野漆树块茎提取物通过调节氧化应激和 TNF-α 炎症途径保护链脲佐菌素诱导的糖尿病肾病大鼠模型。

Acta cirurgica brasileira Pub Date : 2024-08-05 eCollection Date: 2024-01-01 DOI:10.1590/acb395324
Li Fan, Xiaoying Li, Alok Shiomurti Tripathi
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引用次数: 0

摘要

目的:在链脲佐菌素(STZ)诱导的糖尿病肾病(DN)大鼠模型中,评估无患子块茎(Ac)提取物对糖尿病肾病的保护作用:方法:用 STZ(60 毫克/千克,静脉注射)诱导大鼠患糖尿病,并在 STZ 给药六周后通过肾功能测试确认大鼠患有糖尿病肾病。接下来的四周,大鼠接受 Ac 250 mg/kg p.o. 和 500 mg/kg p.o. 治疗。对 DN 大鼠肾组织中的氧化应激和炎症细胞因子水平进行了评估。使用苏木精和伊红染色法对肾组织进行组织病理学检查:结果:与 DN 组相比,Ac 治疗组大鼠的体重有所改善。在方案实施的第 42 天和第 70 天,观察到 Ac 治疗组的血糖水平低于 DN 组。用 Ac 治疗可改善 DN 组大鼠血清中肾功能检测(肌酐和尿素氮)、肝功能酶(天门冬氨酸氨基转移酶和丙氨酸氨基转移酶)和血脂水平的变化。与 DN 组相比,Ac 治疗组组织中的氧化应激参数(丙二醛和活性氧增加,谷胱甘肽和超氧化物歧化酶水平降低)和炎症细胞因子(如白细胞介素-6、肿瘤坏死因子-α 和单核细胞趋化蛋白-1)减少。用 Ac 治疗还可减轻 DN 大鼠肾组织的组织病理学变化:报告表明,Ac 可通过调节炎症细胞因子和氧化应激保护 DN 大鼠的肾损伤。
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Amorphophallus campanulatus tuber extract protects diabetic nephropathy in streptozotocin-induced diabetic nephropathy rat model by regulating oxidative stress and TNF-α inflammatory pathway.

Purpose: To assess the effect of Amorphophallus campanulatus tuber (Ac) extract in the protection of diabetic nephropathy in streptozotocin (STZ) induced diabetic nephropathy (DN) rat model.

Methods: Diabetes was induced with STZ (60 mg/kg, i.p.), and DN was confirmed after six weeks of STZ administration with the estimation of kidney function test. Further rats were treated with Ac 250 and 500 mg/kg p.o. for next four week. Oxidative stress and level of inflammatory cytokines were estimated in the kidney tissue of DN rats. Histopathology of kidney tissue was performed using hematoxylin and eosin staining.

Results: There was improvement in the body weight of Ac treated groups than DN group of rats. Blood glucose level was observed to be reduced in Ac treated groups than DN group on 42nd and 70th day of protocol. Treatment with Ac ameliorated the altered level of kidney function tests (creatinine and BUN), enzymes of liver function (aspartate aminotransferase and alanine aminotransferase), and lipid profile in the serum of DN rats. Oxidative stress parameters (malondialdehyde and reactive oxygen species enhances and reduction in the level of glutathione and superoxide dismutase) and inflammatory cytokines such as interleukin-6, tumour necrosis factor-α, and monocyte chemoattractant protein-1 reduces in the tissue of Ac treated group than DN group. Treatment with Ac also attenuates the altered histopathological changes in the kidney tissue of DN rats.

Conclusions: The report suggests that Ac protects renal injury in DN rats by regulating inflammatory cytokines and oxidative stress.

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