The anti-inflammatory effects of Pyrolae herba extract through the inhibition of the expression of inducible nitric oxide synthase (iNOS) and NO production

Lee, Mu Hong; Lee, Jeong Min; Jun, Sung Hoon; Lee, Seung Ha; Kim, Nam Wook; Lee, Jun Ho; Ko, Na Young; Mun, Se Hwan; Kim, Bo Kyung; Lim, Beong Ou; Choi, Dong Kug; Choi, Wahn Soo

doi:10.1016/j.jep.2007.01.036

Cited by 51 publications

(31 citation statements)

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“…Thus, the degree of inducible NOS or total NO suppression provides a measure to assess the efficacy of a particular treatment in inhibiting an inflammatory process. [31][32][33][34] In the present study, the data obtained during NO assay indicate that all treatment groups exhibited good NO-inhibitory activities in LPS-stimulated macrophages. Further statistical analyses revealed that each group of liposome-encapsulated piroxicam possessed significantly stronger NO inhibition than their respective equivalent dosage of piroxicam.…”

Section: Discussionsupporting

confidence: 59%

Cytoprotective and enhanced anti-inflammatory activities of liposomal piroxicam formulation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Chiong¹,

Yong²,

Ahmad³

et al. 2013

IJN

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Background: Liposomal drug delivery systems, a promising lipid-based nanoparticle technology, have been known to play significant roles in improving the safety and efficacy of an encapsulated drug. Methods: Liposomes, prepared using an optimized proliposome method, were used in the present work to encapsulate piroxicam, a widely prescribed nonsteroidal anti-inflammatory drug. The cytotoxic effects as well as the in vitro efficacy in regulation of inflammatory responses by free-form piroxicam and liposome-encapsulated piroxicam were evaluated using a lipopolysaccharide-sensitive macrophage cell line, RAW 264.7. Results: Cells treated with liposome-encapsulated piroxicam demonstrated higher cell viabilities than those treated with free-form piroxicam. In addition, the liposomal piroxicam formulation resulted in statistically stronger inhibition of pro-inflammatory mediators (ie, nitric oxide, tumor necrosis factor-α, interleukin-1β, and prostaglandin E 2 ) than piroxicam at an equivalent dose. The liposome-encapsulated piroxicam also caused statistically significant production of interleukin-10, an anti-inflammatory cytokine. Conclusion: This study affirms the potential of a liposomal piroxicam formulation in reducing cytotoxicity and enhancing anti-inflammatory responses in vitro.

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Section: Discussionsupporting

confidence: 59%

Cytoprotective and enhanced anti-inflammatory activities of liposomal piroxicam formulation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Chiong¹,

Yong²,

Ahmad³

et al. 2013

IJN

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“…NO is a short-lived free radical synthesized from L-arginine by nitric oxide synthase (NOS) [23] . NOSs can be grouped into two constitutive types (cNOS) in neuronal and epithelial cells and one inducible type (iNOS) produced by immune cells during inflammation.…”

Section: Discussionmentioning

confidence: 99%

Macrophage receptors of polysaccharide isolated from a marine filamentous fungus Phoma herbarum YS4108

et al. 2009

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Aim: YCP, a novel (1,4)-α-D-glucan, was isolated from the mycelium of the marine filamentous fungus Phoma herbarum YS4108. In this work, we investigated a YCP-binding cellular receptor expressed by macrophages and the intracellular signal transduction pathways involved in YCP-induced macrophage activation. Methods: Fluorescence-labeled YCP (fl-YCP) was prepared using the CDAP-activation method. Fluorescence confocal laser microscopy and fluorescence-activated cell sorting (FACS) were used to analyze the effect of fl-YCP on macrophages. To characterize the properties of the YCP receptor, carbohydrates and antibodies were used to inhibit the binding of fl-YCP to macrophages. Moreover, we investigated the role of membrane receptors Toll-like receptor 2 (TLR2), Toll-like receptor 4 (TLR4), Toll-like receptor 6 (TLR6) and complement receptor 3 (CR3). We also examined the role of the p38 kinase pathway in mediating nitric oxide (NO) production. Results: YCP had an in vitro stimulatory effect on the release of NO in macrophage, and fl-YCP can bind directly to receptors on the surface of macrophages in a time-and dose-dependent manner. Competition studies show that LPS, laminarin, anti-TLR4 antibody and anti-CD11b (CR3) antibody could inhibit fl-YCP binding to macrophages. Conversely, mannose, anti-TLR2 and anti-TLR6 antibody could not. Treatment of RAW264.7 cells with YCP resulted in significant activation of p38 in a time-dependent manner. The specific p38 inhibitor SB203580 abrogated YCP-induced NO generation. Treatment of RAW264.7 cells with anti-TLR4 antibody and anti-CR3 antibody significantly reduced YCP-induced NO production and p38 activation. Conclusion: We have demonstrated that YCP-induced NO production occurs through the TLR4 and CR3 membrane receptors in a p38 kinase-dependent manner in macrophages.Keywords: YCP; Phoma herbarum; macrophages; nitric oxide; receptor; p38 kinase Acta Pharmacologica Sinica (2009Sinica ( ) 30: 1008Sinica ( -1014 doi: 10.1038/aps.2009 Original Article Introduction YCP is a polysaccharide with a mean molecular weight of 2.4×10 3 kDa purified from the mycelium of Phoma herbarum YS4108, a marine filamentous fungus that inhabits the sediment at a depth of 50 m in the Yellow Sea near Sheyang Port, Yancheng, China. (YCP is the acronym of Yancheng and polysaccharide.) In an earlier study, YCP was found to be able to increase phagocytic activity of mice in vitro and in vivo, indicating that it may activate macrophages [1] . YCP could significantly increase the production of NO and interleukin-1 (IL-1) by macrophages. It also significantly increased phagocytic activity of macrophages [2] . However, the YCP-binding cellular receptor expressed by macrophages and the intracellular signal transduction pathways involved in YCP-induced macrophage activation are poorly understood.β-glucans are potent stimulators of the innate immune system in invertebrates, while in mammals they are potent activators of the complement system. Soluble and particulate β-glucans interact with cognate receptors on...

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“…After the incubation, quantity of nitrite accumulated in the culture medium was measured as an indicator of NO production (Lee et al, 2007). Briefly, 100 μL of cell culture medium was mixed with 100 μL of Griess reagent (1% sulfanilamide and 0.1% naphthylethylenediamine dihydrochloride in 2.5% phosphoric acid), the mixture was incubated at room temperature for 10 min and the optical density at 540 nm was measured using an enzyme-linked immunosorbent assay (ELISA) microplate reader (Sunrise, Tecan Co. Ltd., Australia).…”

Section: Determination Of Nitric Oxide (No) Productionmentioning

confidence: 99%

Potentiality of benthic dinoflagellate cultures and screening of their bioactivities in Jeju Island, Korea

Shah¹,

Kalpa²,

Ju-Young³

et al. 2014

Afr. J. Biotechnol.

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The anti-inflammatory effects of Pyrolae herba extract through the inhibition of the expression of inducible nitric oxide synthase (iNOS) and NO production

Cited by 51 publications

References 19 publications

Cytoprotective and enhanced anti-inflammatory activities of liposomal piroxicam formulation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Cytoprotective and enhanced anti-inflammatory activities of liposomal piroxicam formulation in lipopolysaccharide-stimulated RAW 264.7 macrophages

Macrophage receptors of polysaccharide isolated from a marine filamentous fungus Phoma herbarum YS4108

Potentiality of benthic dinoflagellate cultures and screening of their bioactivities in Jeju Island, Korea

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