Chrysin attenuates inflammation by regulating M1/M2 status via activating PPARγ

Feng, Xiujing; Qin, Haohan; Shi, Qian; Zhang, Yang; Zhou, Feifei; Wu, Haochen; Ding, Sen; Niu, Zhiyuan; Lu, Yan; Shen, Pingping

doi:10.1016/j.bcp.2014.03.016

Cited by 113 publications

(82 citation statements)

References 60 publications

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“…Among chrysin pharmacological functions, antiatherosclerosis-related effects and associated target spot have been presented (Anandhi et al, 2014;Feng et al, 2014). However, the exact mechanism of anti-atherogenic potential has not been uncovered.…”

Section: Discussionmentioning

confidence: 99%

“…ABCA1, ABCG1, and their transcriptional factors LXRa and PPARg are essential regulators in cholesterol efflux in macrophages. It has been reported that chrysin could activate PPARg (Feng et al, 2014). Therefore, we applied real-time PCR (RT-PCR) to analyze cholesterol efflux-associated genes, such as PPARg, LXRa, ABCA1, and ABCG1.…”

Section: Discussionmentioning

confidence: 99%

“…Various mechanisms are involved in chrysinmediated health benefits such as attenuation of inflammation (Rehman et al, 2013), alleviation of oxidative stress (Mantawy et al, 2014), and induction of cell cycle arrest and apoptosis (Rashid et al, 2014). A recent report revealed that chrysin can inhibit inflammation through activation of PPARg (Feng et al, 2014), a key regulator in glucose and lipid metabolism as well as in cholesterol efflux from macrophages. Furthermore, Anandhi et al (2014) indicated that chrysin significantly lowered the serum levels of total cholesterol, triglycerides, low-density, and very low-density lipoprotein cholesterol and exhibited anti-atherogenic potential in Wistar rats.…”

Section: Introductionmentioning

confidence: 99%

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Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages

Wang

Zhang

Liu

et al. 2015

Pharmaceutical Biology

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Context: Chrysin, a natural flavonoid, has been shown to possess multiple pharmacological activities including anti-atherosclerosis. Objective: The effects of chrysin on foam cell formation and cholesterol flow in RAW264.7 macrophages were investigated in this work to explore the potential mechanism underlying its anti-atherogenic activity. Materials and methods: The inhibitive effect of chrysin on foam cell formation and cholesterol accumulation induced by oxidized low-density lipoprotein cholesterol (ox-LDL) was assessed by oil red O staining and intracellular total cholesterol and triglyceride quantification in RAW264.7 macrophages. The action of chrysin on cholesterol efflux and influx was tested by fluorescent assays. Real-time quantitative PCR was used to quantify the relative expression of cholesterol flow-associated genes and luciferase assay was applied to test the transcription activity of peroxisome proliferator-activated receptor gamma (PPARg). Results: Chrysin dose dependently inhibited the formation of foam cells and prevented the enhanced cholesterol accumulation by ox-LDL. Treatment with chrysin (10 mM) significantly enhanced cholesterol efflux and substantially inhibited cholesterol influx. Simultaneously, chrysin significantly increased the mRNA levels of PPARg, liver X receptor alpha (LXRa), ATPbinding cassette, sub-family A1 (ABCA1), and sub-family G1 (ABCG1), decreased scavenger receptor A1 (SR-A1) and SR-A2, and increased the transcriptional activity of PPARg. Discussion and conclusion: Chrysin is a new inhibitor of foam cell formation that may stimulate cholesterol flow. Up-regulation of the classical PPARg-LXRa-ABCA1/ABCG1 pathway and down-regulation of SR-A1 and SR-A2 may participate in its suppressive effect on intracellular cholesterol accumulation.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages

Wang

Zhang

Liu

et al. 2015

Pharmaceutical Biology

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“…This flavone could ameliorate HFD-induced liver steatosis and inflammation, reducing pro-inflammatory cytokines and inducing anti-inflammatory cytokines and adiponectin levels, via induction of anti-inflammatory M2 phenotype and inhibition of pro-inflammatory M1 phenotype of macrophages through PPARγ upregulation [52]. On the contrary, chrysin displays a lacking triglyceride-lowering effect and a pro-oxidant activity in vitro at concentrations of 1-15 µM [33].…”

Section: Flavonesmentioning

confidence: 99%

Flavonoids and Related Compounds in Non-Alcoholic Fatty Liver Disease Therapy

Pisonero-Vaquero¹,

González‐Gallego²,

Sánchez-Campos³

et al. 2015

CMC

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Non-alcoholic fatty liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is one of the most common chronic liver diseases, which may progress to fibrosis, cirrhosis and hepatocellular carcinoma. NAFLD is characterized by the accumulation of lipids in the liver arising from multiple factors: increased fatty acid uptake, increased de novo lipogenesis, reduced fatty acid oxidation and very low density lipoproteins (VLDL) secretion. Most therapeutic approaches for this disease are often directed at reducing body mass index and improving insulin resistance through lifestyle modifications, bariatric surgery and pharmacological treatments. Nevertheless, there is increasing evidence that the use of natural compounds, as polyphenols, exert multiple benefits on the disorders associated with NAFLD. These molecules seem to be able to regulate the expression of genes mainly involved in de novo lipogenesis and fatty acid oxidation, which contributes to their lipid-lowering effect in the liver. Their antioxidant, anti-inflammatory, antifibrogenic and antilipogenic properties seem to confer on them a great potential as strategy for preventing NAFLD progression. In this review, we summarized the effects of these compounds, especially flavonoids, and their mechanisms of action, that have been reported in several studies carried out in in vitro and in vivo models of NAFLD.

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“…1a) is a naturally occurring flavone-type flavonoid and is found in chamomile, oyster mushroom (Pleurotus ostreatus), and honeycomb. Chrysin has been well documented for involving in various biological activities, including inflammation, cancer, and oxidative stress [18][19][20]. Chrysin has been reported to be an inhibitor of aromatase, an enzyme-converting testosterone into estrogen [21].…”

Section: Introductionmentioning

confidence: 99%

Chrysin inhibits diabetic renal tubulointerstitial fibrosis through blocking epithelial to mesenchymal transition

et al. 2015

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• Glucose increases renal tubular epithelial induction of vimentin, α-SMA and FSP-1. • Glucose enhances renal EMT by blocking tubular epithelial E-cadherin expression. • Chrysin inhibits tubular EMT-mediated tubulointerstitial fibrosis in mouse kidneys. • Chrysin restores renal tubular induction of ZO-1 and occludin downregulated in diabetic mice. • Chrysin blocks glucose-induced renal tubular cell migration with reducing MMP-2 activity.

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Chrysin attenuates inflammation by regulating M1/M2 status via activating PPARγ

Cited by 113 publications

References 60 publications

Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages

Chrysin inhibits foam cell formation through promoting cholesterol efflux from RAW264.7 macrophages

Flavonoids and Related Compounds in Non-Alcoholic Fatty Liver Disease Therapy

Chrysin inhibits diabetic renal tubulointerstitial fibrosis through blocking epithelial to mesenchymal transition

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