我们研究了HM-铬酮（HMC）对C57BL/6J小鼠体内STZ诱导的高血糖和胰岛β细胞的保护作用。给予不同剂量的HMC（10或30mg/kg）治疗STZ诱导的糖尿病小鼠14天，检测其空腹血糖、胰岛素分泌、胰岛细胞组织病理学检查、凋亡蛋白水平和末端脱氧核苷酸转移酶dUTP nick end labeling（TUNEL）的变化。结果显示，HMC剂量依赖性地改善了血糖浓度并减轻了胰岛细胞的损伤。在糖尿病小鼠中观察到胰岛细胞变性，表现为萎缩、透明变性、核溶解和浓缩。然而，在接受HMC（30 mg/kg）治疗的糖尿病小鼠中，胰岛细胞形态得到恢复，核也呈现圆形。此外，与STZ诱导的糖尿病小鼠相比，HMC小鼠β细胞数量明显增加，胰高血糖素染色阳性细胞数量减少。HMC显著降低了原凋亡蛋白的表达，增加了抗凋亡蛋白的表达，TUNEL检测到的凋亡细胞数量增加。HMC降低了糖尿病小鼠中白细胞介素（interleukin，IL）-1β、IL-6和肿瘤坏死因子-α的表达，增加了抗氧化酶活性，降低了活性氧的生成。综上所述，结果表明，HMC具有保护糖尿病小鼠胰岛β细胞和减轻高血糖的潜力。

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.