Molecular mechanism of indomethacin-induced gastropathy

Yadav, Sudhir Kumar; Adhikary, Biplab; Chand, Saswati N.; Maity, Biswanath; Bandyopadhyay, Sandip K.; Chattopadhyay, Subrata

doi:10.1016/j.freeradbiomed.2011.12.023

Cited by 93 publications

(47 citation statements)

References 63 publications

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“…In harmony with the present study, indomethacin administration results in increased amounts of oxidative damage activation of NF-κB [5]. Oxidative stress is known to stimulate transcription factors, including NF-κB [33].…”

Section: Discussionsupporting

confidence: 87%

“…Tumor necrosis factor-α promotes gastric epithelial cell apoptosis and triggers activation of adhesion molecules and leukocyte recruitment, leading to microvascular perturbations [4]. Indomethacin also activates the transcription factor nuclear factor-κB (NF-κB) and all the mitogen-activated protein kinases [5]. Other mechanisms, by which indomethacin induces gastric injury, involve gastric hypermotility and increased production of reactive oxygen and nitrogen species, as well as lipid peroxidation [3].…”

Section: Introductionmentioning

confidence: 99%

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Mechanisms of the Protective Effects of Curcumin against Indomethacin-Induced Gastric Ulcer in Rats

Morsy

El‐Moselhy

2013

Pharmacology

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Background/Aims: Curcumin, a naturally occurring polyphenolic compound, exhibits anti-inflammatory and antioxidant properties that render it an attractive candidate for protection against gastric ulcer. The aim of this study is therefore to evaluate the protective effects of curcumin against indomethacin-induced gastric ulcer in rats. Methods: Gastric ulceration was induced by a single intraperitoneal injection of indomethacin (30 mg/kg). Curcumin (50 mg/kg, p.o.) was administered 30 min before ulcer induction. Results: Curcumin showed gastroprotective effects as evidenced by significant decreases in ulcer index, total acid output and pepsin activity in gastric juice in addition to gastric mucosal malondialdehyde concentration, and concomitant increases in gastric juice mucin concentration, gastric mucosal nitric oxide level and catalase and superoxide dismutase activities as compared to the indomethacin-induced ulcer group. Moreover, immunohistochemical investigations demonstrated that curcumin treatment markedly decreased expression of inducible nitric oxide synthase, nuclear factor-κB, and caspase-3. Conclusion: Curcumin protected the rats' gastric mucosa against indomethacin-induced gastric ulceration possibly, at least in part, by enhancement of the gastric mucosal barrier and reduction in acid secretory parameters in addition to antioxidant and antiapoptotic activities.

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Mechanisms of the Protective Effects of Curcumin against Indomethacin-Induced Gastric Ulcer in Rats

Morsy

El‐Moselhy

2013

Pharmacology

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“…TNF-α, a representative inflammatory cytokine with pleiotropic functions, is involved in the induction of inflammation, injury, and carcinogenesis in a variety of tissues [32]. Moreover, TNF-α was the primary contributor to induce the production of NF-κB and other cytokines [33]. IL-6 is another important pro-inflammatory cytokine involved in inflammation process and modulates the expression of genes participating in cell cycle progression [34].…”

Section: Discussionmentioning

confidence: 99%

Preparation, Characterization and Anti-Ulcer Efficacy of Sanguinarine Loaded Solid Lipid Nanoparticles

Sun¹,

Liu

et al. 2017

Pharmacology

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Aim: This study was designed to develop sanguinarine-loaded solid lipid nanoparticles (SG-SLNs) and investigate its gastroprotective effect on ethanol-induced gastric mucosal lesions in mice. Methods: SG-SLNs were prepared by high temperature melt-cool solidification method using glycerol monostearate as the lipid and a combination of lecithin with poloxamer 188 as the surfactants. Solid lipid nanoparticles (SLNs) were designed at varying lipid concentrations (5, 10, 15, and 20 mg/mL), surfactant mixture concentrations (6, 12, and 18 mg/mL), and drug contents (5, 10, 15, and 20 mg/mL) in “one factor at a time” fashion. Ethanol-induced gastric ulcer model was performed on Kunming mice to examine the anti-inflammatory activity of SG-SLNs and compare it with sanguinarine (SG). Results: The high temperature melt-cool solidification method provided consistent production of SLNs with smaller size and high entrapment efficiency (EE%). The composition of optimal formulation was 10 mg/mL lipid concentration, 18 mg/mL surfactant mixture concentration, and 15 mg/mL drug amount. The mean particle size and EE% of optimized formulation were 238 ± 10.9 nm and 79 ± 2.8%, respectively. Additionally, SG-SLNs significantly decreased tumor necrosis factor-alpha and interleukin-6 levels in the serum and gastric tissue, and reduced the content of NO in serum, and strengthened the protection of mucosal membrane. Moreover, SG-SLNs treatment markedly inhibited ethanol-induced nuclear factor-kappa B (NF-κB) activation when compared with SG. Conclusions: SLNs could be potentially applied as a delivery system of SG. The protective effect of SG-SLNs is due to the suppression of NF-κB expression and subsequent pro-inflammatory cytokines release.

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“…)-induced acute stomach ulceration in mice. Moreover, the protocols of IND-mediated ulceration in mice, and its healing by several anti-ulcer agents have also been extensively studied by our group [23,24]. Hence the present study was carried out under the same experimental conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Group I mice served as normal control, while ulceration in the groups II-V mice was induced by IND (18 mg kg − 1 , p. o., single dose) dissolved in distilled water and suspended in the vehicle, gum acacia (2%). The dose of IND and the treatment regime (drug doses and period of treatment) were standardized in our earlier studies [9,23,24]. The mice of groups I and III (referred to as control) were given the daily oral dose of vehicle (gum acacia in distilled water, 0.2 ml).…”

Section: Experimental Protocol For Ulceration and Biochemical Studiesmentioning

confidence: 99%

dl-trans-3,4-Dihydroxy-1-selenolane (DHSred) heals indomethacin-mediated gastric ulcer in mice by modulating arginine metabolism

Chakraborty

Yadav

Subramanian

et al. 2014

Biochimica et Biophysica Acta (BBA) - General Subjects

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Molecular mechanism of indomethacin-induced gastropathy

Cited by 93 publications

References 63 publications

Mechanisms of the Protective Effects of Curcumin against Indomethacin-Induced Gastric Ulcer in Rats

Mechanisms of the Protective Effects of Curcumin against Indomethacin-Induced Gastric Ulcer in Rats

Preparation, Characterization and Anti-Ulcer Efficacy of Sanguinarine Loaded Solid Lipid Nanoparticles

dl-trans-3,4-Dihydroxy-1-selenolane (DHSred) heals indomethacin-mediated gastric ulcer in mice by modulating arginine metabolism

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