Berberine inhibits gluconeogenesis in spontaneous diabetic rats by regulating the AKT/MAPK/NO/cGMP/PKG signaling pathway
Berberine inhibits gluconeogenesis in spontaneous diabetic rats by regulating the AKT/MAPK/NO/cGMP/PKG signaling pathway
复制标题
DOI：
10.1007/s11010-022-04604-z
复制
发表时间：
2023-01
影响因子：
4.3
通讯作者：
Ming-Qing Lu;Yanpeng Wang;Yuanye Jiang;Cuiping Zhang;Hongping Wang;W. Sha;Lin Chen;T. Lei;Limei Liu
中科院分区：
文献类型：
--
作者：
Ming-Qing Lu;Yanpeng Wang;Yuanye Jiang;Cuiping Zhang;Hongping Wang;W. Sha;Lin Chen;T. Lei;Limei Liu
本工作旨在探讨黄连素(BBR)对糖异生的作用机制。BBR的作用在大鼠原代肝细胞中进行检测，并在自发性糖尿病大鼠体内得到证实。用蛋白质印迹法检测蛋白质水平。免疫荧光染色用于蛋白表达的可视化，而qRT-PCR有助于在mRNA水平上确定基因的表达。此外，cGMP浓度用ELISA法测定，NO水平用分光光度法测定。BBR通过抑制CREB的磷酸化而下调G6Pase和PEPCK，从而抑制糖异生。此外，BBR通过激活AKT1/MAPK轴，增加NO和cGMP浓度，激活NO/cGMP/PKG信号通路。体内实验与体外实验结果基本一致。因此，BBR代表了糖尿病患者的候选药物，其作用机制可能是通过AKT/MAPK/NO/cGMP/PKG通路来驱动的。
This work was aimed to investigate the action mechanism of berberine (BBR) on gluconeogenesis. The effects of BBR were examined in rat primary hepatocytes and confirmed in vivo in spontaneous diabetic rats. Protein levels were assessed by Western blot. Immunofluorescence staining was utilized for visualizing protein expression, while qRT-PCR helped for the determination of gene expression at the mRNA level. Besides, cGMP concentration was measured using ELISA, whereas NO level was assessed by spectrophotometry. BBR inhibited gluconeogenesis by downregulating G6Pase and PEPCK via inhibition of CREB phosphorylation. Moreover, BBR enhanced NO and cGMP concentrations, leading to the activation of the NO/cGMP/PKG signaling via activating AKT1/MAPK axis. The in vivo experiments were consistent with the findings obtained in vitro. Hence, BBR represents a drug candidate for diabetic patients and its mechanism of action may be driven via the AKT/MAPK/NO/cGMP/PKG pathway.