克洛皮多格雷尔通过向氧化应激,亡和凝血通路来保护 gentamicin 诱导的毒性
Asmaa A Akila1, Rania A Gad2, Mohamed Gamal El-Din Ewees3
1Molecular Physiology Division, Department of Zoology, Faculty of Science, Beni-Suef University, Beni-Suef, 62511, Egypt.
Naunyn-Schmiedeberg's archives of pharmacology
|September 5, 2024
概括
克洛皮多格雷尔 (Clop) 通过减少氧化应激,炎症和亡来保护 gentamicin (Genta) 诱导的损伤. 这项研究突出了Clop Clop的重点.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 药理学 药理学是指药理学的学科.
- 生物化学 生化学
背景情况:
- 根他米辛 (Genta) 引起毒性,这是一个重要的临床问题.
- 克洛皮多格雷尔 (Clop) 是一种抗血小板剂,可能具有抗药物诱导的损伤的保护性.
- 凝血级联在Genta诱导的毒性中的作用需要进一步研究.
研究的目的:
- 在大鼠模型中研究克洛皮多格雷尔对根塔米辛诱导的毒性产生的保护作用.
- 阐明克洛皮多格雷尔的保护作用背后的机制,重点关注氧化应激,亡和凝血.
- 评估克洛皮多格雷尔对功能,组织病理学和分子标记物的影响.
主要方法:
- 成年雄性白色老鼠被分为四组:对照组,Genta-only和两个Genta组,先用不同剂量的克洛皮多格雷尔进行预处理.
- 根塔是用腹膜内注射的,而克洛皮多格雷尔是在根塔暴露之前和期间口服的.
- 在脏组织中分析了功能,氧化应激标志物,促炎性细胞因子,亡标志物,凝血概况和纤维素表达.
主要成果:
- 克洛皮多格雷尔治疗显著改善了Genta治疗的老鼠的功能和组织病理学.
- 克洛皮多格雷尔的使用显著降低了促炎性细胞因子,氧化应激指标和促丧性蛋白质的水平.
- 该药物还降低了纤维素蛋白表达,并增强了组织中抗炎和抗亡蛋白的表达.
结论:
- 甘胺素诱导的毒性与氧化应激,亡和凝血系统的激活有关.
- 克洛皮多格雷尔对Genta诱导的损伤具有显著的保护作用.
- 这些保护作用归因于克洛皮多格雷尔的结合抗凝剂,抗氧化剂,抗炎和抗丧性质,使其成为潜在的治疗剂.
相关概念视频
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors
499
Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
499
Anticoagulant Drugs: Low-Molecular-Weight Heparins
654
Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
654
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists
160
Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
160
Anticoagulant Drugs: Vitamin K Antagonists and Direct Oral Anticoagulants
1.2K
Oral anticoagulants are vital tools in preventing and treating blood clotting disorders. This diverse class of medications can be categorized as vitamin K antagonists, exemplified by warfarin, and direct thrombin inhibitors (DTIs), such as dabigatran, as well as factor Xa inhibitors, including rivaroxaban.
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
Warfarin, a prominent vitamin K antagonist family member, exerts its effect by inhibiting the enzyme VKORC1 (vitamin K epoxide reductase complex 1). By hindering this enzyme, warfarin...
1.2K
GPCR Desensitization
5.9K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
5.9K
Enhanced Elimination of Poison
489
Poison can be effectively removed from the gastrointestinal (GI) tract through various decontamination procedures.
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
Antidotes serve a crucial role in counteracting the effects of poison by inhibiting enzymes responsible for producing harmful drug metabolites. In some cases, these toxic metabolites can be neutralized by endogenous cosubstrates, which are maintained at specific concentrations to prevent interaction with cellular macromolecules and subsequent cell death.
Renal excretion is the...
489


