Increased expression of matrix metalloproteinase-9 associated with gastric ulcer recurrence

Li, Senlin; Zhao, Junli; Ren, Xiaohan; Xie, Jia-Ping; Qiang, Ma; Rong, Qiu-Hua

doi:10.3748/wjg.v19.i28.4590

Cited by 38 publications

(39 citation statements)

References 21 publications

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“…Studies by Rautelin HI et al and Li SL et al found that MMP-9 level increased significantly in the gastric mucosa of gastritis patients with positive H. pylori compared to the negative [ 22 , 23 ]. In a study conducted by Oliviera, it was found that H. pylori through a T4SS (Type IV Secretion System) pathway increases the activity of MMP-9 as a response to the invasion of H. pylori on the gastric epithelium [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Serum IL-10, MMP-7, MMP-9 Levels in Helicobacter pylori Infection and Correlation with Degree of Gastritis

Siregar¹,

Halim²,

Sitepu³

2016

Open Access Maced J Med Sci

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AIM:Helicobacter pylori causes gastric mucosal inflammation and immune reaction. However, the increase of IL-10, MMP-7, and MMP-7 levels in the serum is still controversial. The objective of this study was to investigate the serum levels of IL-10, MMP-7 & MMP-9 in gastritis patients with H. pylori infection.MATERIALS AND METHODS:A cross-sectional study was done on seventy gastritis patients that consecutive admitted to endoscopy units. The diagnosis of gastritis was made based on histopathology and diagnosis of H. pylori infection was based on rapid urease test. Serum samples were obtained to determine to circulate IL-10, MMP-7, and MMP-9 level. Univariate and bivariate analysis were done by SPSS version 22.RESULTS:Forthy percentages of the patients were infected with H. pylori. The IL-10 level was significantly higher in H. pylori-infected patients compared to non-infected patients. However, there were no differences between serum levels of MMP-7 and MMP-9 in infected and non-infected H. pylori patients.CONCLUSIONS:The immune response to H. pylori promotes systemic inflammation, which was reflected by the increased levels of serum IL-10. However, there were no significant differences in MMP-7 and MMP-9 serum levels between positive and negative infected H. pylori patients.

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Section: Discussionmentioning

confidence: 99%

Serum IL-10, MMP-7, MMP-9 Levels in Helicobacter pylori Infection and Correlation with Degree of Gastritis

Siregar¹,

Halim²,

Sitepu³

2016

Open Access Maced J Med Sci

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“…Other studies have reported that the ulceration process induced by acetic acid involves an elevation in the gelatinases, which return to normal levels during the healing process [27]. Li et al [28] demonstrated that an increase in MMP-9 in gastric tissue is often associated with the development and progression of gastric ulcers. In the present study, we observed a reduction in MMP-9 in the chrysin-treated group, compared with that in the vehicle-treated group (Figure 6), which is consistent with that demonstrated in myocardial infarction [29].…”

Section: Resultsmentioning

confidence: 97%

Chrysin Modulates Genes Related to Inflammation, Tissue Remodeling, and Cell Proliferation in the Gastric Ulcer Healing

Fagundes

Piffer

Périco

et al. 2020

IJMS

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Chrysin exhibits anti-inflammatory and antioxidant activities. Here, the gastroprotective effect of chrysin was investigated in mouse models of gastric ulcer induced by absolute ethanol, acetic acid, and ischemia-reperfusion injury. The gastric-healing effect was evaluated at 7 and 14 days after treatment; the mechanism of action was verified using the expression of metalloproteinase 2 (MMP-2) and 9 (MMP-9), caspase-3, cyclooxygenase 1 (COX-1) and 2 (COX-2), epidermal growth factor (EGF), and interleukin-10. Chrysin (10 mg/kg) inhibited macroscopic lesions and increased catalase activity in the mouse model established using absolute ethanol. It ameliorated the gastric ulcer caused by acetic acid by improving the expression of inflammatory genes such as COX-2, inhibiting negative remodeling promoted by MMP-9, increasing cell proliferation effect via EGF, and reducing cellular apoptosis by modulating caspase-3. A faster healing effect was evident in the first 7 days of treatment compared to 14 days of treatment, indicating the pharmacological potential of chrysin. Overall, these results demonstrate the potent effect of chrysin in the gastrointestinal tract and elucidate the genes involved in the healing of gastric ulcers. Moreover, an increase in the levels of gastric mucosa defensive factors is involved in the activity of chrysin in the gastric mucosa.

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“…Degradation and remodeling of the extracellular matrix (ECM) is a process of major importance during gastric ulcer formation, in which matrix metalloproteinases (MMPs) are essential. Among the different subtypes of MMPs, MMP-9 is known to play an important role in gastric damage [101]. MMP-9 expression is associated with the production and release of inflammatory mediators, such as interleukin-4 (IL-4), interleukin-1β (IL-1β), and most importantly TNF-α [102,103].…”

Section: Mechanisms Of Action Of the Peptic Ulcersmentioning

confidence: 99%

“…MMP-9 expression is associated with the production and release of inflammatory mediators, such as interleukin-4 (IL-4), interleukin-1β (IL-1β), and most importantly TNF-α [102,103]. Oxidative stress and ROS in gastric glands enhance the expression of MMP-9, intensifying the gastric mucosal injury [101,103]. Thymol protects against ethanol-induced gastric ulcer by downregulating the expression of MMP-9 [69,70].…”

Section: Mechanisms Of Action Of the Peptic Ulcersmentioning

confidence: 99%

Systematic Analysis of Monoterpenes: Advances and Challenges in the Treatment of Peptic Ulcer Diseases

et al. 2020

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Peptic ulcer disease (PUD) is a multifactorial and complex disease caused by an imbalance of protective and aggressive factors (endogenous and exogenous). Despite advances in recent years, it is still responsible for substantial mortality and triggering clinical problems. Over the last decades, the understanding of PUD has changed a lot with the discovery of Helicobacter pylori infection. However, this disease continues to be a challenge due to side-effects, incidence of relapse from use of various anti-ulcer medicines, and the rapid appearance of antimicrobial resistance with current H. pylori therapies. Consequently, there is the need to identify more effective and safe anti-ulcer agents. The search for new therapies with natural products is a viable alternative and has been encouraged. The literature reports the importance of monoterpenes based on the extensive pharmacological action of this class, including wound healing and anti-ulcerogenic agents. In the present study, 20 monoterpenes with anti-ulcerogenic properties were evaluated by assessing recent in vitro and in vivo studies. Here, we review the anti-ulcer effects of monoterpenes against ulcerogenic factors such as ethanol, nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori, highlighting challenges in the field.Biomolecules 2020, 10, 265 2 of 18 PUD results from an imbalance in mucosal defensive factors, such as mucus secretion, bicarbonate efflux, endogenous antioxidant, cell regeneration, continuous synthesis and release of prostaglandin E 2 (PGE 2 ), nitric oxide (NO), and sulfhydryl compounds (SH); and aggressive agents such as smoking, alcohol consumption, dietary factors, stress, prolonged and excessive intake of nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori (H. pylori) infection, among others [6][7][8][9]. For a long time, it was believed that the main factor implicated in the development and progression of peptic ulceration was an hypersecretory acidic environment and together with dietary factors and/or stress was thought to cause most of PUD. But the discovery of H. pylori infection and the widespread use of NSAIDs in the second half of the 20 th century changed this perception. In recent years, peptic ulcer has been found to have multiple causes-H. pylori infection, NSAIDs, smoking, alcohol consumption, stress, lifestyle, and genetic predispositions are determined as major risk factors for the development of PUD [2]. PathophysiologyUnder normal conditions, gastric and duodenal mucosa integrity is maintained by the mucus-bicarbonate barrier, the neutral pH, and continuous epithelial cell renewal [10,11]. PGE 2 stimulates cell proliferation, mucus, and bicarbonate production, promoting a crucial function in mucosa preservation. Another vital factor in gastric homeostasis is adequate blood flow. The NO and PGs are responsible for the maintenance of proper perfusion to the gastric mucosa, assuring the delivery of oxygen and nutrients, as well as removing toxic metabolites, preventing damages to the ti...

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Increased expression of matrix metalloproteinase-9 associated with gastric ulcer recurrence

Abstract: MMP-9 may perform an important function in gastric ulcer formation and recurrence.

Cited by 38 publications

References 21 publications

Serum IL-10, MMP-7, MMP-9 Levels in Helicobacter pylori Infection and Correlation with Degree of Gastritis

Serum IL-10, MMP-7, MMP-9 Levels in Helicobacter pylori Infection and Correlation with Degree of Gastritis

Chrysin Modulates Genes Related to Inflammation, Tissue Remodeling, and Cell Proliferation in the Gastric Ulcer Healing

Systematic Analysis of Monoterpenes: Advances and Challenges in the Treatment of Peptic Ulcer Diseases

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