Last update 01 Nov 2024

Acute gastric mucosal lesion

Last update 01 Nov 2024

Basic Info

Synonyms

Acute gastric mucosal lesion, 急性胃粘膜病変, ｷｭｳｾｲｲﾈﾝﾏｸﾋﾞｮｳﾍﾝ

Introduction-

Drugs associated with Acute gastric mucosal lesion

KB-5492

Target

Opioid receptors

Mechanism

Opioid receptors antagonists

Active Org.

Kyoto Pharmaceutical University

Originator Org.

Organon KK

Active Indication

Acute gastric mucosal lesion

Inactive Indication

Peptic Ulcer

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with Acute gastric mucosal lesion

JPRN-jRCT1080222498 / Unknown statusNot Applicable

Takepron Intravenous 30 mg specified drug-use survey [Hemostatic effect/rebleeding rate]

Start Date27 May 2014

Sponsor / Collaborator

Takeda Pharmaceutical Co., Ltd.

NCT01190657 / CompletedPhase 4

A Multiple-center, Self-controlled Open Study to Evaluate Efficacy and Safety of Teprenone in Patients With Acute Gastritis, Acute Gastric Lesion of Chronic Gastritis With Acute Exacerbation or Gastric Ulcer

This is a self-controlled, open, multiple-center clinical trial.

Start Date01 May 2010

Sponsor / Collaborator

Eisai Co., Ltd.

NCT02151786 / CompletedNot Applicable

Takepron Intravenous 30 mg Specified Drug-use Survey [Hemostatic Effect/Rebleeding Rate]

The purpose of this survey is to evaluate the safety (i.e., frequency of adverse events) and efficacy (i.e., hemostatic effect, rate of rebleeding after confirmation of hemostasis) of administration of lansoprazole intravenous 30 milligram (mg) (Takepron Intravenous 30 mg) to a large number of patients in daily medical practice.

Start Date01 Jan 2007

Sponsor / Collaborator

Takeda Pharmaceutical Co., Ltd.

100 Clinical Results associated with Acute gastric mucosal lesion

100 Translational Medicine associated with Acute gastric mucosal lesion

0 Patents (Medical) associated with Acute gastric mucosal lesion

1,098

Literatures (Medical) associated with Acute gastric mucosal lesion

01 Dec 2024·Molecular Biology Reports

Probiotic bacteria protect against indomethacin-induced gastric ulcers through modulation of oxidative stress, inflammation, and apoptosis

Article

Author: Gelen, Volkan ; Makav, Mustafa ; Şengül, Emin ; Gedikli, Semin ; Gelen, Sevda Urçar

BACKGROUNDIndomethacin is an anti-inflammatory drug that causes ulcers on the gastric mucosa due to its use. Probiotic bacteria are live microorganisms, and it has been stated by various studies that these bacteria have antioxidant and anti-inflammatory effects. In this study, we investigated the possible protective effect of various types of probiotic bacteria (Lactobacillus rhamnosus, Lactobacillus fermentum, and Lactobacillus brevis) against acute gastric mucosal damage caused by indomethacin.METHODSControl group - Physiological saline was administered daily for 10 days. Indo group-Physiological saline was administered daily for 10 days. Ranitidine + Indo group 5 mg/kg ranitidine dose was administered daily for 5 days. On day 11, a single dose of 100 mg/kg of indomethacin was given to the same group. Probiotic + Indo group 1 ml/kg of oral probiotic bacteria was administered daily for 10 days. On day 11, a single 100 mg/kg dose of indomethacin was given. After the application, the rats were anesthetized with ketamine xylazine, killed under appropriate conditions, the abdominal cavity was opened and the stomach tissues were removed. The obtained gastric tissues were used in the biochemical and histopathological analyses discussed below. All data were statistically evaluated by one-way ANOVA using SPSS 20.00, followed by Duncan Post hoc test. The data were expressed as mean ± SD. P < 0.05 was considered statistically significant.RESULTSAs a result, the administration of indomethacin caused gastric damage, stimulating oxidative stress, inflammation, and apoptosis. We found that the use of probiotic bacteria reduces oxidative stress (TOC), increases the activity of antioxidant enzymes (TAC), suppresses inflammation (IL-6 and Tnf-α), and inhibits apoptosis (Bax and Bcl-2) (P < 0.05).CONCLUSIONProbiotic treatment can mitigate gastric damage and apoptosis caused by indomethacin-induced gastric damage in rats. Probiotic also enhances the restoration of biochemical oxidative enzymes as it has anti-inflammatory, antioxidant, and antiapoptotic properties.

01 Dec 2024·Journal of Ethnopharmacology

Targeting TRPV1 signaling: Galangin improves ethanol-induced gastric mucosal injury

Article

Author: Lin, Kaiwen ; Liu, Xiaofei ; Wang, Zhongtao ; Wang, Erhao ; Zhang, Xueer ; Yi, Guohui ; Wang, Yan ; Yu, Xiaodan ; Feng, Faming

ETHNOPHARMACOLOGICAL RELEVANCEGalangin, a bioactive compound extracted from Alpinia officinarum Hance (Zingiberaceae), a plant with significant ethnopharmacological importance, has been used for thousands of years as a spice, condiment, and medicinal agent for various conditions, including gastrointestinal disorders. Although there is evidence suggesting its potential to improve gastric ulcers, the molecular mechanisms underlying its anti-ulcer properties are not fully understood.OBJECTIVEof the Study: This study aimed to investigate the effects of galangin on ethanol-induced acute gastric mucosal injury (AGMI) in mice and elucidate its molecular mechanisms.MATERIALS AND METHODSSixty BALB/c mice were randomly assigned into two main groups: a normal control group (n = 10) and an ethanol-induced group (n = 50). After establishing the AGMI model in mice using a combination of 40% ethanol and anhydrous ethanol, the ethanol-induced group was further subdivided into five subgroups (n = 10): an omeprazole control group (20 mg/kg), an untreated ethanol group, and three treatment groups receiving high-dose (50 mg/kg) or low-dose (25 mg/kg) galangin or capsazepine (CPZ, 2 mg/kg). The protective effects of galangin were evaluated through mucosal injury indices, hematoxylin and eosin staining, and quantification of inflammatory markers (IL-1β, IL-6, IL-8, and TNF-α). Oxidative stress levels and matrix metalloproteinase activity were measured using specific assay kits. Molecular docking was conducted to assess the binding affinity of galangin to key proteins within the transient receptor potential vanilloid 1 (TRPV1) pathway. Real-time fluorescence quantitative PCR (qPCR) was used to determine mRNA expression levels of TRPV1, calmodulin (CaM), substance P (SP), and CGRP in gastric tissues. Protein expression levels of TRPV1, nerve growth factor (NGF), tropomyosin receptor kinase A (TRKA), transforming growth factor beta (TGF-β), cyclooxygenase-2 (COX-2), and nuclear factor kappa B (NF-κB) were assessed through Western blot analysis. In cellular experiments, Culture of Human Gastric Epithelial Cells (GES-1) were treated with various concentrations of galangin after 7% ethanol induction. Cell proliferation, apoptosis, and migration were evaluated using Hoechst 33258 staining and transwell migration assays. TRPV1 protein expression was detected using immunofluorescence, and the expression levels of Bcl-2, BCL2-Associated X (BAX), and Caspase-3 were quantified by qPCR. Additionally, specific probe kits were used to measure intracellular calcium ions (Ca²⁺) and mitochondrial membrane potential.RESULTSThe findings indicate that galangin significantly improved mucosal pathology by reducing ulcer indices and inflammatory levels, while enhancing superoxide dismutase (SOD) activity and decreasing malondialdehyde (MDA) concentration. Galangin also reduced matrix metalloproteinase-2 (MMP-2), m metalloproteinase-9 (MMP-9) levels, promoting mucosal repair. At the cellular level, galangin decreased intracellular calcium ion concentration and mitigated the decline in mitochondrial membrane potential, enhance the restoration of mucosal cells, increased migration and proliferation, and reduced apoptosis. Molecularly, galangin demonstrated favorable binding to TRPV1, NGF, TRKA, TGF-β, COX-2, and NF-κB, and reversed the elevated expression of these proteins. Additionally, galangin downregulated the mRNA expression of TRPV1, CaM, SP, CGRP, BAX, and Caspase-3 in gastric tissues/cells, while upregulating Bcl-2 mRNA expression.CONCLUSIONGalangin mitigates AGMI by inhibiting the overactivation of the TRPV1 pathway, thereby blocking aberrant signal transduction. This study suggests that galangin has therapeutic potential against ethanol-induced AGMI and may be a viable alternative for the treatment of alcohol-induced gastric mucosal injuries.

01 Nov 2024·Journal of the Science of Food and Agriculture

Dendrobium officinale flos water extract ameliorates ethanol‐induced acute gastric mucosal injury via inhibiting oxidative stress and inflammation

Article

Author: He, Jiajiang ; Xu, Lieqiang ; Fan, Pinglong ; Xie, Shuchun ; Yuan, Quan ; Zhang, ZhiQian ; Liu, Xiaoyi ; Liu, Xinyue ; Zhang, Jie

AbstractBACKGROUNDDendrobium officinale flos (DOF), a novel food raw material, is used in Chinese folk medicine to nourish the stomach. However, there is still no available study to evaluate the effects of DOF on animal models of acute gastric injury and its mechanism by modern pharmacological research.RESULTSHerein, we characterized the major components of an aqueous extract of DOF and assessed its potential ameliorative effects in a rat model of acute gastric mucosal injury. The DOF water extract showed significant protective effects on the gastric mucosa and exhibited excellent antioxidant and anti‐inflammatory activities. Acute gastric injury rat models induced by ethanol (6 mL kg−1) were pretreated with different doses of DOF water extract (50–100 mg kg−1 day−1), and the biological effects of DOF extract in gastric tissues were evaluated. DOF extract alleviated the symptoms of ethanol‐stimulated acute gastric mucosal injury, as evidenced by a significant reduction in gastric injury index and the degree of gastric pathological changes. Additionally, treatment with DOF extract upregulated mucin expression in the gastric mucosa, attenuated oxidative stress, decreased the release of inflammatory mediators (TNF‐α, IL‐6), suppressed the expression of key proinflammatory enzymes (COX‐2 and iNOS), reduced the phosphorylation of p38 MAPK and p65 NF‐κB and increased the level of PGE2 in gastric tissues.CONCLUSIONDOF exerts protective effects against ethanol‐induced acute gastric mucosal injury, mainly by inhibiting inflammation and oxidative stress. © 2024 Society of Chemical Industry.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

Acute gastric mucosal lesion

Basic Info

Related

Analysis