Ginkgo biloba extract (egb 761): inhibitory effect on nitric oxide production in the macrophage cell line raw 264.7

Kobuchi, Hirotsugu; Droy-Lefaix, Marie-Thérèse; Christen, Yves; Packer, Lester

doi:10.1016/s0006-2952(96)00873-8

Cited by 147 publications

(59 citation statements)

References 26 publications

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“…Quercetin has also been reported to inhibit IgE-mediated release of histamine, tryptase and production and gene expression of inflammatory cytokines, such as TNF-, IL-1 , IL-6 and IL-8 in phorbol 12-myristate 13-acetate and calcium ionophore-stimulated cultured human mast cells (Kempuraj et al, 2005;Min et al, 2007). These results are consistent with studies reporting that quercetin inhibits NO and TNF-release from LPS-stimulated rat Kupffer cells (Kawada et al, 1998) and inhibits iNOS mRNA and NO production in LPS/IFN--activated macrophage cells (Kobuchi et al, 1997).…”

Section: Inflammatory Cytokinessupporting

confidence: 93%

Anti-Inflammatory Role of Natural Polyphenols and Their Degradation Products

Veres¹

2012

Severe Sepsis and Septic Shock - Understanding a Serious Killer

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Section: Inflammatory Cytokinessupporting

confidence: 93%

Anti-Inflammatory Role of Natural Polyphenols and Their Degradation Products

Veres¹

2012

Severe Sepsis and Septic Shock - Understanding a Serious Killer

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“…The mechanisms of EGb 761 neuroprotective effects are believed to be mediated via several of its properties, including roles as an antioxidant, a free-radical scavenger, a membrane stabilizer, and an inhibitor of platelet-activating factor (PAF). 33,34 The flavonoids, the major component of EGb 761, have been shown to be neuroprotective through their potent antioxidant activity. 29 Alteration of intracellular redox has long been linked to HIV-associated dementia and/or Tat neurotoxicity.…”

Section: Neurotherapeutic Function Of Egb 761 Against Tat Neurotoxicitymentioning

confidence: 99%

Protection against Human Immunodeficiency Virus Type 1 Tat Neurotoxicity by Ginkgo biloba Extract EGb 761 Involving Glial Fibrillary Acidic Protein

Zou

Kim

Zhou

et al. 2007

The American Journal of Pathology

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Human immunodeficiency virus (HIV)-1 Tat protein isan important pathogenic factor in HIV-associated neuropathogenesis. Despite recent progress, the molecular mechanisms underlying Tat neurotoxicity are still not completely understood. However, few therapeutics have been developed to specifically target HIV infection in the brain. Recent development of an inducible brain-specific Tat transgenic mouse model has made it possible to define the mechanisms of Tat neurotoxicity and evaluate anti-neuroAIDS therapeutic candidates in the context of a whole organism. Herein, we demonstrate that administration of EGb 761, a standardized formulation of Ginkgo biloba extract, markedly protected Tat transgenic mice from Tat-induced developmental retardation, inflammation, death, astrocytosis, and neuron loss. EGb 761 directly down-regulated glial fibrillary acidic protein (GFAP) expression at both protein and mRNA levels. This down-regulation was, at least in part, attributable to direct effects of EGb 761 on the interactions of the AP1 and NF-B transcription factors with the GFAP promoter. Most strikingly, Tat-induced neuropathological phenotypes including macrophage/microglia activation, central nervous system infiltration of T lymphocytes, and oxidative stress were significantly alleviated in GFAP-null/Tat transgenic mice. Taken together, these results provide the first evidence to support the potential for clinical use of EGb 761 to treat HIV-associated neurological diseases. Moreover, these findings suggest for the first time that GFAP activation is directly involved in Tat neurotoxicity, supporting the notion that astrocyte activation or astrocytosis may directly contribute to HIV-associated neurological disorders.

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“…Recently, the effects of selected polyphenolics on NO production in lipopolysaccharide (LPS)-activated RAW 264.7 macrophage cells have been reported. These studies have shown that some polyphenolics or methanol extracts of plants inhibit NO production [4][5][6][7] . Most clinically important medicines belong to steroidal or non-steroidal anti-inflammatory chemical therapeutics for treatment of inflammation-related diseases.…”

Section: Introductionmentioning

confidence: 99%