Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

Tsai, Cheng-Fang; Chen, Guan‐Wei; Chen, Yen-Chang; Shen, Ching-Kai; Lu, Dah‐Yuu; Yang, Liang-Yo; Chen, Jiahong; Yeh, Wei-Lan

doi:10.3390/nu14010067

Cited by 138 publications

(82 citation statements)

References 101 publications

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“…There are many studies on the regulation of M2 polarization of microglia by AMPK pathway. The enhanced effect of quercetin on M2 markers and endogenous antioxidants is activated by amp activated protein kinase (AMPK) and Akt signaling pathway [43]. Salidroside regulates the polarization of microglia to M2 type through AMPK -/ mTOR mediated autophagy ux, so as to reduce neuroin ammation and improve functional recovery after spinal cord injury [44].…”

Section: Discussionmentioning

confidence: 99%

PD-L1/PD-L2 deficiency alters numbers and types of microglia and transcriptomic landscape of neural retina

Sheng

Zou

et al. 2022

Preprint

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Background To investigate the effects of PD-1 ligands signaling pathway on microglia and transcriptomic expression and function of neural retina. Methods PD-L1/PD-L2 deficient mice were generated by Cyagen Biosciences Inc. (Suzhou, China). We performed quantitative and qualitative analyses of retinal microglia using mouse retinal western blotting and immunofluorescence experiments. The transcriptomic sequencing of neural retina was performed and analyzed by OE Biotech Co. Ltd. (Shanghai, China). The morphology of neural retina in PD-L1/PD-L2 deficient mice was evaluated using haematoxylin and eosin (HE) staining and in vivo optical coherence tomography (OCT). The visual evoked potential (VEP) test and measuring the photo negative response (PhNR) test assist in approaching changes in visual function in mice. Results PD-L1/PD-L2 deficiency decreased the total number of retinal microglia in neural retina. The activated microglia (M2 microglia) was increased in PD-L1/PD-L2 deficient mice, accompanied by increased STAT6 pathway activation. Transcriptome sequencing and analysis revealed the activation of the PI3K-Akt and MAPK signalling pathways in neural retina of PD-L1/PD-L2 knockout mice. The PD-L1/PD-L2 deficiency did not impact on the morphology and visual function of the neural retina. Conclusions PD-L1/PD-L2 deficiency alters numbers and types of microglia and transcriptomic landscape of neural retina.

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Section: Discussionmentioning

confidence: 99%

PD-L1/PD-L2 deficiency alters numbers and types of microglia and transcriptomic landscape of neural retina

Sheng

Zou

et al. 2022

Preprint

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“…By scavenging ROS, quercetin-loaded ceria nanocomposite can also increase the M2/M1 ratio of macrophage polarization in periodontal inflammation models (241). Besides, quercetin has been suggested to suppress the expression of iNOS and COX-2, as well as the secretion of IL-6, TNF-a, and IL-1b of M1 macrophages with the decrease in ROS and chemokines related to M1 polarization, including CCL2 and CXCL10, while IL-10 of M2 macrophages has been found up-regulated, with the increase in HO-1 and NQO1 via AMPK and AKT signaling pathways (242). Notably, potential mechanisms underlying the effects of quercetin in the immunoregulation of macrophages can also involve the inhibitive effects on the activity of NLRP3 inflammasome via TLR2/Myd88/NF-kB and ROS/AMPK pathway (243).…”

Section: Quercetinmentioning

confidence: 99%

Nrf2-mediated anti-inflammatory polarization of macrophages as therapeutic targets for osteoarthritis

Wang

2022

Front. Immunol.

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Macrophages are the most abundant immune cells within the synovial joints, and also the main innate immune effector cells triggering the initial inflammatory responses in the pathological process of osteoarthritis (OA). The transition of synovial macrophages between pro-inflammatory and anti-inflammatory phenotypes can play a key role in building the intra-articular microenvironment. The pro-inflammatory cascade induced by TNF-α, IL-1β, and IL-6 is closely related to M1 macrophages, resulting in the production of pro-chondrolytic mediators. However, IL-10, IL1RA, CCL-18, IGF, and TGF are closely related to M2 macrophages, leading to the protection of cartilage and the promoted regeneration. The inhibition of NF-κB signaling pathway is central in OA treatment via controlling inflammatory responses in macrophages, while the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway appears not to attract widespread attention in the field. Nrf2 is a transcription factor encoding a large number of antioxidant enzymes. The activation of Nrf2 can have antioxidant and anti-inflammatory effects, which can also have complex crosstalk with NF-κB signaling pathway. The activation of Nrf2 can inhibit the M1 polarization and promote the M2 polarization through potential signaling transductions including TGF-β/SMAD, TLR/NF-κB, and JAK/STAT signaling pathways, with the regulation or cooperation of Notch, NLRP3, PI3K/Akt, and MAPK signaling. And the expression of heme oxygenase-1 (HO-1) and the negative regulation of Nrf2 for NF-κB can be the main mechanisms for promotion. Furthermore, the candidates of OA treatment by activating Nrf2 to promote M2 phenotype macrophages in OA are also reviewed in this work, such as itaconate and fumarate derivatives, curcumin, quercetin, melatonin, mesenchymal stem cells, and low-intensity pulsed ultrasound.

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“…In addition, quercetin increases the levels of M2 marker IL-10 and endogenous antioxidant heme oxygenase (H2O)-1 through the activation of AMPK and protein kinase B(AKT) signaling pathways. It is expected to be a potential drug for treating inflammatory diseases of the central nervous system [ 74 ].…”

Section: Therapeutic Targets For Microglia Polarizationmentioning

confidence: 99%

Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage

et al. 2022

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Intracerebral hemorrhage (ICH) is the most lethal subtype of stroke, but effective treatments are lacking, and neuroinflammation plays a key role in the pathogenesis. In the innate immune response to cerebral hemorrhage, microglia first appear around the injured tissue and are involved in the inflammatory cascade response. Microglia respond to acute brain injury by being activated and polarized to either a typical M1-like (pro-inflammatory) or an alternative M2-like (anti-inflammatory) phenotype. These two polarization states produce pro-inflammatory or anti-inflammatory. With the discovery of the molecular mechanisms and key signaling molecules related to the polarization of microglia in the brain, some targets that regulate the polarization of microglia to reduce the inflammatory response are considered a treatment for secondary brain tissue after ICH damage effective strategies. Therefore, how to promote the polarization of microglia to the M2 phenotype after ICH has become the focus of attention in recent years. This article reviews the mechanism of action of microglia’s M1 and M2 phenotypes in secondary brain injury after ICH. Moreover, it discusses compounds and natural pharmaceutical ingredients that can polarize the M1 to the M2 phenotype.

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Regulatory Effects of Quercetin on M1/M2 Macrophage Polarization and Oxidative/Antioxidative Balance

Cited by 138 publications

References 101 publications

PD-L1/PD-L2 deficiency alters numbers and types of microglia and transcriptomic landscape of neural retina

PD-L1/PD-L2 deficiency alters numbers and types of microglia and transcriptomic landscape of neural retina

Nrf2-mediated anti-inflammatory polarization of macrophages as therapeutic targets for osteoarthritis

Mechanism and Regulation of Microglia Polarization in Intracerebral Hemorrhage

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