diseases. Natural chemicals have unique advantages in inhibiting microglia-mediated neuroinflammation and improving neuronal function. Here, we examined the effects of asperosaponin Ⅵ (ASA Ⅵ) on LPS-activated primary microglia. Microglia were isolated from mice and pretreated with different doses of ASA Ⅵ, following lipopolysaccharide (LPS) administration. Activation and inflammatory response of microglia cells were evaluated by q-PCR, immunohistochemistry and ELISA. Signaling pathways were detected by western blotting. We found that the ASA Ⅵ inhibited the morphological expansion of microglia cells, decreased the expression and release of proinflammatory cytokines, and promoted the expression of antiinflammatory cytokines in a dose-dependent manner. ASA Ⅵ also activated PPAR-γ signaling pathway in LPS-treated microglia. The anti-inflammatory effects of ASA Ⅵ in microglia were blocked by treating PPAR-γ antagonist (GW9662). These results showed that ASA Ⅵ promote the transition of microglia cells from proinflammatory to anti-inflammatory by regulating PPAR-γ pathway.

show abstract

Procyanidin B2 Activates PPARγ to Induce M2 Polarization in Mouse Macrophages

Cited by 49 publications

References 52 publications

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

Bone marrow mesenchymal stem cell-derived exosomal microRNA-124-3p attenuates neurological damage in spinal cord ischemia-reperfusion injury by downregulating Ern1 and promoting M2 macrophage polarization

Asperosaponin VI inhibits LPS-induced inflammatory response by activating PPAR-γ pathway in primary microglia

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