Biswas Astrid Mukta, Emran Tushar, Khan Sabrin Islam, Shabnam Sadia, Jain Preeti, Bepari Asim Kumar, Shill Manik Chandra, Hossain Md Murad, Reza Hasan Mahmud
Department of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Department of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Eur J Pharmacol. 2025 Jun 5;996:177559. doi: 10.1016/j.ejphar.2025.177559. Epub 2025 Mar 26.
Uncontrolled hypertension is a primary contributor to tissue damage in multiple organs, including the heart and kidneys. In this study, we explored the protective roles of L-arginine in a mineralocorticoid-induced rat model of hypertension. To induce hypertension and subsequent organ damage, rats were nephrectomized unilaterally and fed with the mineralocorticoid fludrocortisone acetate and dietary salt (FCA-Salt). These rats were treated with L-arginine for 28 days, and subsequent tests were performed. Biochemical analysis revealed the increased level of inflammation and oxidative stress biomarkers in the plasma, heart, and kidney of the FCA-salt-treated rats. L-arginine treatment decreased the oxidative stress marker malondialdehyde (MDA) by 18 %, 22 %, and 18 % in the heart, kidney, and plasma, respectively. L-arginine also attenuated the advanced oxidative protein products (AOPP). The activity of superoxide dismutase (SOD) increased by 62 %, 45 %, and 16 % in the heart, kidney, and plasma, respectively, in the L-arginine-treated animals compared to the FCA-Salt group. Significant augmentation was also revealed for the nitric oxide (NO), catalase (CAT), and reduced glutathione (GSH). The plasma levels of the kidney function biomarkers uric acid and creatinine were significantly improved after L-arginine treatment. Furthermore, L-arginine remarkably reduced the elevated plasma cytokines IL-1β, IL-17A, TNF-α, and TGF-β1 in FCA-salt-induced hypertensive rats. Histopathological data showed a reduction in fibrosis and tissue damage by L-arginine in the FCA-salt-treated group. We propose that L-arginine could be an effective agent in preventing cardiac and renal dysfunction in hypertensive rats.
uncontrolled高血压是包括心脏和肾脏在内的多个器官组织损伤的主要促成因素。在本研究中，我们探讨了L-精氨酸在盐皮质激素诱导的大鼠高血压模型中的保护作用。为了诱导高血压及随后的器官损伤，大鼠单侧肾切除，并喂食盐皮质激素醋酸氟氢可的松和高盐饮食（FCA-盐）。这些大鼠用L-精氨酸治疗28天，然后进行后续测试。生化分析显示，FCA-盐处理的大鼠血浆、心脏和肾脏中的炎症和氧化应激生物标志物水平升高。L-精氨酸处理使心脏、肾脏和血浆中的氧化应激标志物丙二醛（MDA）分别降低了18%、22%和18%。L-精氨酸还减弱了晚期氧化蛋白产物（AOPP）。与FCA-盐组相比，L-精氨酸处理的动物心脏、肾脏和血浆中的超氧化物歧化酶（SOD）活性分别增加了62%、45%和16%。一氧化氮（NO）、过氧化氢酶（CAT）和还原型谷胱甘肽（GSH）也有显著增加。L-精氨酸治疗后，肾功能生物标志物尿酸和肌酐的血浆水平显著改善。此外，L-精氨酸显著降低了FCA-盐诱导的高血压大鼠血浆中升高的细胞因子IL-1β、IL-17A、TNF-α和TGF-β1。组织病理学数据显示，L-精氨酸可减少FCA-盐处理组的纤维化和组织损伤。我们认为，L-精氨酸可能是预防高血压大鼠心脏和肾脏功能障碍的有效药物。
