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gallic acid/necrosis
L'enllaç es desa al porta-retalls
Pàgina 1 des de 164 resultats
Molecular mechanisms of gallic acid-induced growth inhibition, apoptosis, and necrosis in hypertrophic scar fibroblasts.
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OBJECTIVE
To explore the effect and molecular mechanism of gallic acid (GA) on the cytostatic and cytotoxicity of hypertrophic scar fibroblasts (HSFs).
METHODS
HSFs were treated with a serial dose of GA for indicated time. The cytostatic and cytotoxicity of GA were evaluated by microscopy, trypan
Gallic acid caused cultured mice TM4 Sertoli cells apoptosis and necrosis.
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The study was designed to determine the cytotoxic effect of gallic acid (GA), obtained by the hydrolysis of tannins, on mice TM4 Sertoli cells apoptosis.
UNASSIGNED
In the present study, non-tumorigenic mice TM4 Sertoli cells were treated with different concentrations of GA for 24 h.
Gallic acid selectively induces the necrosis of activated hepatic stellate cells via a calcium-dependent calpain I activation pathway.
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OBJECTIVE
The activation of hepatic stellate cells (HSCs) in response to liver injury is critical to the development of liver fibrosis, thus, the blockage of the activation of HSCs is considered as a rational approach for anti-fibrotic treatment. In this report, we investigated the effects and the
Gallic acid inhibits the growth of HeLa cervical cancer cells via apoptosis and/or necrosis.
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Gallic acid (GA) is widely distributed in various plants and foods, and its various biological effects have been reported. Here, we evaluated the effects of GA on HeLa cells in relation to cell growth inhibition and death. HeLa cell growth was diminished with an IC(50) of approximately 80 microM GA
The teratogenicity and the action mechanism of gallic acid relating with brain and cervical muscles.
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Gallic acid (3,4,5-trihydroxybenzoic acid) (GA) and other flavanoids are extensively used in nutraceuticals because of their antioxidant and antiinflammatory properties. While examining whether GA is effective in alleviating valproic-acid-induced teratogenesis in a chicken embryo model (CEM), we
In vitro polyphenolics erythrocyte model and in vivo chicken embryo model revealed gallic acid to be a potential hemorrhage inducer: physicochemical action mechanisms.
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The in vivo chicken embryo model (CEM) demonstrated that gallic acid (GA) induced dysvascularization and hypoxia. Inflammatory edema, Zenker's necrosis, hemolysis, and liposis of cervical muscles were the common symptoms. Levels of the gene hif-1α, HIF-1α, TNF-α, IL-6, and NFκB in cervical muscles
Antileishmanial activity of hydrolyzable tannins and their modulatory effects on nitric oxide and tumour necrosis factor-alpha release in macrophages in vitro.
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A series of 27 hydrolyzable tannins and related compounds was tested for antiparasitic effects against both extracellular promastigote and intracellular amastigote Leishmania donovani organisms. In parallel, the compounds were evaluated for their immunomodulatory effects on macrophage functions,
On the benefit of galls of Quercus brantii Lindl. in murine colitis: the role of free gallic acid.
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BACKGROUND
In this study we investigated the effect of gall of Quercus brantii Lindl., a traditional Iranian medicine, in a murine model of experimental colitis induced in male rats by rectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS).
METHODS
Quantification of the main active
Protective effects of co-administration of gallic Acid and cyclosporine on rat myocardial morphology against ischemia/reperfusion.
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BACKGROUND
Irreversible myocardial ischemic injury begins 20 minutes after the onset of coronary occlusion. Then the infarcted cells show signs of necrosis and death.
OBJECTIVE
This study investigated the effects of co-administration of Gallic acid (antioxidant) with cyclosporine (mitochondrial
Gallic acid improved behavior, brain electrophysiology, and inflammation in a rat model of traumatic brain injury.
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Traumatic brain injury (TBI) is one of the main causes of intellectual and cognitive disabilities. In the clinic it is essential to limit the development of cognitive impairment after TBI. In this study, the effects of gallic acid (GA; 100 mg/kg, per oral, from 7 days before to 2 days after TBI
Bioactive monoterpene glycosides conjugated with gallic acid from the leaves of Eucalyptus globulus.
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Two monoterpene glycosides, conjugated with gallic acid [globulusin A (1) and B (2)], together with four known compounds, cypellocarpin A (3), eucaglobulin (4), cuniloside (5) and (1S, 2S, 4R)-trans-2-hydroxy-1,8-cineole beta-d-glucopyranoside (6), were isolated from hot-water extracts of the leaves
Involvement of lipid peroxidation in necrosis of skin flaps and its suppression by ellagic acid.
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To evaluate the pathogenesis of lipid peroxidation in skin-flap necrosis and to select a novel herbal antioxidant to suppress lipid peroxidation and salvage the flaps, in vitro and in vivo experiments were instituted. In vitro studies revealed (1) the potentiality of the cutaneous microsomal system
The effects of mitogen-activated protein kinase inhibitors or small interfering RNAs on gallic acid-induced HeLa cell death in relation to reactive oxygen species and glutathione.
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Gallic acid (GA) is widely distributed in various plants and foods and has various biological properties including anticancer effects. In this study, we investigated the effects of mitogen-activated protein kinase (MAPK) [MAP 20 kinase or ERK kinase (MEK), c-Jun N-terminal kinase (JNK), or p38)]
Gallic acid-grafted chitooligosaccharides suppress antigen-induced allergic reactions in RBL-2H3 mast cells.
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In this study, a bioactive derivative of chitooligosaccharides (3-5 kDa) was synthesized via grafting of gallic acid onto chitooligosaccharides (G-COS) to enhance anti-allergic activity. Hence, G-COS was evaluated for its capabilities against allergic reactions in RBL-2H3 mast cells sensitized with
GALLIC ACID IMPROVES OXIDATIVE STRESS AND INFLAMMATION THROUGH REGULATING MICRORNAS EXPRESSIONS IN THE BLOOD OF DIABETIC RATS.
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