益参通络方能改善链脲佐菌素诱导的糖尿病肾病小鼠的肾损伤,调节炎症和细胞凋亡。

Yuan Jiayao, W U Suhui, Meng Yufan, L I Hanbing, L I Genlin, X U Jiangyan
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引用次数: 0

摘要

目的:探讨益肾通络方(YSTLF)对链脲佐菌素诱导的糖尿病肾病小鼠(DKD)的作用及其机制。方法:30只肿瘤研究所小鼠(无特异性病原体,SPF级)分为5组(每组n = 6):对照组、DKD模型、DKD模型加YSTLF (4.9 g/kg)、DKD模型加YSTLF (9.8 g/kg)、DKD模型加卡托普利。单次腹腔注射链脲佐菌素(150 mg/kg)诱导DKD。测量体重、空腹血糖和尿c肽水平,以评估stlf对代谢的调节作用。用肾小球和肾小管健康指标评价肾功能。通过测定天冬氨酸转氨酶和丙氨酸转氨酶水平来评估肝功能。采用苏木精/伊红染色及透射电镜检查肾脏病理改变。通过酶联免疫吸附法、免疫组织化学和Western blot分析炎症和凋亡相关因素。结果:DKD小鼠空腹血糖、c肽、24小时尿蛋白(UP)水平升高,肾损害升高,伴有炎症和细胞凋亡增加。YSTLF显著降低DKD小鼠24小时UP和c肽水平,改善肾脏和肝脏功能。YSTLF还能减轻肾小球肥大、基底膜增厚和足细胞足突消退。上调足细胞标记物podocalyxin的表达。此外,YSTLF可能通过降低DKD小鼠肾脏中单核细胞趋化蛋白(MCP-1)、Bax和Caspase-3的过度表达来减轻炎症和细胞凋亡。结论:这些发现表明,YSTLF通过调节炎症细胞因子MCP-1和Bax/Caspase-3凋亡通路的表达来改善肾损伤,为DKD的治疗提供了一种潜在的方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Yishen Tongluo formula ameliorates kidney injury modulating inflammation and apoptosis in streptozotocin-induced diabetic kidney disease mice.

Objective: To investigate the effect and mechanism of Yishen Tongluo formula (, YSTLF) in streptozotocin-induced diabetic kidney disease mice (DKD) mice.

Methods: Thirty Institute of Cancer Research mice (specific pathogen free, SPF grade) were divided into five groups (n = 6 per group): control, DKD model, DKD model with YSTLF (4.9 g/kg), DKD model with YSTLF (9.8 g/kg), and DKD model with captopril. DKD was induced through a single intraperitoneal injection of streptozotocin (150 mg/kg). Body weight, fasting blood glucose and urine C-peptide levels were measured to assess metabolic regulation by YSTLF. Renal function was evaluated using indicators of glomerular and tubular health. Liver function was assessed by measuring aspartate aminotransferase and alanine aminotransferase levels. Renal pathological changes were examined using hematoxylin/eosin staining and transmission electron microscopy. Inflammatory and apoptosis-related factors were analyzed through enzyme-linked immunosorbent assay, immunohistochemistry, and Western blot analysis.

Results: In DKD mice, fasting blood glucose, C-peptide, 24-hour urine protein (UP) levels, and renal damage were elevated, accompanied by increased inflammation and apoptosis. YSTLF significantly reduced 24-hour UP and C-peptide levels and improved kidney and liver function in DKD mice. YSTLF also mitigated glomerular hypertrophy, basement membrane thickening, and podocyte foot process effacement. It upregulated the expression of the podocyte marker podocalyxin. Furthermore, YSTLF alleviated inflammation and apoptosis, likely by reducing the overexpression of monocyte chemoattractant protein (MCP-1), Bax, and Caspase-3 in the kidneys of DKD mice.

Conclusions: These findings suggest that YSTLF ameliorates kidney injury by modulating the expression of inflammatory cytokine MCP-1 and the Bax/Caspase-3 apoptosis pathway, providing a potential therapeutic approach for DKD.

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