Chrysin attenuates inflammation by regulating M1/M2 status via activating PPARγ.
Chrysin (5,7-di-OH-flavone), a widely distributed natural flavonoid, has been well documented for involving in various biological activities, especially in regulation of peroxisome proliferator activated receptor γ (PPARγ) activity as a modest modulator. However, the exact molecular mechanism is still unrevealed. In the current study, for the first time, we discovered that, chrysin not only significantly attenuated inflammation in high-fat feeding mice, but also alleviated high fat diet-induced hepatic, muscular steatosis in obese mice without altering the body weight. Chrysin decreases the infiltration of macrophages into adipose tissue in obese mice. In addition, chrysin was also found to induce an anti-inflammatory M2 phenotype and decreases M1 phenotype, both in peritoneal macrophages of obese mice and cultured macrophages in vitro, and thereby, chrysin changed the M1/M2 status. Our data further showed that chrysin regulated the phenotype of macrophages through enhancing the transcriptional activation of PPARγ and the expression of its target genes. Taken together, we conclude that chrysin may serve as an effective modulator of PPARγ during the pathogenesis of inflammation, thereby our findings shed light on the potential therapeutic feature of chrysin in recovering inflammatory diseases via regulating M1/M2 status.
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Xiujing
X
Feng
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Haohan
H
Qin
Department of Medicine, University of Texas Health Science Center at San Antonio (UTHSCSA), TX 78229, USA.
Qian
Q
Shi
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Yang
Y
Zhang
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Feifei
F
Zhou
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Haochen
H
Wu
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Sen
S
Ding
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China.
Zhiyuan
Z
Niu
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China. Electronic address: yanlu@nju.edu.cn.
Yan
Y
Lu
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animal for Disease Study, Model Animal Research Center, Nanjing Biomedical Research Institute, Nanjing University, Nanjing 210093, China. Electronic address: ppshen@nju.edu.cn.
Pingping
P
Shen
D000273:Adipose Tissue / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D002455:Cell Division / Q000187:drug effects*; D002461:Cell Line, Transformed; D002470:Cell Survival / Q000187:drug effects; D002478:Cells, Cultured; D004305:Dose-Response Relationship, Drug; D005234:Fatty Liver / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D005419:Flavonoids / Q000008:administration & dosage / Q000009:adverse effects / Q000494:pharmacology / Q000627:therapeutic use*; D006801:Humans; D008099:Liver / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000187:drug effects / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D009220:Myositis / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D065626:Non-alcoholic Fatty Liver Disease; D009765:Obesity / Q000503:physiopathology; D047495:PPAR gamma / Q000819:agonists* / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms; D014158:Transcription, Genetic / Q000187:drug effects
D000894:Anti-Inflammatory Agents, Non-Steroidal; D005419:Flavonoids; D047495:PPAR gamma; C043561:chrysin
Chrysin; Inflammation; M1/M2 status; PPARγ