Ethylacetate extract from Draconis Resina inhibits LPS-induced inflammatory responses in vascular smooth muscle cells and macrophages via suppression of ROS production

Heo, Sook-Kyoung; Yi, Hyo-Seung; Yun, Hyun-Jeong; Ko, Changhyun; Choi, Jin-Ho; Park, Sun-Dong

doi:10.1016/j.fct.2009.06.043

Cited by 28 publications

(17 citation statements)

References 30 publications

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“…1 and 3). Moreover, pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6 secreted by macrophages are required for the synergistic induction of NO synthesis in LPS-stimulated macrophages and induce a number of physiological progression, including inflammation, cytotoxicity, and fever [18,19]. In the present study, we found that GAC significantly inhibited the secretion and mRNA expression of TNF-α, IL-1β, and IL-6 in LPS-stimulated macrophages (Fig.…”

Section: Discussionmentioning

confidence: 99%

Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways

et al. 2015

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Chitosan is a naturally occurring polysaccharide, which has exhibited antioxidant, antimicrobial, and anti-cancer activities among others. Modification of chitosan by grafting phenolic compounds is a good strategy for improvement of bioactivities of chitosan. We investigated the anti-inflammatory action of gallic acid-grafted-chitosan (GAC) in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. GAC inhibited the production of nitric oxide (NO) and prostaglandin E2 (PGE2) by inhibiting inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in LPS-stimulated RAW264.7 macrophages. GAC also suppressed the production and mRNA expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). GAC inactivated nuclear factor-κB (NF-κB) via inhibiting the phosphorylation and degradation of the NF-κB inhibitor, IκB. In addition, GAC suppresses the activation of activator protein-1 (AP-1) through the phosphorylation of mitogen-activated protein kinase (MAPK) such as extracellular signal-regulated kinase (ERK1/2), p38 MAPK, and c-Jun N-terminal kinase/stress-activated protein kinase (JNK). These results suggest that GAC has the potential anti-inflammatory action by downregulating transcriptional factors (NF-κB and AP-1) through MAPK signaling pathways.

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Section: Discussionmentioning

confidence: 99%

Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways

et al. 2015

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“…7 demonstrating that FABP4/aP2 Ϫ/Ϫ macrophages were protected from LPS-induced loss of mitochondrial respiration capacity support this concept. Interestingly, it has been shown that LPS-induced mitochondrial dysfunction mainly relies on the increased ROS production and that suppression of ROS not only protects cells from LPS-induced mitochondrial dysfunction but also greatly attenuates LPS-induced inflammatory responses (46,47). Further work is still required to determine if the decreased hydrogen peroxide level in FABP4/aP2 Ϫ/Ϫ macrophages is responsible for the protection from LPS-induced mitochondrial dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Uncoupling Lipid Metabolism from Inflammation through Fatty Acid Binding Protein-Dependent Expression of UCP2

Hertzel

Steen

et al. 2015

Molecular and Cellular Biology

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cChronic inflammation in obese adipose tissue is linked to endoplasmic reticulum (ER) stress and systemic insulin resistance. Targeted deletion of the murine fatty acid binding protein (FABP4/aP2) uncouples obesity from inflammation although the mechanism underlying this finding has remained enigmatic. Here, we show that inhibition or deletion of FABP4/aP2 in macrophages results in increased intracellular free fatty acids (FFAs) and elevated expression of uncoupling protein 2 (UCP2) without concomitant increases in UCP1 or UCP3. Silencing of UCP2 mRNA in FABP4/aP2-deficient macrophages negated the protective effect of FABP loss and increased ER stress in response to palmitate or lipopolysaccharide (LPS). Pharmacologic inhibition of FABP4/aP2 with the FABP inhibitor HTS01037 also upregulated UCP2 and reduced expression of BiP, CHOP, and XBP-1s. Expression of native FABP4/aP2 (but not the non-fatty acid binding mutant R126Q) into FABP4/aP2 null cells reduced UCP2 expression, suggesting that the FABP-FFA equilibrium controls UCP2 expression. FABP4/aP2-deficient macrophages are resistant to LPS-induced mitochondrial dysfunction and exhibit decreased mitochondrial protein carbonylation and UCP2-dependent reduction in intracellular reactive oxygen species. These data demonstrate that FABP4/aP2 directly regulates intracellular FFA levels and indirectly controls macrophage inflammation and ER stress by regulating the expression of UCP2.O besity-linked metabolic disorders, including insulin resistance, fatty liver disease, and coronary arterial disease, share the common signature of chronic inflammation and endoplasmic reticulum (ER) stress (1, 2). Macrophage and T cell infiltration and activation in adipose tissue play a key role in affecting adipokine synthesis and secretion, thereby regulating systemic insulin resistance (3). Inflammatory cytokines increase oxidative stress and decrease the protein-folding efficiency of the ER, initiating a counterregulatory unfolded protein response (UPR) (4) involving pancreatic ER kinase (PERK), activating transcription factor-6 (ATF6), and inositol-requiring enzyme 1 (IRE1). Such concomitant activation leads to the downstream activation of response pathways and the induction of inflammatory signaling networks via c-Jun N-terminal kinase (JNK) and/or NF-B (nuclear factor kappa B) (1).Lipid metabolism in macrophages has been shown to play an important role in triggering inflammation and ER stress (5, 6) and has led to the identification of critical proteins that regulate the obesity-metabolic disease axis. For example, genetic ablation of the fatty acid binding protein (FABP4, also known as aP2) in macrophages alone is sufficient to protect mice from development of atherosclerosis and dyslipidemia (7). FABP4/aP2 is a cytoplasmic fatty acid (FA) carrier protein that mediates intracellular fatty acid trafficking, and a number of hypotheses have been proposed to explain why the loss of FABP4/aP2 results in metabolic improvement (6). Moreover, small molecules that target FABP4/aP2 have ...

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“…[1] It can be obtained from several different plant sources,w hich has led to some confusion regarding its composition and pharmacology.Aresin variety obtained from the palm tree Daemonorops draco has recently received renewed attention as as ource of bioactive molecules.I tw as shown to have antiviral [2] and anticancer [3] effects as well as activity against osteoporosis, [4] diabetes, [5] inflammation, [6] and platelet aggregation. [1] It can be obtained from several different plant sources,w hich has led to some confusion regarding its composition and pharmacology.Aresin variety obtained from the palm tree Daemonorops draco has recently received renewed attention as as ource of bioactive molecules.I tw as shown to have antiviral [2] and anticancer [3] effects as well as activity against osteoporosis, [4] diabetes, [5] inflammation, [6] and platelet aggregation.…”

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confidence: 99%

Biomimetic Synthesis of Complex Flavonoids Isolated from Daemonorops “Dragon's Blood”

Schmid

Trauner

2017

Angew Chem Int Ed

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The dragonbloodins are a pair of complex flavonoid trimers that have been isolated from the palm tree Daemonorops draco, one of the sources of the ancient resin known as "dragon's blood". We present a short synthesis that clarifies their relative configurations and sheds light on their origin in Nature. This synthesis features biomimetic cascade reactions that involve both ionic and radical intermediates. The biogenetic relationships between dracorhodin, the dracoflavans C, and the dragonbloodins A1 and A2 are discussed.

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Ethylacetate extract from Draconis Resina inhibits LPS-induced inflammatory responses in vascular smooth muscle cells and macrophages via suppression of ROS production

Cited by 28 publications

References 30 publications

Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways

Gallic Acid-g-Chitosan Modulates Inflammatory Responses in LPS-Stimulated RAW264.7 Cells Via NF-κB, AP-1, and MAPK Pathways

Uncoupling Lipid Metabolism from Inflammation through Fatty Acid Binding Protein-Dependent Expression of UCP2

Biomimetic Synthesis of Complex Flavonoids Isolated from Daemonorops “Dragon's Blood”

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