scholarly journals AP-1/IRF-3 Targeted Anti-Inflammatory Activity of Andrographolide Isolated fromAndrographis paniculata

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Ting Shen ◽  
Woo Seok Yang ◽  
Young-Su Yi ◽  
Gi-Ho Sung ◽  
Man Hee Rhee ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Peritoneal Macrophages ◽  
Luciferase Reporter ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Molecular Signaling ◽  
Luciferase Reporter Gene ◽  
Necrosis Factor Alpha ◽  
Anti Inflammatory

Andrographolide (AG) is an abundant component of plants of the genusAndrographisand has a number of beneficial properties including neuroprotective, anticancer, anti-inflammatory, and antidiabetic effects. Despite numerous pharmacological studies, the precise mechanism of AG is still ambiguous. Thus, in the present study, we investigated the molecular mechanisms of AG and its target proteins as they pertain to anti-inflammatory responses. AG suppressed the production of nitric oxide (NO) and prostaglandin E2(PGE2), as well as the mRNA abundance of inducible NO synthase (iNOS), tumor necrosis factor-alpha (TNF-α), cyclooxygenase (COX)-2, and interferon-beta (IFN-β) in a dose-dependent manner in both lipopolysaccharide- (LPS-) activated RAW264.7 cells and peritoneal macrophages. AG also substantially ameliorated the symptoms of LPS-induced hepatitis and EtOH/HCl-induced gastritis in mice. Based on the results of luciferase reporter gene assays, kinase assays, and measurement of nuclear levels of transcription factors, the anti-inflammatory effects of AG were found to be clearly mediated by inhibition of both (1) extracellular signal-regulated kinase (ERK)/activator protein (AP)-1 and (2) IκB kinaseε(IKKε)/interferon regulatory factor (IRF)-3 pathways. In conclusion, we detected a novel molecular signaling pathway by which AG can suppress inflammatory responses. Thus, AG is a promising anti-inflammatory drug with two pharmacological targets.

scholarly journals IKKβ-Targeted Anti-Inflammatory Activities of a Butanol Fraction of Artificially CultivatedCordyceps pruinosaFruit Bodies

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Han Gyung Kim ◽  
Woo Seok Yang ◽  
Gi-Ho Sung ◽  
Ji Hye Kim ◽  
Gwang-Soo Baek ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Responses ◽  
Immunoblot Analysis ◽  
Culture Conditions ◽  
Gastric Ulcers ◽  
Luciferase Reporter ◽  
Necrosis Factor Alpha ◽  
Butanol Fraction ◽  
Reporter Assays ◽  
Anti Inflammatory

The inhibitory activities of theCordyceps pruinosabutanol fraction (Cp-BF) were investigated by determining inflammatory responses of lipopolysaccharide (LPS)-treated RAW264.7 macrophage cells and by evaluating HCl/ethanol (EtOH)-triggered gastric ulcers in mice. The molecular mechanisms of the inhibitory effects of Cp-BF were investigated by identifying target enzymes using biochemical and molecular biological approaches. Cp-BF strongly inhibited the production of NO and TNF-α, release of reactive oxygen species (ROS), phagocytic uptake of FITC-dextran, and mRNA expression levels of interleukin (IL)-6, inducible NO synthase (iNOS), and tumour necrosis factor-alpha (TNF)-αin activated RAW264.7 cells. Cp-BF also strongly downregulated the NF-κB pathway by suppressing IKKβaccording to luciferase reporter assays and immunoblot analysis. Furthermore, Cp-BF blocked both increased levels of NF-κB-mediated luciferase activities and phosphorylation of p65/p50 observed by IKKβoverexpression. Finally, orally administered Cp-BF was found to attenuate gastric ulcer and block the phosphorylation of IκBαinduced by HCl/EtOH. Therefore, these results suggest that the anti-inflammatory activity of Cp-BF may be mediated by suppression of IKKαand its downstream NF-κB activation. Since our group has established the mass cultivation conditions by developing culture conditions forCordyceps pruinosa, the information presented in this study may be useful for developing new anti-inflammatory agents.

scholarly journals The Dietary Flavonoid Kaempferol Mediates Anti-Inflammatory Responses via the Src, Syk, IRAK1, and IRAK4 Molecular Targets

2015 ◽  
Vol 2015 ◽  
pp. 1-15 ◽  
Author(s):  
Shi Hyoung Kim ◽  
Jae Gwang Park ◽  
Jongsung Lee ◽  
Woo Seok Yang ◽  
Gye Won Park ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Molecular Targets ◽  
Peritoneal Macrophages ◽  
Cellular Adhesion ◽  
Inflammatory Activity ◽  
Prostaglandin E ◽  
Genes Encoding ◽  
Anti Inflammatory

Even though a lot of reports have suggested the anti-inflammatory activity of kaempferol (KF) in macrophages, little is known about its exact anti-inflammatory mode of action and its immunopharmacological target molecules. In this study, we explored anti-inflammatory activity of KF in LPS-treated macrophages. In particular, molecular targets for KF action were identified by using biochemical and molecular biological analyses. KF suppressed the release of nitric oxide (NO) and prostaglandin E2(PGE2), downregulated the cellular adhesion of U937 cells to fibronectin (FN), neutralized the generation of radicals, and diminished mRNA expression levels of inflammatory genes encoding inducible NO synthase (iNOS), TNF-α, and cyclooxygenase- (COX-) 2 in lipopolysaccharide- (LPS-) and sodium nitroprusside- (SNP-) treated RAW264.7 cells and peritoneal macrophages. KF reduced NF-κB (p65 and p50) and AP-1 (c-Jun and c-Fos) levels in the nucleus and their transcriptional activity. Interestingly, it was found that Src, Syk, IRAK1, and IRAK4 responsible for NF-κB and AP-1 activation were identified as the direct molecular targets of KF by kinase enzyme assays and by measuring their phosphorylation patterns. KF was revealed to havein vitroandin vivoanti-inflammatory activity by the direct suppression of Src, Syk, IRAK1, and IRAK4, involved in the activation of NF-κB and AP-1.

Eucommiae Cortex Inhibits TNF-α and IL-6 Through the Suppression of Caspase-1 in Lipopolysaccharide-Stimulated Mouse Peritoneal Macrophages

2012 ◽  
Vol 40 (01) ◽  
pp. 135-149 ◽  
Author(s):  
Min-Cheol Kim ◽  
Dae-Seung Kim ◽  
Su-Jin Kim ◽  
Jinbong Park ◽  
Hye-Lin Kim ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Inflammatory Diseases ◽  
Pharmacological Action ◽  
Underlying Mechanism ◽  
Peritoneal Macrophages ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Caspase 1 ◽  
Factor Alpha ◽  
Mouse Peritoneal Macrophages

Eucommiae cortex (EC) is used in various traditional Korean medicines in the form of tonics, analgesics, and sedatives. However, the underlying mechanism of its anti-inflammatory effect remains unclear. This study attempts to determine the effects of EC on lipopolysaccharide (LPS)-induced inflammatory responses in mouse peritoneal macrophages. The findings of the study show that EC inhibits the LPS-induced production of tumor necrosis factor-alpha and interleukin-6. Exposure to EC also reduces an inflammation-induced increase in the levels of cyclooxigenase-2 and the production of prostaglandin E 2 and nitric oxide in mouse peritoneal macrophages. Furthermore, EC suppresses the activation of nuclear factor-kappa B and caspase-1. These results provide novel insights into the pharmacological action of EC and indicate that EC has a potential in the treatment of inflammatory diseases.

scholarly journals ATP-Binding Pocket-Targeted Suppression of Src and Syk by Luteolin Contributes to Its Anti-Inflammatory Action

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Jeong-Oog Lee ◽  
Deok Jeong ◽  
Mi-Yeon Kim ◽  
Jae Youl Cho
Keyword(s):  
Nuclear Translocation ◽  
Binding Pocket ◽  
Luciferase Reporter ◽  
Prostaglandin E ◽  
Atp Binding ◽  
Luciferase Reporter Gene ◽  
Gene Assay ◽  
Anti Inflammatory ◽  
Inflammatory Action ◽  
Artemisia Asiatica

Luteolin is a flavonoid identifiedas a major anti-inflammatory componentofArtemisia asiatica. Numerous reports have demonstrated the ability of luteolin to suppress inflammation in a variety of inflammatory conditions. However, its exact anti-inflammatory mechanism has not been fully elucidated. In the present study, the anti-inflammatory mode of action in activated macrophages of luteolin fromArtemisia asiaticawas examined by employing immunoblotting analysis, a luciferase reporter gene assay, enzyme assays, and an overexpression strategy. Luteolin dose-dependently inhibited the secretion of nitric oxide (NO) and prostaglandin E2(PGE2) and diminished the levels of mRNA transcripts of inducible NO synthase (iNOS), tumor necrosis factor- (TNF-)α, and cyclooxygenase-2 (COX-2) in lipopolysaccharide- (LPS-) and pam3CSK-treated macrophage-like RAW264.7 cells without displaying cytotoxicity. Luteolin displayed potent NO-inhibitory activity and also suppressed the nuclear translocation of NF-κB (p65 and p50) via blockade of Src and Syk, but not other mitogen-activated kinases. Overexpression of wild type Src and point mutants thereof, and molecular modelling studies, suggest that the ATP-binding pocket may be the luteolin-binding site in Src. These results strongly suggest that luteolin may exert its anti-inflammatory action by suppressing the NF-κB signaling cascade via blockade of ATP binding in Src and Syk.

scholarly journals Caragana rosea Turcz Methanol Extract Inhibits Lipopolysaccharide-Induced Inflammatory Responses by Suppressing the TLR4/NF-κB/IRF3 Signaling Pathways

Molecules ◽  
2021 ◽  
Vol 26 (21) ◽  
pp. 6660
Author(s):  
Ankita Mitra ◽  
Akash Ahuja ◽  
Laily Rahmawati ◽  
Han Gyung Kim ◽  
Byoung Young Woo ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Methanol Extract ◽  
Inflammatory Responses ◽  
Eastern China ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory

Caragana rosea Turcz, which belongs to the Leguminosae family, is a small shrub found in Northern and Eastern China that is known to possess anti-inflammatory properties and is used to treat fever, asthma, and cough. However, the underlying molecular mechanisms of its anti-inflammatory effects are unknown. Therefore, we used lipopolysaccharide (LPS) in RAW264.7 macrophages to investigate the molecular mechanisms that underlie the anti-inflammatory activities of a methanol extract of Caragana rosea (Cr-ME). We showed that Cr-ME reduced the production of nitric oxide (NO) and mRNA levels of iNOS, TNF-α, and IL-6 in a concentration-dependent manner. We also found that Cr-ME blocked MyD88- and TBK1-induced NF-κB and IRF3 promoter activity, suggesting that it affects multiple targets. Moreover, Cr-ME reduced the phosphorylation levels of IκBα, IKKα/β and IRF3 in a time-dependent manner and regulated the upstream NF-κB proteins Syk and Src, and the IRF3 protein TBK1. Upon overexpression of Src and TBK1, Cr-ME stimulation attenuated the phosphorylation of the NF-κB subunits p50 and p65 and IRF3 signaling. Together, our results suggest that the anti-inflammatory activity of Cr-ME occurs by inhibiting the NF-κB and IRF3 signaling pathways.

Momordica charantia Inhibits Inflammatory Responses in Murine Macrophages via Suppression of TAK1

2018 ◽  
Vol 46 (02) ◽  
pp. 435-452 ◽  
Author(s):  
Woo Seok Yang ◽  
Eunju Yang ◽  
Min-Jeong Kim ◽  
Deok Jeong ◽  
Deok Hyo Yoon ◽  
...  
Keyword(s):  
Mrna Expression ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Momordica Charantia ◽  
Luciferase Reporter ◽  
No Production ◽  
Dependent Manner ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory ◽  
Dose Dependent

Momordica charantia known as bitter melon is a representative medicinal plant reported to exhibit numerous pharmacological activities such as antibacterial, antidiabetic, anti-inflammatory, anti-oxidant, antitumor, and hypoglycemic actions. Although this plant has high ethnopharmacological value for treating inflammatory diseases, the molecular mechanisms by which it inhibits the inflammatory response are not fully understood. In this study, we aim to identify the anti-inflammatory mechanism of this plant. To this end, we studied the effects of its methanol extract (Mc-ME) on lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. Specifically, we evaluated nitric oxide (NO) production, mRNA expression of inflammatory genes, luciferase reporter gene activity, and putative molecular targets. Mc-ME blocked NO production in a dose-dependent manner in RAW264.7 cells; importantly, no cytotoxicity was observed. Moreover, the mRNA expression levels of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 were decreased by Mc-ME treatment in a dose-dependent manner. Luciferase assays and nuclear lysate immunoblotting analyses strongly indicated that Mc-ME decreases the levels of p65 [a nuclear factor (NF)-[Formula: see text]B subunit] and c-Fos [an activator protein (AP)-1 subunit]. Whole lysate immunoblotting assays, luciferase assays, and overexpression experiments suggested that transforming growth factor [Formula: see text]-activated kinase 1 (TAK1) is targeted by Mc-ME, thereby suppressing NF-[Formula: see text]B and AP-1 activity via downregulation of extracellular signal-regulated kinases (ERKs) and AKT. These results strongly suggest that Mc-ME exerts its anti-inflammatory activity by reducing the action of TAK1, which also affects the activation of NF-[Formula: see text]B and AP-1.

scholarly journals Myrrh Inhibits LPS-Induced Inflammatory Response and Protects from Cecal Ligation and Puncture-Induced Sepsis

2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Min-Sun Kim ◽  
Gi-Sang Bae ◽  
Kyoung-Chel Park ◽  
Bon Soon Koo ◽  
Byung-Jin Kim ◽  
...  
Keyword(s):  
Inflammatory Mediators ◽  
Inflammatory Responses ◽  
Cecal Ligation ◽  
Inhibitory Effect ◽  
Peritoneal Macrophages ◽  
Prostaglandin E ◽  
Cecal Ligation And Puncture ◽  
Extracellular Signal ◽  
Alanine Aminotransferase Level ◽  
Anti Inflammatory

Myrrh has been used as an antibacterial and anti-inflammatory agent. However, effect of myrrh on peritoneal macrophages and clinically relevant models of septic shock, such as cecal ligation and puncture (CLP), is not well understood. Here, we investigated the inhibitory effect and mechanism(s) of myrrh on inflammatory responses. Myrrh inhibited LPS-induced productions of inflammatory mediators such as nitric oxide, prostaglandin E2, and tumor necrosis factor-αbut not of interleukin (IL)-1βand IL-6 in peritoneal macrophages. In addition, Myrrh inhibited LPS-induced activation of c-jun NH2-terminal kinase (JNK) but not of extracellular signal-regulated kinase (ERK), p38, and nuclear factor-κB. Administration of Myrrh reduced the CLP-induced mortality and bacterial counts and inhibited inflammatory mediators. Furthermore, administration of Myrrh attenuated CLP-induced liver damages, which were mainly evidenced by decreased infiltration of leukocytes and aspartate aminotransferase/alanine aminotransferase level. Taken together, these results provide the evidence for the anti-inflammatory and antibacterial potential of Myrrh in sepsis.

scholarly journals Anti-inflammatory Effect of d-(+)-Cycloserine Through Inhibition of NF-κB and MAPK Signaling Pathways in LPS-Induced RAW 264.7 Macrophages

2020 ◽  
Vol 15 (4) ◽  
pp. 1934578X2092048 ◽  
Author(s):  
Hyun-Kyu Kang ◽  
Chang-Gu Hyun
Keyword(s):  
Nitric Oxide ◽  
Mtt Assay ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Prostaglandin E ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Raw 264.7 Macrophages ◽  
Anti Inflammatory

Recently, additional therapeutic potentials of classical antibiotics are gaining considerable attention. The discovery of penicillin in the 1920s had a major impact on the history of human health. Penicillin has been used for the treatment for fatal microbial infections in humans and has led to the discovery of several new antibiotics. d-(+)-Cycloserine (DCS) is an antibiotic isolated from Streptomyces orchidaceous and is used in conjunction with other drugs in the treatment of tuberculosis. However, there have been no studies on the anti-inflammatory effects of DCS in RAW 264.7 macrophage cell line. To investigate the anti-inflammatory effects of DCS, we examined the ability of DCS to inhibit the inflammatory responses in lipopolysaccharide (LPS)-induced RAW 264.7 macrophages in this study. Cell viability was analyzed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The cells were pretreated with various concentrations (2, 4, and 6 mM) of DCS, then treated with 1 μg/mL LPS to detect its anti-inflammatory effects. d-(+)-Cycloserine inhibited the production of nitric oxide (NO) in a concentration-dependent manner, and to some extent, inhibited the production of prostaglandin E2. Consistent with these findings, DCS suppressed the expression of pro-inflammatory cytokines such as interleukin (IL)-1β and IL-6. However, it had no effect on the expression of tumor necrosis factor-α. Western blot analysis demonstrated that DCS inhibited inducible nitric oxide synthase and suppressed cyclooxygenase type-2 (COX-2) expression. In addition, investigation of its effects on nuclear factor kappa B signaling showed that DCS inhibited phosphorylation of inhibitory kappa B-α (IκB-α) and increased intracellular IκB-α in a concentration-dependent manner. Furthermore, DCS inhibited the phosphorylation of LPS-induced extracellular signal-regulated kinase, however it did not affect phosphorylation of c-jun N-terminal kinase and p38. Further studies confirmed that the inhibition of phosphorylation of IκB-α was mediated through the inhibition of phosphoinositide 3-kinase/Akt (PI3K/Akt) pathway. To determine the applicability of DCS to the skin, cytotoxicity on HaCaT keratinocytes was measured following treatment with various concentrations (2, 4, 6, 8, and 10 mM) of DCS using MTT assay. These results suggest that DCS may be used as a potential drug for the treatment of inflammatory diseases.

Molecular mechanisms for the growth factor action of gastrin

1997 ◽  
Vol 273 (4) ◽  
pp. G891-G898 ◽  
Author(s):  
Andrea Todisco ◽  
Yoshiaki Takeuchi ◽  
Andrej Urumov ◽  
Junko Yamada ◽  
Vinzenz M. Stepan ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Molecular Mechanisms ◽  
Luciferase Activity ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Luciferase Reporter Gene ◽  
Promoting Effect ◽  
Ar42j Cells ◽  
Gf 109203X ◽  
Growth Promoting

We have previously observed that gastrin has a cholecystokinin B (CCK-B) receptor-mediated growth-promoting effect on the AR42J rat pancreatic acinar cell line and that this effect is paralleled by induction of expression of the early response gene c- fos. We undertook these experiments to elucidate the mechanism for induction of c- fos and the linkage of this action to the trophic effects of gastrin. Gastrin (0.1–10 nM) dose dependently induced luciferase activity in AR42J cells transfected with a construct consisting of a luciferase reporter gene coupled to the serum response element (SRE) of the c- fos promoter. This effect was blocked by the specific CCK-B receptor antagonist D2 but not by the specific CCK-A receptor antagonist L-364,718 or by pertussis toxin, indicating that gastrin targets the SRE via specific CCK-B receptors through a mechanism independent of Gi. Inhibition of protein kinase C (PKC) either by prolonged (24 h) exposure of the cells to the phorbol ester 12- O-tetradecanoylphorbol 13-acetate (100 nM) or by incubation with the selective inhibitor GF-109203X (3.5 μM) resulted in an 80% reduction in luciferase activity. Similar results were observed in the presence of the specific extracellular signal-regulated kinase (ERK) kinase (MEK) inhibitor PD-98059 (50 μM). We measured ERK2 activity in AR42J cells via in-gel kinase assays and observed that gastrin (1 pM-100 nM) induced ERK2 enzyme activity in a dose-dependent manner. Addition of GF-109203X and PD-98059, either alone or in combination, produced, respectively, partial and total inhibition of gastrin-induced ERK2 activity. Gastrin induction of ERK2 activity also resulted in a threefold increase in the transcriptional activity of Elk-1, a factor known to bind to the c- fos SRE and to be phosphorylated and activated by ERK2. PD-98059 blocked the growth-promoting effect of gastrin on the AR42J cells, demonstrating that this effect depends on activation of MEK. Our data lead us to conclude that the trophic actions of gastrin are mediated by ERK2-induced c- fos gene expression via PKC-dependent and -independent pathways.

scholarly journals Nuciferine Inhibited the Differentiation and Lipid Accumulation of 3T3-L1 Preadipocytes by Regulating the Expression of Lipogenic Genes and Adipokines

2021 ◽  
Vol 12 ◽  
Author(s):  
Hanyuan Xu ◽  
Linjie Wang ◽  
Kemin Yan ◽  
Huijuan Zhu ◽  
Hui Pan ◽  
...  
Keyword(s):  
Lipid Accumulation ◽  
Molecular Mechanisms ◽  
Luciferase Reporter ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Luciferase Reporter Gene ◽  
Aporphine Alkaloid ◽  
Lipogenic Genes ◽  
Proliferation And Differentiation

Purposes: Nuciferine, a main aporphine alkaloid component found in lotus leaf (Nelumbo nucifera), has been demonstrated to possess the property of reducing fat mass and alleviating dyslipidemia in vivo. The purpose of this study is to explore the effects of nuciferine on the proliferation and differentiation of 3T3-L1 cells and further investigate the possible underlying molecular mechanisms.Methods: 3T3-L1 preadipocytes were treated with 0∼20 μM nuciferine for 24∼120 h, the cell viability was assessed using CCK8. 3T3-L1 preadipocytes and human primary preadipocytes were then induced differentiation and the effects of nuciferine on the lipid metabolism in differentiating and fully differentiated adipocytes were observed by the methods of intracellular triglyceride (TG) assay, Oil Red O staining, RT-qPCR and western blot. Transient transfection and dual luciferase reporter gene methods were used to assess the effects of nuciferine on FAS promoter activities.Results: Nuciferine inhibited the proliferation of 3T3-L1 preadipocytes in a dose- and time-dependent manner. 20 μM nuciferine significantly attenuated lipid accumulation and reduced intracellular TG contents by 47.2, 59.9 and 55.4% on the third, sixth and ninth day of preadipocytes differentiation, respectively (all p < 0.05). Moreover, the mRNA levels of PPARγ, C/EBPα, C/EBPβ, FAS, ACC, HSL and ATGL were notably decreased by 39.2∼92.5% in differentiating preadipocytes when treated with 5∼20 μM nuciferine (all p < 0.05). In fully differentiated adipocytes treated with 20 μM nuciferine for 48 h, the mRNA levels of FAS, ACC and SREBP1 were remarkably downregulated by 22.6∼45.2% compared with the controls (0 μM) (all p < 0.05), whereas the expression of adipokines FGF21 and ZAG were notably promoted by nuciferine. Similarly, in fully differentiated human primary adipocytes, the mRNA levels of FAS, ACC, SREBP1 were decreased and the expression of FGF21 and ZAG were elevated after treated with nuciferine (all p < 0.05). Further mechanism studies showed that 2.5∼20 μM nuciferine significantly decreased FAS promoter activities in 3T3-L1 preadipocytes.Conclusion: Nuciferine inhibited the proliferation and differentiation of 3T3-L1 preadipocytes. The inhibitory effects of nuciferine on adipogenesis might be due to the downregulation of PPARγ, C/EBPα and C/EBPβ, which led to the reduction of intracellular lipid accumulation in 3T3-L1 cells and by downregulating the expression of critical lipogenic enzymes, especially of FAS, which was achieved by inhibiting the FAS promoter activities. Besides, nuciferine promoted the expression of adipokines in fully differentiated adipocytes.

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