Effect of Compounds Isolated from Natural Products on IFN-<b>γ</b>/LPS–Induced Nitric Oxide Production in RAW 264.7 Macrophages

Ahmad, Sadeem; Israf, Daud Ahmad; Lajis, Nordin H.; Khozirah, S.; Habsah, M.; Jasril,; Permana, Dharma; Norhadiani, I.

doi:10.1080/13880200500530765

Cited by 16 publications

(17 citation statements)

References 29 publications

(29 reference statements)

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“…This assertion is supported by the demonstration that pre‐treatment with the substrate for NOS, l‐ arginine, significantly attenuated the antinociceptive effects caused by administration of FKB and an inhibitor of NOS, l‐ NOARG. In addition, the present study was in agreement with the reported in vitro studies which showed that FKB attenuated the NO production in LPS‐induced RAW 264.7 cell line and reduced the over‐expression of inducible NO synthase [17,18].…”

Section: Discussionsupporting

confidence: 92%

“…As activation of the NO cascade is known to take place secondary to NMDA receptor activation and a great deal of evidence has demonstrated the role of NO in various models of nociception [13–16], this has led to the speculation that the mechanism of FKB‐induced antinociception, at least in part, involved an interaction of FKB with the glutaminergic system and/or inhibition of NO production. In addition, previous studies have demonstrated that FKB was able to inhibit NO production in lipopolysaccharide (LPS)‐induced murine monocytic macrophage, RAW 264.7 cell line [17,18]. Furthermore, it also reduced the over‐expression of inducible NO synthase and nuclear factor‐κB protein expression in mouse liver [18].…”

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confidence: 99%

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Possible Participation of Nitric Oxide/Cyclic Guanosine Monophosphate/Protein Kinase C/ATP-Sensitive K+ Channels Pathway in the Systemic Antinociception of Flavokawin B

Mohamad

Akhtar

Khalivulla

et al. 2011

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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The possible mechanisms of action in the antinociceptive activity induced by systemic administration (intraperitoneal, i.p.) of flavokawin B (FKB) were analysed using chemical models of nociception in mice. It was demonstrated that i.p. administration of FKB to the mice at 0.3, 1.0, 3.0 and 10 mg ⁄ kg produced significant dose-related reduction in the number of abdominal constrictions. The antinociception induced by FKB in the acetic acid test was significantly attenuated by i.p. pretreatment of mice with L-arginine, the substrate for nitric oxide synthase or glibenclamide, the ATP-sensitive K + channel inhibitor, but was enhanced by methylene blue, the non-specific guanylyl cyclase inhibitor. FKB also produced dose-dependent inhibition of licking response caused by intraplantar injection of phorbol 12-myristate 13-acetate, a protein kinase C activator (PKC). Together, these data indicate that the NO ⁄ cyclic guanosine monophosphate ⁄ PKC ⁄ ATP-sensitive K + channel pathway possibly participated in the antinociceptive action induced by FKB.Chalcones or 1,3-diaryl-2-propen-1-ones are a well-known class of flavonoids that have been reported to possess both in vitro and in vivo biological activities including antimicrobial, anticancer, antiprotozoal, antiplatelet, antinociceptive and anti-inflammatory [1][2][3][4][5][6]. It has been reported elsewhere that chalcones and their derivatives inhibited the synthesis of nitric oxide (NO), lipoxygenase as well as cyclo-oxygenase activities which constitute the major pro-inflammatory pathways and remain most targeted for anti-inflammatory and antinociceptive drug development [7][8][9][10].In attempts to obtain active derivatives from chalcone that possesses anti-inflammatory and antinociceptive activities, our group previously isolated 6¢-hydroxy-2¢,4¢-dimethoxychalcone or flavokawin B (FKB) from Alpinia nutans Rosc. along with other chalcones such as cardamonin (6), 5,6-dehydrokawain, (-)-pinocembrin, (-)-pinostrobin and 2¢,3¢,4¢,6¢-tetrahydroxychalcone [11]. Recently, we chemically synthesized FKB and demonstrated that systemic administration of FKB exerted potent dose-dependent antinociceptive activity when assessed in the chemical and thermal models of nociception in mice, indicating involvement of the peripheral and central antinociceptive activities [12]. Moreover, in the same study, we demonstrated that the central antinociceptive activity of FKB was not mediated by the activation of opioid receptors. Besides, we also demonstrated that FKB produced marked inhibition of the nociceptive response caused by intraplantar injection of glutamate into mouse hind paw in the glutamate-induced nociception test and perhaps the inhibition of peripheral N-Methyl-D-aspartic acid (NMDA) receptors contributes to the antinociceptive effect of FKB [12]. As activation of the NO cascade is known to take place secondary to NMDA receptor activation and a great deal of evidence has demonstrated the role of NO in various models of nociception [13][14][15][16], this has led to the ...

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Section: Discussionsupporting

confidence: 92%

mentioning

confidence: 99%

Possible Participation of Nitric Oxide/Cyclic Guanosine Monophosphate/Protein Kinase C/ATP-Sensitive K+ Channels Pathway in the Systemic Antinociception of Flavokawin B

Mohamad

Akhtar

Khalivulla

et al. 2011

Basic &Amp; Clinical Pharmacology &Amp; Toxicology

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“…Nitric oxide synthesized by nitric oxide synthase in activated inflammatory cells acts as a secondary mediator of some actions of pro-inflammatory cytokines [2,25,[27][28][29][30]. Therefore, anti-inflammatory effects may be related to the inhibition of nitric oxide synthases, especially the iNOS [2,25].…”

Section: Discussionmentioning

confidence: 97%

“…In addition to neutrophil-derived free radicals, production of nitric oxide (NO) plays an important role in the development of the edema caused by various factors, including the effects induced by prostaglandins and cytokines [2,[25][26][27][28][29]. Nitric oxide synthesized by nitric oxide synthase in activated inflammatory cells acts as a secondary mediator of some actions of pro-inflammatory cytokines [2,25,[27][28][29][30].…”

Section: Discussionmentioning

confidence: 99%

“…The first mediators of the early phase of this type of inflammation are histamine, 5-hydroxytryptamine, and bradykinin [1]. An acute inflammatory process is comprised of inflammation mediators including neutrophil-derived reactive oxygen species (ROS), nitric oxide (NOÁ) [2,3], prostaglandins, and cytokines [4]. ROS play an important role in the pathogenesis of many diseases, such as respiratory distress syndrome, rheumatoid arthritis, local or systemic inflammatory disorders, diabetes, atherosclerosis, cancer, and neurodegenerative diseases [3,5].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of anti-inflammatory and antioxidant activities of Peltigera rufescens lichen species in acute and chronic inflammation models

et al. 2009

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The anti-inflammatory effects of the methanol extract of the lichen species Peltigera rufescens (Weis.) Humb (MEPR) (Peltigeraceae) on acute (carrageenan-induced) and chronic (cotton pellet granule) phases of inflammation were investigated. The MEPR was capable of reducing carrageenan-induced inflammation and showed a potent antiproliferative effect (63.5%) in the chronic inflammation model. Inflammation is related to neutrophil infiltration and the production of neutrophil-derived mediators and free radicals. The MEPR reduced the myeloperoxidase and inducible nitric oxide synthase (NOS) activities, which were increased by carrageenan injection. Carrageenan injection also increased the lipid peroxidation (LPO) as compared with untreated paw tissues. The administration of MEPR, diclofenac, and indomethacin reduced the LPO in paw tissues through amelioration of the antioxidant defense systems. Neutrophil infiltration and neutrophil-derived free radicals in tissues therefore appeared to play an important role in the inflammation process induced by carrageenan. The anti-inflammatory effect of MEPR could be attributed to its reducing effect on the neutrophil-derived free radicals and its ameliorating effect on the antioxidant defense systems.

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Phytol from Scoparia dulcis prevents NF-κB-mediated inflammatory responses during macrophage polarization

Duraisamy,

Angusamy,

Ravi

et al. 2024

3 Biotech

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Effect of Compounds Isolated from Natural Products on IFN-γ/LPS–Induced Nitric Oxide Production in RAW 264.7 Macrophages

Cited by 16 publications

References 29 publications

Possible Participation of Nitric Oxide/Cyclic Guanosine Monophosphate/Protein Kinase C/ATP-Sensitive K+ Channels Pathway in the Systemic Antinociception of Flavokawin B

Possible Participation of Nitric Oxide/Cyclic Guanosine Monophosphate/Protein Kinase C/ATP-Sensitive K+ Channels Pathway in the Systemic Antinociception of Flavokawin B

Evaluation of anti-inflammatory and antioxidant activities of Peltigera rufescens lichen species in acute and chronic inflammation models

Phytol from Scoparia dulcis prevents NF-κB-mediated inflammatory responses during macrophage polarization

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