亚洲酸通过抑制与性结肠炎发展相关的分子,生化和病理学变化来拯救肠道组织
Maha S Lokman1,2, Rami B Kassab2,3, Fatma A M Salem4
1Department of Biology, College of Science and Humanities in Al-Kharj, Prince Sattam bin Abdul Aziz University, Al-Kharj, Saudi Arabia.
Bioscience reports
|May 3, 2024
概括
亚洲酸 (AA) 通过减少炎症和氧化应激,在治疗性结肠炎 (UC) 中表现有前途. 这项研究发现,在UC的老鼠模型中,AA有效地减弱了分子,生化和组织学损伤.
科学领域:
- 药理学 药理学是指药理学的学科.
- 胃肠病学 胃肠病学
- 生物化学 生物化学
背景情况:
- 性结肠炎 (UC) 涉及显著的炎症和氧化应激.
- 亚洲酸 (AA) 是一种多,具有已知的抗氧化和抗炎性质.
- 关于AA减轻UC相关损害的潜力,需要进行调查.
研究的目的:
- 评估亚洲酸 (AA) 在酸诱导的性结肠炎 (UC) 鼠模型中的疗效.
- 评估AA对UC分子,生化和组织学标记物的影响.
- 为了比较AA的效果与标准治疗 (5-氨基酸).
主要方法:
- 在老鼠中使用乙酸诱导UC.
- 治疗组包括对照组,UC,UC + 5-ASA,UC + 20 mg/kg AA和UC + 40 mg/kg AA.
- 对氧化应激标记物 (LPO,NO),抗氧化蛋白 (Nrf2通路),炎症调解物 (MPO,NF-κB通路) 和亡标记物 (caspase-3,Bcl2/Bax) 的分析.
- 结肠组织的组织病理学检查.
主要成果:
- UC诱导显著增加了脂质过氧化,氧化,炎症媒介和亡标志物.
- 在UC诱导下调节了关键的抗氧化蛋白 (Nrf2,CAT,SOD,GSH,GPx,GR).
- 在两种测试剂量中服用AA改善了这些UC诱导的分子,生化和组织病理变化.
结论:
- 亚洲酸对性结肠炎具有显著的治疗潜力.
- AA有效地改善抗氧化状态,并减少UC结肠中的炎症和亡.
- AA代表了一种有前途的天然化合物,用于管理UC相关的病理.
相关概念视频
Drugs for Treatment of Ulcerative Colitis in IBD
138
Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
138
Acid Suppressive Drugs for Peptic Ulcer Disease: Proton Pump Inhibitors
387
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...
387
Acid Suppressive Drugs for Peptic Ulcer Disease: Antacids
355
In the complex environment of the gastric lumen, excessive acid secretion can lead to the formation or worsening of ulcers within the delicate mucosal layer. Antacids, such as sodium bicarbonate and calcium carbonate, provide relief by neutralizing this acid, transforming it into harmless salt and water. This neutralization process raises the gastric pH from a highly acidic level of 1 to a more basic 3-4, reducing the acidity within the stomach.
However, this neutralization reaction between...
However, this neutralization reaction between...
355
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists
432
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...
432
Drugs for Peptic Ulcer Disease: Sucralfate as Mucosal Protective Agents
465
In the intricate landscape of the gastric lumen, excessive acid secretion disrupts the natural defense mechanisms, weakening the mucus-bicarbonate barrier. This vulnerability allows pepsin to infiltrate epithelial cells, digesting mucosal proteins and triggering erosion, leading to ulcer formation.
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
In this scenario, mucosal protective agents like sucralfate play an essential role. Sucralfate, a complex of sulfated sucrose and aluminum hydroxide, demonstrates its usefulness in acidic conditions,...
465
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents
418
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...
418


