Ursolic acid: a potent Inhibitor of superoxides produced in the cellular system

Ali, Muhammad; Ibrahim, Syed Amir; Jalil, Saima; Choudhary, M. Iqbal

doi:10.1002/ptr.2108

Cited by 66 publications

(40 citation statements)

References 9 publications

(11 reference statements)

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“…In order to identify the flavonoids, the NaOCH 3 , AlCl 3 /HCl, and NaOAc/H 3 BO 3 UV spectrum were also used (Mabry et al, 1970). All these data were in good agreement with the respective literature data (Ahmad et al, 1987;Ali et al, 2007;Lendl et al, 2005;Markham, 1982;Markham & Geiger, 1993;Mizushina et al, 2006;Wang et al, 2009). …”

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confidence: 79%

Compounds fromSedum caeruleumwith antioxidant, anticholinesterase, and antibacterial activities

Bensouici

Kabouche

Karioti

et al. 2015

Pharmaceutical Biology

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Context: This is the first study on the phytochemistry, antioxidant, anticholinesterase, and antibacterial activities of Sedum caeruleum L. (Crassulaceae). Objective: The objective of this study is to isolate the secondary metabolites and determine the antioxidant, anticholinesterase, and antibacterial activities of S. caeruleum. Materials and methods: Six compounds (1-6) were isolated from the extracts of S. caeruleum and elucidated using UV, 1D-, 2D-NMR, and MS techniques. Antioxidant activity was investigated using DPPH , CUPRAC, and ferrous-ions chelating assays. Anticholinesterase activity was determined against acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) enzymes using the Ellman method. Antibacterial activity was performed according to disc diffusion and minimum inhibitory concentration (MIC) methods. Results: Isolated compounds were elucidated as ursolic acid (1), daucosterol (2), b-sitosterol-3-O-b-D-galactopyranoside (3), apigenin (4), apigetrin (5), and apiin (6). The butanol extract exhibited highest antioxidant activity in all tests (IC 50 value: 28.35 ± 1.22 mg/mL in DPPH assay, IC 50 value: 40.83 ± 2.24 mg/L in metal chelating activity, and IC 50 value: 23.52 ± 0.44 mg/L in CUPRAC), and the highest BChE inhibitory activity (IC 50 value: 36.89 ± 0.15 mg/L). Moreover, the chloroform extract mildly inhibited (MIC value: 80 mg/mL) the growth of all the tested bacterial strains. Discussion and conclusion: Ursolic acid (1), daucosterol (2), b-sitosterol-3-O-b-D-galactopyranoside (3), apigenin (4), apigetrin (5), and apiin (6) were isolated from Sedum caeruleum for the first time. In addition, a correlation was observed between antioxidant and anticholinesterase activities of bioactive ingredients of this plant.

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supporting

confidence: 79%

Compounds fromSedum caeruleumwith antioxidant, anticholinesterase, and antibacterial activities

Bensouici

Kabouche

Karioti

et al. 2015

Pharmaceutical Biology

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“…It has been reported that UA has anti-inflammatory effects on macrophages (26). To investigate the effects of UA on pro-inflammatory cytokines such as IL-1, IL-6, and TNF, pMs were treated with LPS (100 ng/ml) and/or UA (10 M) for 6 h, and the expression of the abovementioned cytokines was examined using qPCR.…”

Section: Ua Suppresses Il-1 Production In Macrophagesmentioning

confidence: 99%

Ursolic acid enhances macrophage autophagy and attenuates atherogenesis

Leng

Iwanowycz

Saaoud

et al. 2016

Journal of Lipid Research

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This article is available online at http://www.jlr.org recycled for downstream metabolism (1). Among the three major kinds of autophagy, macroautophagy, microautophagy, and chaperone-mediated autophagy, macroautophagy is the most prevalent form and, thus, commonly referred to as autophagy (2, 3). Over the past decade, research efforts regarding this ancient biological process have been revived due to the realization that alterations in autophagy play crucial pathological roles in many diseases (4, 5) for which current therapeutic means are limited. While many basic aspects of autophagy have been unraveled, little has been translated into clinical benefit, and no autophagy-modulating therapies have been approved for clinical use.The autophagy process starts with the formation of a double-membrane autophagosome, which engulfs cytoplasmic materials. Autophagosomes are targeted to the lysosomal compartment and single-membrane autolysosomes are generated in which the sequestered cargos are degraded in the highly acidic environment and the resulting simple products are reused (6, 7). There are many molecules involved in autophagy, including Beclin-1 (involved in vesicle nucleation); Atg5, Atg7, and Atg16L1 (involved in vesicle elongation); and LC3 (involved in the expansion of autophagosome membrane and autophagosome-lysosome fusion) (8). Autophagy occurs in almost all cell types, including macrophages. Macrophages primarily use phagocytosis as the first line of defense against exogenous pathogens and endogenous waste products. They adopt autophagy to process bulky materials (e.g., damaged mitochondria and excessive lipids) in unfavorable microenvironments, thus mitigating cytotoxicity. Recently, autophagy has been shown to play a critical role in inflammatory responses in macrophages by interacting with inflammasomes or directly targeting pro-interleukin Abstract Macrophage autophagy has been shown to be protective against atherosclerosis. We previously discovered that ursolic acid (UA) promoted cancer cell autophagy. In the present study, we aimed to examine whether UA enhances macrophage autophagy in the context of atherogenesis. Cell culture study showed that UA enhanced autophagy of macrophages by increasing the expression of Atg5 and Atg16l1, which led to altered macrophage function. UA reduced pro-interleukin (IL)-1 protein levels and mature IL-1 secretion in macrophages in response to lipopolysaccharide (LPS), without reducing IL-1 mRNA expression. Confocal microscopy showed that in LPS-treated macrophages, UA increased LC3 protein levels and LC3 appeared to colocalize with IL-1. In cholesterolloaded macrophages, UA increased cholesterol efflux to apoAI, although it did not alter mRNA or protein levels of ABCA1 and ABCG1. Electron microscopy showed that UA induced lipophagy in acetylated LDL-loaded macrophages, which may result in increased cholesterol ester hydrolysis in autophagolysosomes and presentation of free cholesterol to the cell membrane. In LDLR / mice fed a Western diet to induce atherogenesi...

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“…As UA exhibits antioxidant activity in certain cell models or cell-free models (10)(11)(12), the present study aimed to determine whether UA interferes in antioxidant ability in colon tissues. The content of MDA, a marker of lipid peroxidative damage, and activity of SOD, an important anti-oxidative enzyme were measured.…”

Section: Ua Decreases Mda Content and Mpo Activity And Increases Sodmentioning

confidence: 99%

“…UA is well known to possess various biological activities, including anti-inflammatory (5,6), anticancer (7,8), hypoglycemic (9), antioxidant (10)(11)(12) and immunomodulatory activities (13). Previously, UA was reported to be involved in colitis in a number of publications (4,14,15).…”

Section: Introductionmentioning

confidence: 99%

Ursolic acid protects against ulcerative colitis via anti-inflammatory and antioxidant effects in mice

Liu

Piao

Guo

et al. 2016

Molecular Medicine Reports

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Abstract. Ursolic acid (UA) has been reported to have a protective effect in colitis. However, the underlying mechanisms remain to be elucidated. In the present study, experimental ulcerative colitis was induced in male BALB/c mice by the administration of 5% dextran sulfate sodium (DSS) for 7 days, followed by treatment with UA for another 7 days. Hematoxylin & eosin staining was performed to evaluate colon tissue damage, and enzyme assays were used to measure malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in colon homogenate. In addition, serum levels of interleukin (IL)-1β and tumor necrosis factor (TNF)-α were measured using an ELISA, and the level of nuclear factor (NF)-κB p65 in the colonic tissues was assessed by western blotting. The 7-day DSS administration induced marked colon damage, increased the serum levels of IL-1β and TNF-α, increased MDA content and decreased SOD activity in the colon homogenate. These changes were significantly improved by treatment with UA. UA also reduced the DSS-stimulated high nuclear level of NF-κB p65 in the colon tissues. These results demonstrate a protective role of UA in ulcerative colitis, and suggest that anti-inflammatory and antioxidant activities are involved in the underlying mechanisms.

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Ursolic acid: a potent Inhibitor of superoxides produced in the cellular system

Cited by 66 publications

References 9 publications

Compounds fromSedum caeruleumwith antioxidant, anticholinesterase, and antibacterial activities

Compounds fromSedum caeruleumwith antioxidant, anticholinesterase, and antibacterial activities

Ursolic acid enhances macrophage autophagy and attenuates atherogenesis

Ursolic acid protects against ulcerative colitis via anti-inflammatory and antioxidant effects in mice

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