针对Helicobacter pylori胃殖民的创新性胃透性配方的先进互穿透的聚合物网络
Roberto Grosso1, Elena Benito1, Ana I Carbajo-Gordillo1
1Departamento de Química Orgánica y Farmacéutica, Facultad de Farmacia, Universidad de Sevilla, C/ Prof. García González, n. 2, 41012, Seville, Spain.
概括
新的胃性聚合物网络增强了阿莫西林的输送,用于治疗Helicobacter pylori感染. 这些可生物降解的粘膜粘合系统提供了改善的药物释放和组合治疗的潜力,以打击胃癌风险.
科学领域:
- 聚合物科学和药物输送
- 胃肠病学和传染病学
背景情况:
- 与Helicobacter pylori感染相关的抗生素耐药性和癌症风险的增加需要新的治疗策略.
- 目前的治疗方法在达到有效的药物度和克服胃环境方面面临挑战.
研究的目的:
- 开发和评估新型的半互穿透聚合物网络 (半IPN) 作为阿莫西西林 (AMOX) 的胃透矩阵.
- 评估这些矩阵在模拟的胃条件下的性能,包括粘膜粘附,浮力,胀和受控的药物释放.
- 探索将vonoprazan (VONO) 纳入药物的潜力,以提高治疗疗效.
主要方法:
- 制造设计用于胃保留和控制性阿莫西西林释放的半IPN矩阵.
- 评估矩阵属性,包括膨胀指数,微观结构,粘膜粘合,浮力和生物降解性.
- 在24小时内,在pH 1.2和pH 5.0下进行体外药物释放研究.
- 对阿莫西西林和诺普拉桑联合配方的研究.
主要成果:
- 开发的半IPN表现出显著的胀 (>360%),超的微结构,粘膜粘合和浮力.
- 矩阵在24小时内保持了结构完整性,在pH 1.2和pH 5.0两种情况下都显示了受控的阿莫西西林释放 (10%-100%).
- 使用实验设计阐明了释放机制,突出显示了矩阵对胃状况的适用性.
- 3D脚手架的生物降解性和稳定性证实了它们对高药物负载的潜力.
结论:
- 量身定制的半IPN矩阵代表了一种有前途的胃药物输送系统,用于对抗H. pylori的阿莫西林.
- 粘粘性和浮力性质,加上受控释放,为H. pylori根除提供了有效的策略.
- 与诺普拉桑联合配方是一种潜在的协同方法,可以对抗H. pylori并预防胃癌.
相关概念视频
Treating Helicobacter pylori in Peptic Ulcers: Antimicrobial Therapy
358
Helicobacter pylori, a resilient gram-negative bacterium, can thrive in the stomach's harsh, acidic environment. Infection with H. pylori leads to a cascade of events within the stomach lining. One of the critical disruptions caused by this bacterium is the interference with somatostatin production, a hormone responsible for regulating acid secretion. This interference tips the balance, escalating acid secretion and diminishing bicarbonate levels. This imbalance compromises the defensive...
358
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors
374
Peptic ulcers, often induced by H. pylori infections or NSAID usage, arise from disruptions in the delicate balance of gastric acid production. Peptic ulcers stem from heightened gastric acid levels due to H. pylori infections or NSAID use. The protective mucus layer diminishes in the presence of these factors, allowing gastric acid to erode the stomach lining and form ulcers.
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
Gastric acid, a potent cocktail of hydrogen and chloride ions, is produced in specialized parietal cells within the...
374
Peptic Ulcer Disease IV: Management
87
Medical treatment strategies for peptic ulcers encompass various methods. The primary goal of treatment is to diminish gastric acidity and strengthen mucosal defense mechanisms.
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
The therapeutic approach involves ensuring adequate rest, implementing drug therapy, promoting smoking cessation, making dietary modifications, and emphasizing long-term follow-up care.
Pharmacological management
The prevailing therapy for peptic ulcers involves a combination of managing the patient's current...
87
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
403
The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
403
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists
423
Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
423
Gastritis III: Clinical Manifestations and Management
214
The clinical manifestations of gastritis can vary depending on the cause and type of gastritis, but some common symptoms may include the following.
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
Clinical manifestations of acute gastritis
The patient with acute gastritis may have a rapid onset of symptoms, such as epigastric pain or discomfort, dyspepsia, anorexia, hiccups, or nausea and vomiting, which can last from a few hours to a few days. Erosive or hemorrhagic gastritis may cause bleeding, which may manifest as blood in vomit or as...
214


