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aristolochic acid/inflammation
Врската е зачувана во таблата со исечоци
Страница 1 од 83 резултати
Patterns of interstitial inflammation during the evolution of renal injury in experimental aristolochic acid nephropathy.
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BACKGROUND
Interstitial inflammation is a prominent feature associated with the severity of renal injury and progressive kidney failure. We utilized an animal model of aristolochic acid (AA)-induced nephropathy (AAN) to assess patterns of infiltration and inflammation during the evolution of
Metabolomics analysis reveals the association between lipid abnormalities and oxidative stress, inflammation, fibrosis, and Nrf2 dysfunction in aristolochic acid-induced nephropathy.
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Alternative medicines are commonly used for the disease prevention and treatment worldwide. Aristolochic acid (AAI) nephropathy (AAN) is a common and rapidly progressive interstitial nephropathy caused by ingestion of Aristolochia herbal medications. Available data on pathophysiology and molecular
Isolation, structural elucidation and anti-inflammatory activity of astragalin, (-)hinokinin, aristolactam I and aristolochic acids (I & II) from Aristolochia indica.
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Astragalin was isolated for the first time along with (-)hinokinin, aristolactam I and aristolochic acids (I & II) from the extracts of Aristolochia indica L. using a new, efficient preparative HPLC method. A reversed-phase HPLC method of analysis was developed to analyse the isolated compounds. The
Effect of aristolochic acid on arachidonic acid cascade and in vivo models of inflammation.
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Recently, it has been reported that aristolochic acid inhibits phospholipase A2 (PLA2) in vitro and also decrease either oedema induced by snake venom and human synovial fluid PLA2. The aim of this research was to study the antiinflammatory activity of aristolochic acid and to investigate the effect
A comparison between the effects of ochratoxin A and aristolochic acid on the inflammation and oxidative stress in the liver and kidney of weanling piglets.
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Ochratoxin A (OTA) and aristolochic acid (AA) are toxins that can frequently contaminate cereals and cereals-based products. The present study has realized a comparison between the effect of OTA and AA on oxidative stress and inflammation in both the liver and kidney of pigs as major organs involved
Aristolochic Acid induces heart failure in zebrafish embryos that is mediated by inflammation.
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Aristolochic Acid (AA) is a component of Chinese herbs that has been found to be toxic to multiple organs in adults. Its toxicity to developing embryos has not been reported. Here, we describe that AA specifically causes heart defects in developing zebrafish embryos in a dosage-dependent manner. The
[ON THE EFFICACY OF ARISTOLOCHIC ACID ON CHRONIC INFLAMMATORY TISSUE PROCESSES].
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[Studies on the problem of the possible use of aristolochic acid in chronic inflammatory processes of the jaw region. Preliminary report].
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Evidence for inflammation-mediated memory dysfunction in gastropods: putative PLA2 and COX inhibitors abolish long-term memory failure induced by systemic immune challenges.
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BACKGROUND
Previous studies associate lipid peroxidation with long-term memory (LTM) failure in a gastropod model (Lymnaea stagnalis) of associative learning and memory. This process involves activation of Phospholipase A2 (PLA2), an enzyme mediating the release of fatty acids such as arachidonic
Nephroprotective role of resveratrol and ursolic Acid in aristolochic Acid intoxicated zebrafish.
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The nephrotoxicity of aristolochic acid (AA) is well known, but information regarding the attenuation of AA-induced toxicity is limited. The aim of the present study was to study the nephroprotective effects of resveratrol (Resv) and ursolic acid (UA) in a zebrafish model. We used two transgenic
Aristolochic acid I aggravates renal injury by activating the C3a/C3aR complement system.
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Previous studies have reported that the complement system is unconventionally activated in many kinds of glomerulonephritis. Multiple complement components participate in the pathogenic process by triggering immune response or other intracellular signaling pathways. Here, we have investigated the
Microarray analysis reveals the inhibition of nuclear factor-kappa B signaling by aristolochic acid in normal human kidney (HK-2) cells.
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OBJECTIVE
To study the molecular mechanism underlying the effect of aristolochic acid (AA), a major active component of plants from the Aristolochiaceae family using microarray analysis.
METHODS
Human kidney (HK-2) cells were treated with AA (0, 10, 30, and 90 micromol/L) for 24 h, and the cell
Involvement of p38 MAPK phosphorylation and nitrate formation in aristolochic acid-mediated antiplatelet activity.
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Aristolochic acid (AsA) is produced from Aristolochia fangchi, and has been used as a Chinese herbal medicine. AsA possesses various biological activities including antiplatelet, antifungal, and anti-inflammatory properties. The aim of this study was to examine the mechanisms of AsA in inhibiting
Targeting c-fms kinase attenuates chronic aristolochic acid nephropathy in mice.
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Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by some Chinese herbal medicines, but treatment remains ineffective. Macrophage accumulation is an early feature in human and experimental AAN; however, the role of macrophages in chronic AAN is unknown. We report here that
Quantitation of N6-Formyl-lysine Adduct Following Aristolochic Acid Exposure in Cells and Rat Tissues by Liquid Chromatography-Tandem Mass Spectrometry Coupled with Stable Isotope-Dilution Method.
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N6-Formyl-lysine (FLys) is an abundant and lasting protein adduct formed when formaldehyde generated by nitrosative/oxidative stress and inflammation reacts with lysine residues. It is believed that the post-translational N6-formylation of lysine is associated
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