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Modified Citrus Pectin (MCP) Confers a Renoprotective Effect on Early‐Stage Nephropathy in Type‐2 Diabetic Mice
Chemistry & Biodiversity ( IF 2.9 ) Pub Date : 2024-04-08 , DOI: 10.1002/cbdv.202400104
Hager M Mahmoud 1 , Abdel-Razik H Abdel-Razik 2 , Mahmoud A Elrehany 3 , Eman M. Othman 4 , Amany A. Bekhit 5
Affiliation  

Diabetic nephropathy (DN) is a significant global health concern with a high morbidity rate. Accumulating evidence reveals that Galectin‐3 (Gal‐3), a β‐galactoside‐binding lectin, is a biomarker in kidney diseases. Our study aimed to assess the advantageous impacts of modified citrus pectin (MCP) as an alternative therapeutic strategy for the initial and ongoing progression of DN in mice with type 2 diabetes mellitus (T2DM). The animal model has been split into four groups: control group, T2DM group (mice received intraperitoneal injections of nicotinamide (NA) and streptozotocin (STZ), T2DM+MCP group (mice received 100 mg/kg/day MCP following T2DM induction), and MCP group (mice received 100 mg/kg/day). After 4 weeks, kidney weight, blood glucose level, serum kidney function tests, histopathological structure alterations, oxidative stress, inflammation, apoptosis, and fibrosis parameters were determined in renal tissues. Our findings demonstrated that MCP treatment reduced blood glucose levels, renal histological damage, and restored kidney weight and kidney function tests. Additionally, MCP reduced malondialdehyde level and restored glutathione level, and catalase activity. MCP demonstrated a notable reduction in inflammatory and apoptosis mediators TNF‐α, iNOS, TGF‐βRII and caspase‐3. Overall, MCP could alleviate renal injury in an experimental model of DN by suppressing renal oxidative stress, inflammation, fibrosis, and apoptosis mediators.

中文翻译:

改良柑橘果胶 (MCP) 对 2 型糖尿病小鼠的早期肾病具有肾脏保护作用

糖尿病肾病(DN)是一个重要的全球健康问题,发病率很高。越来越多的证据表明,半乳糖凝集素-3 (Gal-3) 是一种 β-半乳糖苷结合凝集素,是肾脏疾病的生物标志物。我们的研究旨在评估改良柑橘果胶 (MCP) 作为替代治疗策略对 2 型糖尿病 (T2DM) 小鼠 DN 初始和持续进展的有利影响。动物模型分为四组:对照组、T2DM组(小鼠腹腔注射烟酰胺(NA)和链脲佐菌素(STZ))、T2DM+MCP组(小鼠在T2DM诱导后接受100 mg/kg/天的MCP),和MCP组(小鼠接受100 mg/kg/天)4周后,测定肾脏重量、血糖水平、血清肾功能测试、组织病理学结构改变、氧化应激、炎症、细胞凋亡和肾组织纤维化参数。我们的研究结果表明,MCP 治疗可降低血糖水平、肾脏组织学损伤,并恢复肾脏重量和肾功能测试。此外,MCP 还可降低丙二醛水平并恢复谷胱甘肽水平,并且过氧化氢酶活性显着降低炎症和细胞凋亡介质 TNF。 ‐α、iNOS、TGF-βRII 和 caspase-3 总体而言,MCP 可以通过抑制肾脏氧化应激、炎症、纤维化和凋亡介质来减轻 DN 实验模型中的肾损伤。
更新日期:2024-04-08
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