Magnolol stimulates lipolysis in lipid‐laden RAW 264.7 macrophages

Chen, Jin Shan; Chen, Yuh‐Lien; Greenberg, Andrew S.; Chen, Yi Jen; Wang, Seu Mei

doi:10.1002/jcb.20361

Cited by 26 publications

(25 citation statements)

References 35 publications

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“…In a series of magnolol‐related studies, we found that magnolol also induces lipolysis in lipid‐laden RAW264.7 macrophages [13] and sterol ester‐loaded 3T3‐L1 preadipocytes, and the signaling pathway of the latter event involves ERK [14]. However, whether the same signaling pathway accounts for magnolol‐induced steroidogenesis in adrenal cells has not yet been elucidated.…”

Section: Introductionmentioning

confidence: 99%

Signaling pathways of magnolol‐induced adrenal steroidogensis

et al. 2005

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This study focused on identifying the signalling mediating the effect of magnolol on corticosterone production. Magnolol-induced corticosterone production was completely inhibited by mitogen-activated protein kinase kinase (MEK)-inhibitor PD98059, tyrosine kinase (TK)-inhibitor genistein or Janus tyrosine kinase 2 (JAK2)-inhibitor AG490, suggesting that extracellular signal-regulated kinase (ERK) and JAK2 are both involved in this signaling cascade. Further, magnolol induced the transient phosphorylation of MEK, ERK, cAMP response-element binding protein (CREB) and the expression of 32 and 30 kDa steroidogenic acute regulatory protein (StAR) in a time-dependent manner. Inhibition of TK or JAK2 activities blocked magnolol-induced phosphorylation of MEK and ERK, again supporting the upstream role of JAK2. The activation of JAK2 or MEK apparently mediated the magnolol-induced phosphorylation of CREB and the upregulation of StAR. These findings demonstrate a novel pathway for magnolol to induce the expression of StAR, which regulates the rate-limiting step in sterodiogenesis.

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Section: Introductionmentioning

confidence: 99%

Signaling pathways of magnolol‐induced adrenal steroidogensis

et al. 2005

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“…[1] This transformation is exploited for the construction of complex carbon architectures. [5,6] In particular, nonsymmetric 2,2'-biphenols have exceptional properties as building blocks for ligands in molecular catalysis, [7] bioactive materials, [3] and natural products. [5,6] In particular, nonsymmetric 2,2'-biphenols have exceptional properties as building blocks for ligands in molecular catalysis, [7] bioactive materials, [3] and natural products.…”

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confidence: 99%

Selective Synthesis of Partially Protected Nonsymmetric Biphenols by Reagent‐ and Metal‐Free Anodic Cross‐Coupling Reaction

et al. 2016

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The oxidative cross-coupling of aromatic substrates without the necessity of leaving groups or catalysts is described. The selective formation of partially protected nonsymmetric 2,2'-biphenols via electroorganic synthesis was accomplished with a high yield of isolated product. Since electric current is employed as the terminal oxidant, the reaction is reagent-free; no reagent waste is generated as only electrons are involved. The reaction is conducted in an undivided cell, and is suitable for scale-up and inherently safe. The implementation of O-silyl-protected phenols in this transformation results in both significantly enhanced yields and higher selectivity for the desired nonsymmetric 2,2'-biphenols. The use of a bulky silyl group to block one hydroxyl moiety makes the final product less prone to oxidation. Furthermore, the partially silyl-protected 2,2'-biphenols are versatile building blocks that usually require tedious or low-yielding synthetic pathways. Additionally, this strategy facilitates a large variety of new substrate combinations for oxidative cross-coupling reactions.

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“…Since magnolol stimulated steroidogenesis in rat adrenal cells (Wang et al, 2000) and lipolysis in lipid-laden macrophages (Chen et al, 2005) through a pathway independent of the cAMP-PKA system, all these results indicate that lipolysis in adipocytes and lipid-laden macrophages is mediated via different signal transduction pathways. Further studies are required to investigate the underlying mechanism through which magnolol regulates lipid metabolism in macrophages.…”

Section: Effect Of No On Lipolysis In Lipid-laden Macrophages (A)mentioning

confidence: 85%

Nitric oxide-independent lipid metabolism in RAW 264.7 macrophages loaded with oleic acid

Huang

Chen

2006

Cell Biology International

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The role of nitric oxide (NO) in the regulation of lipogenesis and lipolysis in RAW 264.7 macrophages loaded with oleic acid (OA) was investigated in this paper. Magnolol stimulated full lipolysis without affecting NO levels. Both inhibition and elevation of NO production in OA-loaded macrophages did not induce lipolysis. Besides, lipopolysaccharide (LPS)-induced increased accumulation of lipid droplets was not reduced by down-regulation of NO levels. Moreover, incubation of macrophages with sodium nitroprusside (SNP), an NO donor, stimulated significant NO production without altering the lipid droplet accumulation. All these results clearly demonstrate that NO is not involved in the modulation of lipid metabolism in macrophages loaded with OA.

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Magnolol stimulates lipolysis in lipid‐laden RAW 264.7 macrophages

Cited by 26 publications

References 35 publications

Signaling pathways of magnolol‐induced adrenal steroidogensis

Signaling pathways of magnolol‐induced adrenal steroidogensis

Selective Synthesis of Partially Protected Nonsymmetric Biphenols by Reagent‐ and Metal‐Free Anodic Cross‐Coupling Reaction

Nitric oxide-independent lipid metabolism in RAW 264.7 macrophages loaded with oleic acid

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