Inhibitory effect of curcumin on nitric oxide production from lipopolysaccharide-activated primary microglia

Jung, Kyoung Hwa; Lee, Hae Sung; Cho, Jae Youl; Shin, Wan Seon; Rhee, Man Hee; Kim, Tae Kyun; Kang, Ju Hye; Kim, Seung Hee; Hong, Sungyoul; Kang, Seog Youn

doi:10.1016/j.lfs.2006.06.048

Cited by 148 publications

(107 citation statements)

References 68 publications

(74 reference statements)

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“…Considering that oxidative stress is central to KA induced excitotoxic damage, anti-oxidant and anti-inflammatory treatments may attenuate or prevent the KA mediated neurodegeneration . It has been reported that anti-inflammatory substances lucidone (Senthil Kumar et al, 2010), curcumin (Jung et al, 2006), and phenantroindolizdine alkaloids reduce NO production observed in inflammation (Yang et al, 2006). The results of this study showed the prevention of increased NOS activity and NO concentration is in favor of our earlier report .…”

Section: Swamy Et Al Afr J Tradit Complement Altern Med (2014) 11(5)contrasting

confidence: 52%

Propolis Ameliorates Tumor Nerosis Factor-α, Nitric Oxide levels, Caspase-3 and Nitric Oxide Synthase Activities in Kainic Acid Mediated Excitotoxicity in Rat Brain

Swamy¹,

Suhaili²,

Sirajudeen³

et al. 2014

Afr. J. Trad. Compl. Alt. Med.

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Background: Increased nitric oxide (NO), neuronal inflammation and apoptosis have been proposed to be involved in excitotoxicity plays a part in many neurodegenerative diseases. To understand the neuro-protective effects of propolis, activities of Nitric oxide synthase (NOS) and caspase-3 along with NO and tumor necrosis factor-α (TNF-α) levels were studied in cerebral cortex (CC), cerebellum (CB) and brain stem (BS) in rats supplemented with propolis prior to excitotoxic injury with kainic acid (KA). Materials and methods: Male Sprague-Dawley rats were divided into four groups (n=6 rats per group) as Control, KA, Propolis and KA+Propolis. The control group and KA group have received vehicle and saline. Propolis group and propolis + KA group were orally administered with propolis (150mg/kg body weight), five times every 12 hours. KA group and propolis +KA group were injected subcutaneously with kainic acid (15mg/kg body weight) and were sacrificed after 2 hrs. CC, CB and BS were separated, homogenized and used for estimation of NOS, caspase-3, NO and TNF-α by commercial kits. Results were analyzed by one way ANOVA, reported as mean + SD (n=6 rats), and p<0.05 was considered statistically significant. Results: The concentration of NO, TNF-α, NOS and caspase-3 activity were increased significantly (p<0.001) in all the three brain regions tested in KA group compared to the control. Propolis supplementation significantly (p<0.001) prevented the increase in NOS, NO, TNF-α and caspase-3 due to KA. Conclusion:Results of this study clearly demonstrated that the propolis supplementation attenuated the NOS, caspase-3 activities, NO, and TNF-α concentration and in KA mediated excitotoxicity. Hence propolis can be a possible potential protective agent against excitotoxicity and neurodegenerative disorders.

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Section: Swamy Et Al Afr J Tradit Complement Altern Med (2014) 11(5)contrasting

confidence: 52%

Propolis Ameliorates Tumor Nerosis Factor-α, Nitric Oxide levels, Caspase-3 and Nitric Oxide Synthase Activities in Kainic Acid Mediated Excitotoxicity in Rat Brain

Swamy¹,

Suhaili²,

Sirajudeen³

et al. 2014

Afr. J. Trad. Compl. Alt. Med.

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“…3,28) It is well known that curcumin inhibits NO production indirectly by inhibition of inducible nitric oxide synthase (iNOS) though suppression of nuclear factor-kappa B (NF-κB). 10,29) Our EPR study suggests that the direct interaction of curcumin and THC with NO may partially contribute to their anti-inflammatory activity. Despite only moderate NO scavengers, this mechanism of direct interaction should be considered in the development or use of curcumin analogues as anti-inflammatory agent.…”

Section: Resultsmentioning

confidence: 85%

Electron Paramagnetic Resonance Study of the Free Radical Scavenging Capacity of Curcumin and Its Demethoxy and Hydrogenated Derivatives

Morales

Sirijaroonwong

Yamanont

et al. 2015

Biological & Pharmaceutical Bulletin

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The quantitative free radical scavenging capacity of curcumin and its demethoxy derivatives (demethoxycurcumin (Dmc) and bisdemethoxycurcumin (Bdmc)) and hydrogenated derivatives (tetrahydrocurcumin (THC), hexahydrocurcumin (HHC) and octahydrocurcumin (OHC)) towards 1,1-diphenyl-2-picryl hydrazyl (DPPH), nitric oxide radical (NO), hydroxyl radical (HO · ) and superoxide anion radical (O 2 · ) were investigated by electron paramagnetic resonance (EPR) spectroscopy. One mole of the hydrogenated derivatives scavenged about 4 mol of the DPPH radical, while curcumin and Dmc scavenged about 3 mol of the DPPH radical. Curcumin and THC showed moderate scavenging activity towards NO, yielding 200 mmol of NO scavenged per 1 mol of the scavenger. In contrast, curcumin and its derivatives showed very low scavenging activity towards HO · and O 2 · , yielding approximately only 3-12 mmol scavenged per 1 mol of the tested compounds. Our results suggest that curcumin and its derivatives principally act as chain breaking antioxidants rather than as direct free radical scavengers. Furthermore, we showed that the ortho-methoxyphenolic group and the heptadione linkage of these molecules greatly contributed to their DPPH and NO scavenging activity.Key words curcumin; electron paramagnetic resonance; free radical scavenger; spin trapping Curcumin [1,7-bis(4-hydroxy-3-methoxyphenyl)-1,6-heptadiene-3,5-dione] is the primary biologically active constituent that is isolated from the spice, turmeric (Curcuma longa LINN). It shows various therapeutically beneficial activities, including anti-oxidant, anti-inflammatory, anti-cancer, and anti-viral activities 1,2) mediated through its interactions with several molecular targets such as enzymes, receptors, and transcription factors.3,4) As a potent anti-oxidant, several mechanisms have been proposed which describe the direct interaction of curcumin with reactive oxygen species (ROS) as well as its involvement in ROS-independent mechanisms (i.e., induction of antioxidant enzymes). 5,6) The structure-antioxidant activity relationship of curcumin and the compound it reduces has been demonstrated in both in vitro and in vivo models, for example, 1,1-diphenyl-2-picrylhydrazyl (DPPH) kinetic analysis, γ-radiolysis of rat liver microsomes, 7) 2,2′-azobis(2-amidinopropane)dihydrochloride (AAPH)-induced low density lipoprotein (LDL) oxidation, 8) AAPH-induced linoleic oxidation. 9) Lastly, the protective effects of curcumin on oxidative injury have been demonstrated in vivo in several animal diseases models. [10][11][12] Free radicals are normally formed by the physiological processes of the cell. For example superoxide anion radical (O 2 −· ) is produced during the mitochondrial respiratory chain reaction and the nitric oxide radical (NO) is generated by the activation of nitric oxide synthase. In some circumstances, the overproduction of those radicals, as well as the formation of toxic radicals such as the hydroxyl radical (HO · ) leads to the damage of biological molecules, thus resulting in many ...

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“…The cells were used for experiments 48 h after transfection. Luciferase assays were performed using the Luciferase Assay System (Promega) as reported previously (23).…”

Section: Luciferase Reporter Gene Activity Assaymentioning

confidence: 99%

Akt Cys-310-targeted Inhibition by Hydroxylated Benzene Derivatives Is Tightly Linked to Their Immunosuppressive Effects

Lee

et al. 2010

Journal of Biological Chemistry

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The hydroxylated benzene metabolite hydroquinone (HQ) is mainly generated from benzene, an important industrial chemical, and is also a common dietary component. Although numerous reports have addressed the tumorigenesis-inducing effects of HQ, few papers have explored its molecular regulatory mechanism in immunological responses. In this study we characterized Akt (protein kinase B)-targeted regulation by HQ and its derivatives, in suppressing inflammatory responses using cellular, molecular, biochemical, and immunopharmacological approaches. HQ down-regulated inflammatory responses such as NO production, surface levels of pattern recognition receptors, and cytokine gene expression with IC 50 values that ranged from 5 to 10 M. HQ inhibition was mediated by blocking NF-B activation via suppression of its translocation pathway, which is composed of Akt, IB␣ kinase ␤, and IB␣. Of the targets in this pathway, HQ directly targeted and bound to the sulfhydryl group of Cys-310 of Akt and sequentially interrupted the phosphorylation of both Thr-308 and Ser-473 by mediation of ␤-mercaptoethanol, according to the liquid chromatography/ mass spectroscopy analysis of the interaction of HQ with an Aktderived peptide. Therefore, our data suggest that Akt and its target site Cys-310 can be considered as a prime molecular target of HQ-mediated immunosuppression and for novel antiAkt-targeted immunosuppressive drugs.

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Inhibitory effect of curcumin on nitric oxide production from lipopolysaccharide-activated primary microglia

Cited by 148 publications

References 68 publications

Propolis Ameliorates Tumor Nerosis Factor-α, Nitric Oxide levels, Caspase-3 and Nitric Oxide Synthase Activities in Kainic Acid Mediated Excitotoxicity in Rat Brain

Propolis Ameliorates Tumor Nerosis Factor-α, Nitric Oxide levels, Caspase-3 and Nitric Oxide Synthase Activities in Kainic Acid Mediated Excitotoxicity in Rat Brain

Electron Paramagnetic Resonance Study of the Free Radical Scavenging Capacity of Curcumin and Its Demethoxy and Hydrogenated Derivatives

Akt Cys-310-targeted Inhibition by Hydroxylated Benzene Derivatives Is Tightly Linked to Their Immunosuppressive Effects

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