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没食子酸丙酯对链脲佐菌素-烟酰胺诱导的糖尿病大鼠氧化应激和血糖的影响。

Effect of madecassoside in reducing oxidative stress and blood glucose in streptozotocin-nicotinamide-induced diabetes in rats.

机构信息

School of Postgraduate Studies, International Medical University, Kuala Lumpur, Malaysia.

Faculty of Medicine, University of Adelaide, Adelaide, Australia.

出版信息

J Pharm Pharmacol. 2023 Aug 1;75(8):1034-1045. doi: 10.1093/jpp/rgad063.

Abstract

OBJECTIVES

Madecassoside (MAD) is a triterpenoid constituent of Centella asiatica (L.) Urb., an ethnomedical tropical plant, extracts of which were shown to reduce blood glucose in experimental diabetes. This study examines MAD for its anti-hyperglycaemic effects and tests the hypothesis that it reduces the blood glucose in experimentally induced diabetic rats by protecting the β-cells.

METHODS

Diabetes was induced using streptozotocin (60 mg/kg, i.v.) followed by nicotinamide (210 mg/kg, intraperitoneal (i.p.)). MAD (50 mg/kg) was administered orally for 4 weeks, commencing 15 days after induction of diabetes; resveratrol (10 mg/kg) was used as a positive control. Fasting blood glucose, plasma insulin, HbA1c, liver and lipid parameters were measured, along with antioxidant enzymes and malondialdehyde as an index of lipid peroxidation; histological and immunohistochemical studies were also undertaken.

KEY FINDINGS

MAD normalized the elevated fasting blood glucose levels. This was associated with increased plasma insulin concentrations. MAD alleviated oxidative stress by improving enzymatic antioxidants and reducing lipid peroxidation. Histopathological examination showed significant recovery of islet structural degeneration and an increased area of islets. Immunohistochemical staining showed increased insulin content in islets of MAD-treated rats.

CONCLUSIONS

The results demonstrate an antidiabetic effect of MAD associated with preservation of β-cell structure and function.

摘要

目的

积雪草苷(MAD)是一种来自于积雪草(Centella asiatica(L.)Urb.)的三萜类化合物,这种热带植物的提取物已被证明可降低实验性糖尿病中的血糖水平。本研究检验了 MAD 的抗高血糖作用,并提出假设,即通过保护β细胞,MAD 可降低实验性诱导的糖尿病大鼠的血糖。

方法

使用链脲佐菌素(60 mg/kg,静脉内)加烟酰胺(210 mg/kg,腹腔内)诱导糖尿病。糖尿病诱导后 15 天开始,MAD(50 mg/kg)经口给药 4 周;白藜芦醇(10 mg/kg)用作阳性对照。测量空腹血糖、血浆胰岛素、HbA1c、肝和脂质参数,以及抗氧化酶和丙二醛作为脂质过氧化的指标;还进行了组织学和免疫组织化学研究。

主要发现

MAD 使升高的空腹血糖水平正常化。这与血浆胰岛素浓度的增加有关。MAD 通过改善酶抗氧化剂和减少脂质过氧化来减轻氧化应激。组织病理学检查显示胰岛结构退化有明显恢复,胰岛面积增加。免疫组织化学染色显示 MAD 处理大鼠胰岛中胰岛素含量增加。

结论

这些结果表明 MAD 具有抗糖尿病作用,与β细胞结构和功能的保存有关。

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