Minia General Hospital, 65111, Minia, Egypt.
Histology Department, Faculty of Veterinary Medicine, Beni-Suef University, 62511, Beni-Suef, Egypt.
Chem Biodivers. 2024 Jul;21(7):e202400104. doi: 10.1002/cbdv.202400104. Epub 2024 May 31.
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.
糖尿病肾病（DN）是一个全球性的重大健康问题，其发病率很高。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性柑橘果胶（MCP）作为 2 型糖尿病（T2DM）小鼠中 DN 初始和持续进展的替代治疗策略的有利影响。动物模型分为四组：对照组、T2DM 组（小鼠接受烟酰胺（NA）和链脲佐菌素（STZ）腹腔注射）、T2DM+MCP 组（T2DM 诱导后给予 100mg/kg/天 MCP）和 MCP 组（小鼠接受 100mg/kg/天 MCP）。4 周后，测定肾脏组织中的肾脏重量、血糖水平、血清肾功能试验、组织病理学结构改变、氧化应激、炎症、细胞凋亡和纤维化参数。我们的研究结果表明，MCP 治疗可降低血糖水平、肾脏组织损伤，并恢复肾脏重量和肾功能试验。此外，MCP 降低了丙二醛水平并恢复了谷胱甘肽水平和过氧化氢酶活性。MCP 显著减少了 TNF-α、iNOS、TGF-βRII 和 caspase-3 等炎症和凋亡介质。总的来说，MCP 通过抑制肾脏氧化应激、炎症、纤维化和凋亡介质，可减轻 DN 实验模型中的肾脏损伤。
