HM-Chromanone Alleviates Hyperglycemia by Protecting Pancreatic Islet Cells in Streptozotocin-Induced Diabetic Mice

链脲佐菌素 内分泌学 内科学 标记法 小岛 胰腺 细胞凋亡 糖尿病 胰岛 胰高血糖素 化学 胰岛炎 胰岛素 坏死 医学 免疫组织化学 生物化学
作者
Jae Eun Park,Ji-Sook Han
出处
期刊:Journal of Medicinal Food [Mary Ann Liebert, Inc.]
卷期号:26 (6): 357-367
标识
DOI:10.1089/jmf.2022.k.0084
摘要

We examined the effects of HM-chromanone (HMC) on alleviating hyperglycemia and protecting pancreatic β-cells from streptozotocin (STZ)-induced damage in C57BL/6J mice. HMC was administered to STZ-induced diabetic mice at 10 or 30 mg/kg, for 14 days. Thereafter, changes in fasting blood glucose levels, insulin-secretion, histopathological examination of pancreas islet cell and apoptotic protein levels, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay were determined. The results revealed that HMC dose-dependently improved blood glucose concentrations and alleviated pancreatic islet cells damage. In diabetic mice, degeneration of the islet cells was observed wherein they appeared shrunken, with hyaline deterioration, nuclear dissolution, and condensation. However, morphology of the islet cell was restored, and nuclei were visibly rounded in the HMC (30 mg/kg)-administered diabetic mice. In addition, β-cell numbers were markedly increased in HMC mice compared to STZ-induced diabetic mice, and the number of cells stained with glucagon was decreased. HMC markedly decreased the expression of proapoptotic proteins and increased antiapoptotic proteins, and the number of apoptotic cells detected by TUNEL was elevated. HMC decreased expression of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α in diabetic mice. Moreover, HMC increased antioxidant-enzymes activity, and decreased reactive oxygen species generation. In conclusion, the results demonstrate the potential of HMC to alleviate hyperglycemia by protecting the pancreatic β-cells in diabetic mice.

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