Comparison of the therapeutic effects of sildenafil citrate, heparin and neuropeptides in a rat model of acetic acid-induced gastric ulcer

Kalaycı, Mehmet; Koçdor, Mehmet Ali; Kuloğlu, Tuncay; Şahin, İ̇brahim; Saraç, Mehmet; Aksoy, Aziz; Yardım, Meltem; Dalkılıç, Semih; Gursu, Onur; Aydın, Suna; Akkoç, Ramazan Fazıl; Uğraş, Meltem; Artaş, Gökhan; Ozercan, İbrahim Hanifi; Uğur, Kader; Aydın, Süleyman

doi:10.1016/j.lfs.2017.08.013

Cited by 18 publications

(11 citation statements)

References 35 publications

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“…Infection with H. pylori may cause gastritis, gastric and peptic ulcers, and even gastric cancer [32]. Gastric ulcer is considered one of the major public health consequences that occur due to many factors, especially the harmful activity of gastric acid and pepsin [33]. Peptic ulcer is characterized by acid peptic lesions in the digestive tract, which result in mucosa ruptures (reaching the submucosa) that are generally found in the proximal stomach or duodenum [34].…”

Section: Infection Bymentioning

confidence: 99%

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Paz

Alencar

Lima

et al. 2020

Oxidative Medicine and Cellular Longevity

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Omeprazole (OME) is commonly used to treat gastrointestinal disorders. However, long-term use of OME can increase the risk of gastric cancer. We aimed to characterize the pharmacological effects of OME and to correlate its adverse effects and toxicogenetic risks to the genomic instability mechanisms and cancer-based on database reports. Thus, a search (till Aug 2019) was made in the PubMed, Scopus, and ScienceDirect with relevant keywords. Based on the study objective, we included 80 clinical reports, forty-six in vitro, and 76 in vivo studies. While controversial, the findings suggest that long-term use of OME (5 to 40 mg/kg) can induce genomic instability. On the other hand, OME-mediated protective effects are well reported and related to proton pump blockade and anti-inflammatory activity through an increase in gastric flow, anti-inflammatory markers (COX-2 and interleukins) and antiapoptotic markers (caspases and BCL-2), glycoprotein expression, and neutrophil infiltration reduction. The reported adverse and toxic effects, especially in clinical studies, were atrophic gastritis, cobalamin deficiencies, homeostasis disorders, polyp development, hepatotoxicity, cytotoxicity, and genotoxicity. This study highlights that OME may induce genomic instability and increase the risk of certain types of cancer. Therefore, adequate precautions should be taken, especially in its long-term therapeutic strategies and self-medication practices.

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Section: Infection Bymentioning

confidence: 99%

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Paz

Alencar

Lima

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Besides an effect on motility, nesfatin-1 affects secretory functions: ICV injected nesfatin-1 reduced 2-deoxy- d -glucose-stimulated gastric acid production [ 75 ] associated with a lower expression of H + /K + -ATPase in obese rats [ 76 ]. Moreover, nesfatin-1 seems to be implicated in inflammatory processes, because IP [ 77 ] or IV [ 78 ] injected nesfatin-1 improved healing in rat models of gastric ulcer, associated with a decrease in TNF- α and IL-1 β and mediated by downstream cyclooxygenase 2 signaling [ 79 , 80 ].…”

Section: Implications Of Nesfatin-1 In Gastrointestinal Functionsmentioning

confidence: 99%

Current Understanding of the Role of Nesfatin-1

Schalla

Stengel

2018

Journal of the Endocrine Society

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Nesfatin-1 was discovered in 2006 and implicated in the regulation of food intake. Subsequently, its widespread central and peripheral distribution gave rise to additional effects. Indeed, a multitude of actions were described, including modulation of gastrointestinal functions, glucose and lipid metabolism, thermogenesis, mediation of anxiety and depression, as well as cardiovascular and reproductive functions. Recent years have witnessed a great increase in our knowledge of these effects and their underlying mechanisms, which will be discussed in the present review. Lastly, gaps in knowledge will be highlighted to foster further studies.

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“…Several behavioral factors culminate in the development of PUs. They include inadequate eating habits, alcohol and tobacco consumption, stress, and the inadvertent use of nonsteroidal anti-inflammatory drugs (NSAIDs) [9]. In these situations, the defense mechanisms of the gastric mucosa, such as mucus and bicarbonate secretion, acid-base balance, endogenous sulfhydryl groups, and epidermal growth factor [9, 10], are insufficient to maintain tissue homeostasis, favoring the development of lesions.…”

Section: Introductionmentioning

confidence: 99%

Antioxidant and Antiulcerogenic Activity of the Dry Extract of Pods of Libidibia ferrea Mart. ex Tul. (Fabaceae)

Prazeres

Aragão

Brito³

et al. 2019

Oxidative Medicine and Cellular Longevity

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Ethnomedicinal studies in the Amazon community and in the Northeast region of Brazil highlight the use of Libidibia ferrea fruits for the treatment of gastric problems. However, there are no data in the literature of this pharmacological activity. Thus, the aim of this paper is to provide a scientific basis for the use of the dry extract of L. ferrea pods (DELfp) for the treatment of peptic ulcers. Phytochemical characterization was performed by HPLC/MS. In vitro antioxidant activity was assessed using DPPH, ABTS, phosphomolybdenum, and superoxide radical scavenging activity. The gastroprotective activity, the ability to stimulate mucus production, the antisecretory activity, and the influence of -SH and NO compounds on the antiulcerogenic activity of DELfp were evaluated. The healing activity was determined by the acetic acid-induced chronic ulcer model. Anti-Helicobacter pylori activity was investigated. HPLC/MS results identified the presence of phenolic compounds, gallic acid and ellagic acid, in DELfp. The extract showed antioxidant activity in vitro. In ulcers induced by absolute ethanol and acidified ethanol, the ED50 values of DELfp were 113 and 185.7 mg/kg, respectively. DELfp (100, 200, and 400 mg/kg) inhibited indomethacin-induced lesions by 66.7, 69.6, and 65.8%, respectively. DELfp (200 mg/kg) reduced gastric secretion and H+ concentration in the gastric contents and showed to be independent of nitric oxide (NO) and dependent on sulfhydryl (-SH) compounds in the protection of the gastric mucosa. In the chronic ulcer model, DELfp reduced the area of the gastric lesion. DELfp also showed anti-H. pylori activity. In conclusion, DELfp showed antioxidant, gastroprotective, healing, and antiulcerogenic activities. The mechanism of these actions seems to be mediated by different pathways and involves the reduction of gastric secretion and H+ concentration, dependence on sulfhydryl compounds, and anti-H. pylori activity. All these actions support the medicinal use of this species in the management of peptic ulcers.

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Comparison of the therapeutic effects of sildenafil citrate, heparin and neuropeptides in a rat model of acetic acid-induced gastric ulcer

Cited by 18 publications

References 35 publications

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Pharmacological Effects and Toxicogenetic Impacts of Omeprazole: Genomic Instability and Cancer

Current Understanding of the Role of Nesfatin-1

Antioxidant and Antiulcerogenic Activity of the Dry Extract of Pods of Libidibia ferrea Mart. ex Tul. (Fabaceae)

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