Anti-inflammatory mechanism of galangin in lipopolysaccharide-stimulated microglia: Critical role of PPAR-γ signaling pathway

Choi, Min Ji; Lee, Eun Jung; Park, Jin-Sun; Kim, Su Nam; Park, Eun Mi; Kim, Hee Sun

doi:10.1016/j.bcp.2017.07.021

Cited by 114 publications

(79 citation statements)

References 58 publications

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“…Recent data indicate TREM2 is capable of binding to bacteria (Lehnardt, 2010) and impacts the phagocytosis and apoptosis via the PI3K signaling in macrophages (Lehnardt, 2010;Jay et al, 2015;Ull et al, 2017). TREM2 silencing can enhance LPS induced proinflammatory cytokineproduction in microglia (Wu et al, 2015;Choi et al, 2017). Studies also indicate PI3K signaling likely modulate pro-inflammatory signals in microglia (Wang et al, 2016).…”

Section: Introductionmentioning

confidence: 95%

“…TREM2 is highly expressed in microglia with approximately 300-fold higher than that in the neuron and other glial cells (Luo et al, 2014;Wu et al, 2015), and acts as a key regulator of inflammatory response (Torika et al, 2016;Choi et al, 2017;Zhong et al, 2017). TREM2 is highly expressed in microglia with approximately 300-fold higher than that in the neuron and other glial cells (Luo et al, 2014;Wu et al, 2015), and acts as a key regulator of inflammatory response (Torika et al, 2016;Choi et al, 2017;Zhong et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…TLR4 is activated by bacteria to modulate the innate immune responses, which releases pro-and antiinflammatory cytokines to promote robust inflammatory responses (Gawish et al, 2015). TREM2 silencing can enhance LPS induced proinflammatory cytokineproduction in microglia (Wu et al, 2015;Choi et al, 2017). Recent data indicate TREM2 is capable of binding to bacteria (Lehnardt, 2010) and impacts the phagocytosis and apoptosis via the PI3K signaling in macrophages (Lehnardt, 2010;Jay et al, 2015;Ull et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

“…Triggering receptor expressed on myeloid cell-2 (TREM2) is a cellular surface receptor which belongs to the lectin-like immunoglobulin superfamily. TREM2 is highly expressed in microglia with approximately 300-fold higher than that in the neuron and other glial cells (Luo et al, 2014;Wu et al, 2015), and acts as a key regulator of inflammatory response (Torika et al, 2016;Choi et al, 2017;Zhong et al, 2017). TREM-2 down-regulates TLR4-mediated cytokine responses, TNF-a production and the NF-kB activation (Peng et al, 2010;Sharif et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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TREM2 inhibits inflammatory responses in mouse microglia by suppressing the PI3K/NF‐κB signaling

Zhao

Lin

et al. 2018

Cell Biology International

112

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This study aimed to investigate the effects of triggering receptor expressed on myeloid cell-2 (TREM2) on the production of pro-inflammatory mediators and cytokines induced by lipopolysaccharide (LPS) in BV2 microglia. TREM2 expression or TREM2-specific siRNA were used to induce TREM2 overexpression or silencing. The BV2 cells were pre-treated with the PI3 K inhibitor of LY294002 for 1 h and stimulated with LPS for 24 h. Then, the cell viability, apoptosis, phagocytosis, nitric oxide (NO), lactate dehydrogenase (LDH), and cytokine production, as well as the activation of AKT and NF-kB were determined, respectively. We found LPS stimulation significantly reduced BV2 cell viability, enhanced BV2 cell phagocytosis and apoptosis compared to the control groups. In addition, LPS stimulation significantly increased the production of NO, LDH, TNF-α, IL-1β, and the activation of AKT and NF-kB, while decreased the levels of IL-10 and TGF-β1. However, these pro-inflammatory effects were significantly attenuated by TREM2 overexpression or pre-treatment with LY294002, while enhanced by TREM2 silencing. Thus, we concluded that TREM2 inhibited neuroinflammation by down-regulating PI3 K/AKT and NF-kB signaling in BV2 microglia. Above all, therapeutic enhanced TREM2 expression may be a new strategy for intervention of neuroinflammatory diseases.

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Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TREM2 inhibits inflammatory responses in mouse microglia by suppressing the PI3K/NF‐κB signaling

Zhao

Lin

et al. 2018

Cell Biology International

112

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“…PPARs‐γ have been implicated in the phenotypic switch induced in microglia by some neuroprotective natural compounds, such as malibatol A, a resveratrol agonist (Pan et al, ) and galangin, a molecule abundant in honey and medicinal herbs (Choi et al, ).…”

Section: Receptor and Channels Promoting Anti‐inflammatory Microglia mentioning

confidence: 99%

How to reprogram microglia toward beneficial functions

Fumagalli

Lombardi

Gressèns

et al. 2018

Glia

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Microglia, brain cells of nonneural origin, orchestrate the inflammatory response to diverse insults, including hypoxia/ischemia or maternal/fetal infection in the perinatal brain. Experimental studies have demonstrated the capacity of microglia to recognize pathogens or damaged cells activating a cytotoxic response that can exacerbate brain damage. However, microglia display an enormous plasticity in their responses to injury and may also promote resolution stages of inflammation and tissue regeneration. Despite the critical role of microglia in brain pathologies, the cellular mechanisms that govern the diverse phenotypes of microglia are just beginning to be defined. Here we review emerging strategies to drive microglia toward beneficial functions, selectively reporting the studies which provide insights into molecular mechanisms underlying the phenotypic switch. A variety of approaches have been proposed which rely on microglia treatment with pharmacological agents, cytokines, lipid messengers, or microRNAs, as well on nutritional approaches or therapies with immunomodulatory cells. Analysis of the molecular mechanisms relevant for microglia reprogramming toward pro-regenerative functions points to a central role of energy metabolism in shaping microglial functions. Manipulation of metabolic pathways may thus provide new therapeutic opportunities to prevent the deleterious effects of inflammatory microglia and to control excessive inflammation in brain disorders.

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The role of peroxisome proliferator‐activated receptor γ in lipid metabolism and inflammation in atherosclerosis

Yang

Shang

2023

Cell Biology International

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Cardiovascular disease events are the result of functional and structural abnormalities in the arteries and heart. Atherosclerosis is the main cause and pathological basis of cardiovascular diseases. Atherosclerosis is a multifactorial disease associated with dyslipidemia, inflammation, and oxidative stress, among which dyslipidemia and chronic inflammation occur in all processes. Under the influence of lipoproteins, the arterial intima causes inflammation, necrosis, fibrosis, and calcification, leading to plaque formation in specific parts of the artery, which further develops into plaque rupture and secondary thrombosis. Foam cell formation from macrophages is an early event in the development of atherosclerosis. Lipid uptake causes a vascular inflammatory response, and persistent inflammatory infiltration in the lesion area further promotes the development of the disease. Inhibition of macrophage differentiation into foam cell and reduction of the level of proinflammatory factors in macrophages can effectively alleviate the occurrence and development of atherosclerosis. Peroxisome proliferator-activated receptor γ (PPARγ) is a ligandactivated nuclear receptor that plays an important antiatherosclerotic role by regulating triglyceride metabolism, lipid uptake, cholesterol efflux, macrophage polarity, and inhibiting inflammatory signaling pathways. In addition, PPARγ shifts its binding to ligands and co-activators or co-repressors of transcription of target genes through posttranslational modification, thereby affecting the regulation of its downstream target genes. Many ligand agonists have also been developed targeting PPARγ. In this review, we summarized the role of PPARγ in lipid metabolism and inflammation in development of atherosclerosis, the posttranslational regulatory mechanism of PPARγ, and further discusses the value of PPARγ as an antiatherosclerosis target.

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Anti-inflammatory mechanism of galangin in lipopolysaccharide-stimulated microglia: Critical role of PPAR-γ signaling pathway

Cited by 114 publications

References 58 publications

TREM2 inhibits inflammatory responses in mouse microglia by suppressing the PI3K/NF‐κB signaling

TREM2 inhibits inflammatory responses in mouse microglia by suppressing the PI3K/NF‐κB signaling

How to reprogram microglia toward beneficial functions

The role of peroxisome proliferator‐activated receptor γ in lipid metabolism and inflammation in atherosclerosis

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