Objective: The aim of this study was to examine the effect of berberine on diabetes mellitus in vivo and in vitro, and elucidate the underlying mechanisms.

Methods: Rat models of type 2 diabetes mellitus (T2DM) were established and were treated with berberine. Pathological changes in the thoracic aorta, and inflammatory factor and adiponectin levels were investigated. Vascular smooth muscle cells (VSMCs) of the thoracic aorta were cultured and treated with berberine. Cellular proliferation, migration, and inflammatory factor levels were investigated. Responses of vascular rings to phenylephrine (PE) and sodium nitroprusside (SNP) after berberine intervention and the changes of relaxation responses to SNP after adding Iberiotoxin (IbTX) were investigated.

Results: Berberine ameliorated the pathological status of the thoracic aorta in the T2DM rats. Berberine significantly inhibited the C-reactive protein (CRP), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) production, and increased the adiponectin level compared with the model group. Compared with the model group, berberine inhibited the proliferation and migration of VSMCs in vitro, and reduced tumor growth factor-β1 (TGF-β1), IL-6, and TNF-α levels. Furthermore, the contraction of thoracic aorta to PE was reduced, while the relaxation response of thoracic aorta to SNP was increased, after the berberine intervention in the T2DM rats. The relaxation response of thoracic aorta to SNP in the model and berberine groups decreased after the IbTX treatment.

Conclusion: Protective effects of berberine against macrovascular complications induced by diabetes mellitus may be attributed to inhibiting of the inflammation and intervening of the calcium- activated potassium (BK_Ca).

目的：本研究的目的是在体内和体外检测小檗碱对糖尿病的影响，并阐明其潜在机制。

方法：建立2型糖尿病（T2DM）大鼠模型，并给予黄连素治疗。研究了胸主动脉的病理变化、炎症因子和脂联素水平。培养胸主动脉的血管平滑肌细胞 (VSMCs) 并用小檗碱处理。研究了细胞增殖、迁移和炎症因子水平。研究了小檗碱干预后血管环对去氧肾上腺素（PE）和硝普钠（SNP）的反应以及加入伊比利亚毒素（IbTX）后对SNP的松弛反应的变化。

结果：小檗碱改善了T2DM大鼠胸主动脉的病理状态。与模型组相比，小檗碱显着抑制C反应蛋白（CRP）、白细胞介素6（IL-6）和肿瘤坏死因子α（TNF-α）的产生，并增加脂联素水平。与模型组相比，小檗碱在体外抑制VSMCs的增殖和迁移，降低肿瘤生长因子-β1（TGF-β1）、IL-6和TNF-α水平。此外，在小檗碱干预 T2DM 大鼠后，胸主动脉对 PE 的收缩减少，而胸主动脉对 SNP 的舒张反应增加。IbTX 治疗后，模型组和小檗碱组胸主动脉对 SNP 的松弛反应降低。

结论：小檗碱对糖尿病大血管并发症的保护作用可能与抑制炎症和介导钙活化钾（BK _Ca）有关。