Esomeprazole Sodium is a potent and orally active proton pump inhibitor[1]. Esomeprazole Sodium reduces gastric acid secretion by covalently modifying the sulfhydryl groups of the proton pump and inhibiting the activity of H⁺/K⁺-ATPase in gastric parietal cells[2]. Esomeprazole Sodium is commonly used in research on gastroesophageal reflux disease (GERD), peptic ulcers, and Helicobacter pylori infections[3].
In vitro, Esomeprazole Sodium (50μM; 20h) reduced MDA-MB-468 triple-negative breast cancer cell viability and lowered intracellular pH with an EC50=70μM, decreased gastric-type H⁺/K⁺-ATPase expression, and enhanced doxorubicin cytotoxicity but did not have significant effect on non-cancerous breast epithelial MCF-10A cells[4]. Treatment of primary human lung epithelial cells with Esomeprazole Sodium (1–100μM; 24h) dose-dependently suppressed bleomycin-induced iNOS expression, down-regulated TNF-α, IL-1β and IL-6, blocked TGF-β-driven collagen I/III/V transcription, and abolished ECM-related gene up-regulation without measurable cytotoxicity[5].
In vivo, Esomeprazole Sodium (300mg/kg/day; p.o.; 11 days) elevated plasma ADMA, reversed cotton-smoke-induced lung fibrosis, reduced collagen deposition, and lowered circulating TNF-α, IL-1β, MMP7 and NO over-production in C57BL/6J mice without affecting pulmonary inflammation or organ weights[6]. Esomeprazole Sodium (0.5mg/kg/day; i.v.; 13 days) reversed baseline low-pretreatment gastric juice pH (4.25±2.39) to 6.43±1.18 and sustained pH≥4 in 75% of adult Quarter Horse mares, while improving ulcer scores without adverse effects[7].
References:
[1] Thitiphuree S, Talley NJ. Esomeprazole, a new proton pump inhibitor: pharmacological characteristics and clinical efficacy. Int J Clin Pract. 2000;54(8):537-541.
[2] Shin JM, Munson K, Vagin O, Sachs G. The gastric HK-ATPase: structure, function, and inhibition. Pflugers Arch. 2009;457(3):609-622.
[3] Johnson TJ, Hedge DD. Esomeprazole: a clinical review. Am J Health Syst Pharm. 2002;59(14):1333-1339.
[4] Goh W, Sleptsova-Freidrich I, Petrovic N. Use of proton pump inhibitors as adjunct treatment for triple-negative breast cancers. An introductory study. J Pharm Pharm Sci. 2014;17(3):439-446.
[5] Ebrahimpour A, Wang M, Li L, et al. Esomeprazole attenuates inflammatory and fibrotic response in lung cells through the MAPK/Nrf2/HO1 pathway. J Inflamm (Lond). 2021;18(1):17.
[6] Nelson C, Lee J, Ko K, et al. Therapeutic Efficacy of Esomeprazole in Cotton Smoke-Induced Lung Injury Model. Front Pharmacol. 2017;8:16.
[7] Videla R, Sommardahl CS, Elliott SB, Vasili A, Andrews FM. Effects of intravenously administered esomeprazole sodium on gastric juice pH in adult female horses. J Vet Intern Med. 2011;25(3):558-562.
Esomeprazole Sodium是一种强效、具有口服活性的质子泵抑制剂[1]。Esomeprazole Sodium通过共价修饰胃壁细胞质子泵的巯基，抑制H⁺/K⁺-ATPase活性，从而减少胃酸分泌[2]。Esomeprazole Sodium常用于胃食管反流病（GERD）、消化性溃疡及幽门螺杆菌感染的研究[3]。
体外实验中，Esomeprazole Sodium（50μM; 20h）可降低MDA-MB-468三阴性乳腺癌细胞的存活率，降低细胞内pH（EC50=70μM），下调胃型H⁺/K⁺-ATPase表达，并增强多柔比星细胞毒性，但对非癌乳腺上皮MCF-10A细胞无明显影响[4]。在原代人肺上皮细胞中，Esomeprazole Sodium（1–100μM; 24h）剂量依赖性地抑制博来霉素诱导的iNOS表达，下调TNF-α、IL-1β和IL-6，阻断TGF-β诱导的胶原I/III/V转录，并抑制ECM相关基因的上调，且无可见细胞毒性[5]。
体内实验中，在C57BL/6J小鼠中，Esomeprazole Sodium（300mg/kg/天；口服；11天）升高血浆ADMA水平，逆转棉花烟雾诱导的肺纤维化，减少胶原沉积，并降低循环中TNF-α、IL-1β、MMP7和NO的过度生成，但不影响肺部炎症或器官重量[6]。Esomeprazole Sodium（0.5mg/kg/天；静脉注射；13天）将基础低预处理胃液pH（4.25±2.39）逆转至6.43±1.18，并使75%的成年Quarter Horse母马胃液pH维持pH≥4，同时改善溃疡评分且无不良反应[7]。