Effects of N-acetyl-l-cysteine in patients with chronic atrophic gastritis and nonulcer dyspepsia: a phase III pilot study

Farinati, Fabio; Cardin, R.; Libera, G Della; Pallotta, Teresa; Colantoni, A.; Gurrieri, G

doi:10.1016/s0011-393x(97)80106-3

Cited by 3 publications

(3 citation statements)

References 15 publications

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“…There was no significant reduction in the severity of macroscopic and microscopic score when N-acetylcysteine was administered alone. This finding was in discord with the study by Farinati et al that revealed that NAC is fairly well tolerated and apparently leads to an endoscopic, symptomatic, and to some extent histologic improvement that is not clearly related to changes in mucosal GSH and MDA levels in patients with gastritis and non-ulcer dyspepsia (Farinati et al 1997).…”

Section: Discussioncontrasting

confidence: 55%

Efficiency evaluation of Amlodipine combined with N-acetylcysteine on Indomethacin-induced gastritis in rats

Annouf

Laham

Chatty

2022

RRP

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Introduction: It is a well-known phenomenon that nonsteroidal anti-inflammatory drugs cause gastric mucosal damage. Amlodipine is a third generation dihydropyridine-type calcium channel blocker; it can inhibit inflammatory cytokines and enhance antioxidant defenses. N-acetylcysteine can act both as a precursor of reduced glutathione and as a direct ROS scavenger. Moreover, N-acetylcysteine has been purported to have anti-inflammatory properties. Materials and methods: 34 albino Wistar rats were used. The model of gastritis was induced by subcutaneous Indomethacin prepared in 5% sodium bicarbonate administered at a dose rate of 9 mg/kg for two days at 24h intervals. N-acetylcysteine (500 mg/kg), Amlodipine (10 mg/kg) and N-acetylcysteine (500 mg/kg) combined with Amlodipine (5 mg/kg) were administrated for seven consecutive days beginning 24 h after the first Indomethacin injection. Rats were sacrificed under ether anesthesia on the 8th day. The stomach injury was assessed by macroscopic damage and histological study. Results and discussion: The results showed that macroscopic stomach damage scores caused by administration of Indomethacin did not significantly decrease by administration of N-acetylcysteine alone (p>0.05), but it decreased significantly by administration of Amlodipine alone or by its combination with N-acetylcysteine (p<0.05). Microscopic stomach damage scores did not significantly decrease by administration of Amlodipine or N-acetylcysteine alone (p>0.05), but they decreased significantly by administering the combination of Amlodipine with N-acetylcysteine (p<0.05). Administration of Amlodipine with N-acetylcysteine showed significant reduction in the severity of the gastric inflammation induced by Indomethacin, which was evidenced macroscopically and microscopically. Conclusion: This study concluded that administration of Amlodipine with N-acetylcysteine produce obvious enhancement in gastritis induced by Indomethacin. Graphical abstract:

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Section: Discussioncontrasting

confidence: 55%

Efficiency evaluation of Amlodipine combined with N-acetylcysteine on Indomethacin-induced gastritis in rats

Annouf

Laham

Chatty

2022

RRP

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“…It is thought that this may be the result of a reduction in the mucosal oxidant load as a result of the antioxidant properties of NAC rather than its properties as a GSH precursor. Similarly, a previous study investigating NAC administration in patients with chronic atrophic gastritis and nonulcer dyspepsia observed an improvement both endoscopically and histologically with no related increase in GSH levels [60]. Hence, NAC may act primarily as a GSH precursor in non‐ H. pylori settings but predominantly as an antioxidant during H. pylori infection.…”

Section: Novel Therapies For H Pylori Associated Diseasementioning

confidence: 81%

Cellular Mucosal Defense During Helicobacter pylori Infection: A Review of the Role of Glutathione and the Oxidative Pentose Pathway

Matthews

Butler²

2005

Helicobacter

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Helicobacter pylori is the primary cause of gastritis and peptic ulcer disease and is known to infect greater than 50% of the world's population. It is also known to lead to the onset of gastric cancer and unless treated, lasts throughout life in most individuals. Mouse models of H. pylori infection have improved our ability to study this organism and can be used to investigate the host mucosal response to the infection, particularly the early events postinoculation. Previous studies have shown that H. pylori infection leads to an increased production of reactive oxygen species within the gastric mucosa which are thought to play a major role in the mediation of associated disease. Recent studies have shown differences in the availability of an important antioxidant, glutathione, during chronic H. pylori infection. The availability of glutathione is primarily controlled by the activity of the oxidative pentose pathway. This review proposes that the severity of inflammation and damage associated with H. pylori infection is dependent on the ability of mucosal cells to counteract the increased load of reactive oxygen species. It is hypothesized that the oxidative pentose pathway and glutathione availability are important factors modulating this response. It is suggested that the therapeutic regulation of glutathione availability could provide a novel method for preventing or reducing the damage caused during H. pylori infection.

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“…NAC has been shown to enhance the integrity of the mucosal lining, thereby potentially reducing the adhesion of bacteria to the urinary tract epithelium. This protective effect could help prevent the initial attachment and colonization of uropathogenic bacteria, reducing the likelihood of recurrent UTIs [ 71 , 72 ]. All these effects of NAC, in combination with other agents such as mannose and chondroitin sulphate, could be furtherly enhanced, providing synergistic effects by targeting different aspects of UTI pathogenesis, including bacterial adhesion, biofilm formation, and immune modulation.…”

Section: N -Acetylcysteinementioning

confidence: 99%

Novel Key Ingredients in Urinary Tract Health—The Role of D-mannose, Chondroitin Sulphate, Hyaluronic Acid, and N-acetylcysteine in Urinary Tract Infections (Uroial PLUS®)

Crocetto,

Balsamo,

Amicuzi

et al. 2023

Nutrients

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Urinary tract infections represent a common and significant health concern worldwide. The high rate of recurrence and the increasing antibiotic resistance of uropathogens are further worsening the current scenario. Nevertheless, novel key ingredients such as D-mannose, chondroitin sulphate, hyaluronic acid, and N-acetylcysteine could represent an important alternative or adjuvant to the prevention and treatment strategies of urinary tract infections. Several studies have indeed evaluated the efficacy and the potential use of these compounds in urinary tract health. In this review, we aimed to summarize the characteristics, the role, and the application of the previously reported compounds, alone and in combination, in urinary tract health, focusing on their potential role in urinary tract infections.

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Effects of N-acetyl-l-cysteine in patients with chronic atrophic gastritis and nonulcer dyspepsia: a phase III pilot study

Cited by 3 publications

References 15 publications

Efficiency evaluation of Amlodipine combined with N-acetylcysteine on Indomethacin-induced gastritis in rats

Efficiency evaluation of Amlodipine combined with N-acetylcysteine on Indomethacin-induced gastritis in rats

Cellular Mucosal Defense During Helicobacter pylori Infection: A Review of the Role of Glutathione and the Oxidative Pentose Pathway

Novel Key Ingredients in Urinary Tract Health—The Role of D-mannose, Chondroitin Sulphate, Hyaluronic Acid, and N-acetylcysteine in Urinary Tract Infections (Uroial PLUS®)

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