Choi Kung-Ha, Park Mi Hwa, Lee Hyun Ah, Han Ji-Sook
Department of Food and Nutrition, College of Medical and Life Science, Silla University, Busan 46958, Republic of Korea.
Department of Food Science and Nutrition, Pusan National University, Busan 46241, Republic of Korea.
Z Naturforsch C J Biosci. 2018 Jul 26;73(7-8):281-289. doi: 10.1515/znc-2017-0172.
Exposure to high levels of glucose may cause glucotoxicity, leading to pancreatic β cell dysfunction, including cell apoptosis and impaired glucose-stimulated insulin secretion. The aim of this study was to explore the effect of cyanidin-3-rutinoside (C3R), a derivative of anthocyanin, on glucotoxicity-induced apoptosis in INS-1 pancreatic β cells. Glucose (30 mM) treatment induced INS-1 pancreatic β cell death, but glucotoxicity and apoptosis significantly decreased in cells treated with 50 μM C3R compared to that observed in 30 mM glucose-treated cells. Furthermore, hyperglycemia increased intracellular reactive oxygen species (ROS), lipid peroxidation, and nitric oxide (NO) levels, while C3R treatment reduced these in a dose-dependent manner. C3R also increased the activity of antioxidant enzymes, markedly reduced the expression of pro-apoptotic proteins (such as Bax, cytochrome c, caspase 9 and caspase 3), and increased the expression of the anti-apoptotic protein, Bcl-2, in hyperglycemia-exposed cells. Finally, cell death was examined using annexin V/propidium iodide staining, which revealed that C3R significantly reduced high glucose-induced apoptosis. In conclusion, C3R may have therapeutic effects against hyperglycemia-induced β cell damage in diabetes.
暴露于高水平葡萄糖可能会导致糖毒性，进而引发胰腺β细胞功能障碍，包括细胞凋亡以及葡萄糖刺激的胰岛素分泌受损。本研究的目的是探讨花青素衍生物矢车菊素-3-芸香糖苷（C3R）对糖毒性诱导的INS-1胰腺β细胞凋亡的影响。葡萄糖（30 mM）处理可诱导INS-1胰腺β细胞死亡，但与30 mM葡萄糖处理的细胞相比，用50 μM C3R处理的细胞中糖毒性和凋亡显著降低。此外，高血糖会增加细胞内活性氧（ROS）、脂质过氧化和一氧化氮（NO）水平，而C3R处理则以剂量依赖的方式降低这些水平。C3R还增加了抗氧化酶的活性，显著降低了促凋亡蛋白（如Bax、细胞色素c、半胱天冬酶9和半胱天冬酶3）的表达，并增加了高血糖暴露细胞中抗凋亡蛋白Bcl-2的表达。最后，使用膜联蛋白V/碘化丙啶染色检测细胞死亡情况，结果显示C3R显著降低了高糖诱导的细胞凋亡。总之，C3R可能对糖尿病中高血糖诱导的β细胞损伤具有治疗作用。
