Effect of melatonin on secreted and induced matrix metalloproteinase‐9 and ‐2 activity during prevention of indomethacin‐induced gastric ulcer

Ganguly, Krishnendu; Maity, Pallab; Reíter, Russel J.; Swarnakar, Snehasikta

doi:10.1111/j.1600-079x.2005.00250.x

Cited by 53 publications

(56 citation statements)

References 58 publications

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“…The potential antiulcer drugs can exert their protective effect against mucosal lesions through inhibition of neutrophil infiltration in the ulcerated gastric tissue (Ganguly et al, 2005). Furthermore, neutrophil accumulation in a gastric mucosa has been shown to induce microcirculatory abnormalities.…”

Section: Discussionmentioning

confidence: 99%

Anti-ulcerogenic effect of Zuojin Pill against ethanol-induced acute gastric lesion in animal models

Wang

Zhang

Zhu

et al. 2015

Journal of Ethnopharmacology

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Section: Discussionmentioning

confidence: 99%

Anti-ulcerogenic effect of Zuojin Pill against ethanol-induced acute gastric lesion in animal models

Wang

Zhang

Zhu

et al. 2015

Journal of Ethnopharmacology

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“…29 Moreover, melatonin offers protection against fibrosis by preventing oxidative damage caused by lipid peroxidation and glutathione depletion. 30 Pycnogenol, a standardized and patented extract from the bark of the French maritime pine (Pinus pinaster Aiton), consists of a concentrate of polyphenols. 31 Pycnogenol is marketed worldwide as a food supplement or as an herbal drug.…”

mentioning

confidence: 99%

Effects of Melatonin and Pycnogenol on Small Artery Structure and Function in Spontaneously Hypertensive Rats

et al. 2010

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Abstract-It was suggested that oxidative stress has a key role in the development of endothelial dysfunction, as well as microvascular structural alterations. Therefore, we have investigated 2 substances with antioxidant properties: melatonin and Pycnogenol. We treated 7 spontaneously hypertensive rats (SHRs) with melatonin and 7 with Pycnogenol for 6 weeks. We compared results obtained with those observed in 7 SHRs and 7 Wistar-Kyoto normotensive control rats kept untreated. Mesenteric small resistance arteries were dissected and mounted on a wire myograph, and a concentrationresponse curve to acetylcholine was performed. Aortic contents of metalloproteinase 2, Bax, inducible NO synthase, and cyclooxygenase 2 were evaluated, together with the aortic content of total collagen and collagen subtypes and apoptosis rate. A small reduction in systolic blood pressure was observed. A significant improvement in mesenteric small resistance artery structure and endothelial function was observed in rats treated with Pycnogenol and melatonin. Total aortic collagen content was significantly greater in untreated SHRs compared with Wistar-Kyoto control rats, whereas a full normalization was observed in treated rats. Apoptosis rate was increased in the aortas of untreated SHRs compared with Wistar-Kyoto control rats; an even more pronounced increase was observed in treated rats. Bax and metalloproteinase 2 expressions changed accordingly. Cyclooxygenase 2 and inducible NO synthase were more expressed in the aortas of untreated SHRs compared with Wistar-Kyoto control rats; this pattern was normalized by both treatments. In conclusion, our data suggest that treatment with Pycnogenol and melatonin may protect the vasculature, partly independent of blood pressure reduction, probably through their antioxidant effects. Key Words: endothelial function Ⅲ melatonin Ⅲ Pycnogenol oxidative stress R eactive oxygen species (ROS) are generated as byproducts of cellular respiration and other metabolic processes and may contribute to oxidative damage. 1,2 The ROS family includes several molecules that have divergent effects on cellular function, namely, regulation of cell growth and differentiation, modulation of extracellular matrix production and breakdown, inactivation of NO, and stimulation of protein kinases and proinflammatory genes. 3-5 Importantly, some of these actions are associated with pathological changes in cardiovascular tissues. 6 In cardiovascular disease, increased ROS production leads to endothelial dysfunction, increased vascular contractility, vascular smooth muscle cell growth and apoptosis, monocyte migration, lipid peroxidation, inflammation, and increased deposition of extracellular matrix proteins, all processes contributing to vascular damage. 7 ROS may be important in the development and maintenance of hypertension, in terms of excess production of oxidants, decreased NO bioavailability, and decreased antioxidant capacity in the vasculature and kidneys. 6,7 Hypertension may contribute to structural and functional al...

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“…In a rat experimental model, up-regulation of MMP-9 induced intestinal barrier dysfunction and bacterial translocation (Mikami et al, 2009). On the other hand, reduction in MMP-9 activity resulted in attenuation of the development of indomethacin-induced gastric ulcers in rats (Ganguly et al, 2005). In a rat model with ethanol-induced gastric ulcer, MMP-9 down-regulation also prevented the development of gastric ulcer (Singh et al, 2007).…”

Section: Role Of Chymase On Nsaid-induced Small Intestinal Damages 687mentioning

confidence: 99%

“…MMPs are a family of zinc-and calcium-dependent endopeptidases, divided into different subgroups: collagenases, gelatinases, stromilysins, membrane-type MMPs, and other MMPs. Among the MMPs, MMP-9 is known as a gelatinase, and it was recently documented that MMP-9 plays an important role in the development of gastric damage induced by an NSAID in rats (Ganguly et al, 2005). However, very little is known about the involvement of MMPs in NSAID-induced small intestinal enteritis.…”

mentioning

confidence: 99%

Significance of Chymase-Dependent Matrix Metalloproteinase-9 Activation on Indomethacin-Induced Small Intestinal Damages in Rats

Kakimoto

Takai²,

Murano³

et al. 2009

J Pharmacol Exp Ther

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The side effects of nonsteroidal anti-inflammatory drugs (NSAIDs) include gastrointestinal damage not only in the stomach but also in the small intestine. Chymase converts promatrix metalloproteinase-9 to matrix metalloproteinase (MMP)-9, which plays an important role in NSAID-induced gastric damage, but it has been unclear whether chymase-dependent MMP-9 activation is involved in the NSAID-induced small intestinal damage. To clarify the involvement of chymase-dependent MMP-9 activation on NSAID-induced small intestinal damage, the effect of a chymase inhibitor, 2-[4-(5-fluoro-3-methylbenzo[b]thiophen-2-yl)sulfonamido-3-methanesulfonylphenyl] thiazole-4-carboxylic acid (TY-51469), on indomethacin-induced small intestinal damage in rats was evaluated. Until 6 h after oral administration of indomethacin in rats, intestinal MMP-9 activity was unchanged compared with normal rats, but significant increases in MMP-9 activity were observed 12 and 24 h after indomethacin administration. Significant increases in the small intestinal damage score were also observed 12 and 24 h after indomethacin administration. In the extract from the small intestine 24 h after indomethacin administration, the MMP-9 activation was significantly attenuated by TY-51469. Intraperitoneal injection of TY-51469 (10 mg/kg) 3 h before indomethacin administration significantly attenuated the MMP-9 activity in the small intestine compared with placebo treatment. Myeloperoxidase activity, which indicates accumulation of neutrophils, was significantly increased in the small intestine in the placebo-treated rats, but its activity was significantly attenuated by TY-51469 treatment. The area of small intestinal damage was also significantly ameliorated by TY-51469 treatment. These findings suggest that chymase-dependent MMP-9 activation has a significant role in indomethacin-induced small intestinal damage in rats.Nonsteroidal anti-inflammatory drugs (NSAIDs) such as indomethacin have been widely used for their anti-inflammatory effects, but they are known to produce gastric damage. More recently, with the development of capsule endoscopy and double-balloon endoscopy, it has become possible to examine the small intestine endoscopically, and NSAID-induced damage in the small intestine has been clarified (Allison et al., 1992;Maiden et al., 2005). We recently proposed the possibilities of the therapeutic targets in NSAID-induced small intestinal damage (Higuchi et al., 2009). However, the mechanism of NSAID-induced small intestinal damage has been still unclear, and useful medications have not been identified.Matrix metalloproteinases (MMPs) play a crucial role in physiological turnover of extracellular matrix with degradation and remodeling during inflammation. MMPs are a family of zinc-and calcium-dependent endopeptidases, divided into different subgroups: collagenases, gelatinases, stromilysins, membrane-type MMPs, and other MMPs. Among the MMPs, MMP-9 is known as a gelatinase, and it was recently documented that MMP-9 plays an important role i...

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Effect of melatonin on secreted and induced matrix metalloproteinase‐9 and ‐2 activity during prevention of indomethacin‐induced gastric ulcer

Cited by 53 publications

References 58 publications

Anti-ulcerogenic effect of Zuojin Pill against ethanol-induced acute gastric lesion in animal models

Anti-ulcerogenic effect of Zuojin Pill against ethanol-induced acute gastric lesion in animal models

Effects of Melatonin and Pycnogenol on Small Artery Structure and Function in Spontaneously Hypertensive Rats

Significance of Chymase-Dependent Matrix Metalloproteinase-9 Activation on Indomethacin-Induced Small Intestinal Damages in Rats

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