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糙叶稠李中的一个羊毛甾烷三萜改善 2 型糖尿病大鼠的葡萄糖耐量和胰岛β细胞超微结构。

A Lanosteryl Triterpene from Protorhus longifolia Improves Glucose Tolerance and Pancreatic Beta Cell Ultrastructure in Type 2 Diabetic Rats.

机构信息

Department of Biochemistry and Microbiology, University of Zululand, KwaDlangezwa 3886, South Africa.

Biomedical Research and innovation Platform (BRIP), South African Medical Research Council, Tygerberg 7505, South Africa.

出版信息

Molecules. 2017 Jul 26;22(8):1252. doi: 10.3390/molecules22081252.

DOI:10.3390/molecules22081252
PMID:28933769
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6152316/
Abstract

Type 2 diabetes remains one of the leading causes of death worldwide. Persistent hyperglycemia within a diabetic state is implicated in the generation of oxidative stress and aggravated inflammation that is responsible for accelerated modification of pancreatic beta cell structure. Here we investigated whether a lanosteryl triterpene, methyl-3β-hydroxylanosta-9,24-dien-21-oate (RA-3), isolated from can improve glucose tolerance and pancreatic beta cell ultrastructure by reducing oxidative stress and inflammation in high fat diet and streptozotocin-induced type 2 diabetes in rats. In addition to impaired glucose tolerance, the untreated diabetic rats showed increased fasting plasma glucose and C-peptide levels. These untreated diabetic rats further demonstrated raised cholesterol, interleukin-6 (IL-6), and lipid peroxidation levels as well as a destroyed beta cell ultrastructure. Treatment with RA-3 was as effective as metformin in improving glucose tolerance and antioxidant effect in the diabetic rats. Interestingly, RA-3 displayed a slightly more enhanced effect than metformin in reducing elevated IL-6 levels and in improving beta cell ultrastructure. Although the involved molecular mechanisms remain to be established, RA-3 demonstrates a strong potential to improve pancreatic beta cell ultrastructure by attenuating impaired glucose tolerance, reducing oxidative stress and inflammation.

摘要

2 型糖尿病仍然是全球主要的死亡原因之一。糖尿病状态下的持续高血糖与氧化应激和炎症加剧有关,这是导致胰腺β细胞结构加速改变的原因。在这里,我们研究了从 中分离出的一种羊毛甾烷三萜,甲基-3β-羟基羊毛甾-9,24-二烯-21-酸酯(RA-3),是否可以通过降低氧化应激和炎症来改善葡萄糖耐量和胰腺β细胞超微结构在高脂肪饮食和链脲佐菌素诱导的 2 型糖尿病大鼠中。除了葡萄糖耐量受损外,未经治疗的糖尿病大鼠空腹血糖和 C 肽水平升高。这些未经治疗的糖尿病大鼠进一步表现出胆固醇、白细胞介素 6(IL-6)和脂质过氧化水平升高以及β细胞超微结构破坏。RA-3 治疗与二甲双胍一样有效,可以改善糖尿病大鼠的葡萄糖耐量和抗氧化作用。有趣的是,RA-3 在降低升高的 IL-6 水平和改善β细胞超微结构方面比二甲双胍显示出稍强的效果。尽管涉及的分子机制仍有待确定,但 RA-3 具有通过减轻葡萄糖耐量受损、降低氧化应激和炎症来改善胰腺β细胞超微结构的强大潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/b4f052ce7835/molecules-22-01252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/77362369f624/molecules-22-01252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/73cdefa8133c/molecules-22-01252-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/9676054b2843/molecules-22-01252-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/b4f052ce7835/molecules-22-01252-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/77362369f624/molecules-22-01252-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/73cdefa8133c/molecules-22-01252-g002a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/9676054b2843/molecules-22-01252-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f6bf/6152316/b4f052ce7835/molecules-22-01252-g004.jpg

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