Comparative Protective Effect of Hawthorn Berry Hydroalcoholic Extract, Atorvastatin, and Mesalamine on Experimentally Induced Colitis in Rats

Malekinejad, Hassan; Shafie-Irannejad, Vahid; Hobbenaghi, Rahim; Tabatabaie, S. Hamed; Moshtaghion, Seyed-Mehdi

doi:10.1089/jmf.2012.2672

Cited by 19 publications

(27 citation statements)

References 43 publications

(40 reference statements)

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“…SFZ also induced a significant decrease in DSS-stimulated MDA content, and a non-significant increase in SOD activity. Hawthorn berry extract, a source of UA, has been found to decrease neutrophil infiltration in colon tissues in a colitis model (14). In the present study, MPO activity, an important maker of neutrophils, was measured to examine the effect of UA on neutrophil infiltration.…”

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

confidence: 91%

“…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). Hawthorn berry extract containing 0.5% UA decreased edema and the infiltration of neutrophils in the colonic tissues of acetic acid-treated rats (14).…”

Section: Introductionmentioning

confidence: 99%

“…Previously, UA was reported to be involved in colitis in a number of publications (4,14,15). Hawthorn berry extract containing 0.5% UA decreased edema and the infiltration of neutrophils in the colonic tissues of acetic acid-treated rats (14). UA significantly inhibits the production of pro-inflammatory cytokines, including tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, and the expression of cyclooxygenase-2 and inducible nitric oxide (NO) synthetase in lipopolysacharride (LPS)-stimulated macrophages and colonic tissues from 2,4,6-trinitrobenzenesulfonic-treated mice (4,15).…”

Section: Introductionmentioning

confidence: 99%

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

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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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“…Mesalazine is used clinically at oral doses of 10-70 mg·kg −1 per day in patients with IBD (Das et al, 1973;Sandborn and Hanauer, 2003). In many studies of experimental colitis in mice, mesalazine is given at oral doses of 50 or 100 mg·kg −1 (Malekinejad et al, 2013;Sann et al, 2013). However, in our preliminary studies, when we gave mesalazine at 10, 20 or 50 mg·kg −1 to our model of colitis in mice, we could not find any significant difference of anti-colitis effects such as colon shortening and macroscopic score between these doses (data not shown).…”

Section: Figurementioning

confidence: 99%

Penta‐O‐galloyl‐β‐D‐glucose ameliorates inflammation by inhibiting MyD88/NF‐κB and MyD88/MAPK signalling pathways

Jang

Hyam

Jeong

et al. 2013

British J Pharmacology

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BACKGROUND AND PURPOSEThe gallnut of Rhus chinensis MILL and its main constituent penta-O-galloyl-β-D-glucose (PGG) inhibited NF-κB activation in LPS-stimulated peritoneal and colonic macrophages. Here we have investigated PGG mechanisms underlying anti-inflammatory effects of PGG in vitro and in vivo. EXPERIMENTAL APPROACHMale C57BL/6 mice (18-22 g, 6 weeks old) were used to prepare peritoneal and colonic macrophages and for the induction of colitis by intrarectal administration of 2,3,4-trinitrobenzene sulphonic acid (TNBS). A range of inflammatory markers and transcription factors were evaluated by ELISA, immunoblotting, flow cytometry and confocal microscopy. KEY RESULTSExpression of Toll-like receptor (TLR)-4 or Lipopolysaccharide (LPS) binding to TLR-4 in LPS-stimulated peritoneal macrophages was not affected by PGG. However PGG inhibited binding of an anti-MyD88 antibody to peritoneal macrophages, but did not reduce binding of anti-IL-1 receptor-associated kinase (IRAK1) and IRAK4 antibodies to the macrophages with or without transfection with MyD88 siRNA. PGG potently reduced the activation of IRAK1, NF-κB, and MAPKs in LPS-or pepetidoglycan-stimulated peritoneal and colonic macrophages. PGG suppressed IL-1β, TNF-α and IL-6 in LPS-stimulated peritoneal macrophages, while increasing expression of the anti-inflammatorycytokine IL-10. Oral administration of PGG inhibited colon shortening and myeloperoxidase activity in mice with TNBS-induced colitis, along with reducing NF-κB activation and IL-1β, TNF-α, and IL-6 levels, whereas it increased IL-10. CONCLUSIONS AND IMPLICATIONSPGG reduced activation of NF-κB and MAPK signalling pathways by directly interacting with the MyD88 adaptor protein. PGG may ameliorate inflammatory diseases such as colitis.

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“…In recent years, with increasing morbidity, coronary heart disease is most evident in middle-aged and elderly people and seriously threatens life and health of patients. As commonly used drugs for the clinical treatment of coronary heart diseases, atorvastatin and trimetazidine have effects of antiinflammation, lipid reduction, blood vessel protection, cardiac function recovery, and plaque dissolution facilitation with favorable clinical application effect [3,4]. In this study, 98 patients with coronary heart diseases accepted by our hospital from February 2016 to June 2017 were studied to analyse the clinical effect of atorvastatin-trimetazidine combined treatment.…”

Section: Introductionmentioning

confidence: 99%

Clinical effect of atorvastatin-trimetazidine combined treatment of coronary heart disease

Song¹,

Wang²

2018

biomedicalresearch

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Comparative Protective Effect of Hawthorn Berry Hydroalcoholic Extract, Atorvastatin, and Mesalamine on Experimentally Induced Colitis in Rats

Cited by 19 publications

References 43 publications

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

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

Penta‐O‐galloyl‐β‐D‐glucose ameliorates inflammation by inhibiting MyD88/NF‐κB and MyD88/MAPK signalling pathways

Clinical effect of atorvastatin-trimetazidine combined treatment of coronary heart disease

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