Anti-Diabetic Effects of CTB-APSL Fusion Protein in Type 2 Diabetic Mice

被引:20
|
作者
Liu, Yunlong [1 ]
Gao, Zhangzhao [1 ]
Guo, Qingtuo [1 ]
Wang, Tao [1 ]
Lu, Conger [1 ]
Chen, Ying [1 ]
Sheng, Qing [1 ]
Chen, Jian [1 ]
Nie, Zuoming [1 ]
Zhang, Yaozhou [1 ]
Wu, Wutong [1 ]
Lv, Zhengbing [1 ]
Shu, Jianhong [1 ]
机构
[1] Zhejiang Sci Tech Univ, Coll Life Sci, Hangzhou 310018, Zhejiang, Peoples R China
基金
浙江省自然科学基金;
关键词
Bombyx mori pupae; active peptide from shark liver; oral administration; type 2 diabetes mellitus; cholera toxin B subunit; FREE FATTY-ACIDS; TOXIN B-SUBUNIT; BETA-CELL; CHOLERA-TOXIN; BOMBYX-MORI; PANCREATIC-ISLETS; ACTIVE PEPTIDE; EXPRESSION; GENE; PURIFICATION;
D O I
10.3390/md12031512
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
To determine whether cholera toxin B subunit and active peptide from shark liver (CTB-APSL) fusion protein plays a role in treatment of type 2 diabetic mice, the CTB-APSL gene was cloned and expressed in silkworm (Bombyx mori) baculovirus expression vector system (BEVS), then the fusion protein was orally administrated at a dose of 100 mg/kg for five weeks in diabetic mice. The results demonstrated that the oral administration of CTB-APSL fusion protein can effectively reduce the levels of both fasting blood glucose (FBG) and glycosylated hemoglobin (GHb), promote insulin secretion and improve insulin resistance, significantly improve lipid metabolism, reduce triglycerides (TG), total cholesterol (TC) and low density lipoprotein (LDL) levels and increase high density lipoprotein (HDL) levels, as well as effectively improve the inflammatory response of type 2 diabetic mice through the reduction of the levels of inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6). Histopathology shows that the fusion protein can significantly repair damaged pancreatic tissue in type 2 diabetic mice, significantly improve hepatic steatosis and hepatic cell cloudy swelling, reduce the content of lipid droplets in type 2 diabetic mice, effectively inhibit renal interstitial inflammatory cells invasion and improve renal tubular epithelial cell nucleus pyknosis, thus providing an experimental basis for the development of a new type of oral therapy for type 2 diabetes.
引用
收藏
页码:1512 / 1529
页数:18
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