Hou Congcong, Liang Hongyu, Hao Zhangsen, Zhao Ding
College of Pharmacy, Hebei Medical University, No. 361 Zhongshan East Road, Shijiazhuang 050017, PR China.
Beijing Shouyi Group Co., Ltd. Mine Hospital, Tangshan 064400, PR China.
Saudi Pharm J. 2023 Mar;31(3):433-443. doi: 10.1016/j.jsps.2023.01.010. Epub 2023 Feb 2.
It has been reported diabetic gastroparesis is related to diabetic autonomic neuropathy of the gastrointestinal tract, and berberine (BBR) could ameliorate diabetic central and peripheral neuropathy. However, the influence of BBR on the function and motility of the gastric fundus nerve is unclear.
A diabetic rat model was constructed, and HE staining was used to observe the morphological changes in the gastric fundus. The changes in cholinergic and nitrogen-related neurochemical indexes and the effects of BBR on them were measured using Elisa. The effects of BBR on the neural function and motility of gastric fundus were investigated by electric field stimulation (EFS) induced neurogenic response in vitro.
In the early stage of STZ-induced diabetic rats, the contractile response of gastric fundus induced by EFS was disorder, disturbance of contraction amplitude, and the cell bodies of neurons in the myenteric plexus of gastric fundus presented vacuolar lesions. Administration with BBR could improve the above symptoms. BBR further enhanced the contraction response in the presence of a NOS inhibitor or the case of inhibitory neurotransmitters removal. Interestingly, the activity of ACh could affect NO release directly and the enhancement of BBR on contractile response was canceled by calcium channel blockers completely.
In the early stage of STZ-induced diabetic rats, the neurogenic contractile response disorder of the gastric fundus is mainly related to cholinergic and nitrergic nerve dysfunction. BBR promotes the release of ACh mainly by affecting the calcium channel to improve the neurological dysfunction of the gastric fundus.
据报道，糖尿病胃轻瘫与胃肠道糖尿病自主神经病变有关，黄连素（BBR）可改善糖尿病中枢和周围神经病变。然而，BBR对胃底神经功能和运动的影响尚不清楚。
构建糖尿病大鼠模型，采用苏木精-伊红（HE）染色观察胃底形态学变化。用酶联免疫吸附测定法（ELISA）检测胆碱能和氮相关神经化学指标的变化以及BBR对其的影响。通过体外电场刺激（EFS）诱导的神经源性反应研究BBR对胃底神经功能和运动的影响。
在链脲佐菌素（STZ）诱导的糖尿病大鼠早期，EFS诱导的胃底收缩反应紊乱，收缩幅度受到干扰，胃底肌间神经丛神经元胞体出现空泡样病变。给予BBR可改善上述症状。在存在一氧化氮合酶（NOS）抑制剂或去除抑制性神经递质的情况下，BBR进一步增强收缩反应。有趣的是，乙酰胆碱（ACh）的活性可直接影响一氧化氮（NO）释放，BBR对收缩反应的增强作用被钙通道阻滞剂完全消除。
在STZ诱导的糖尿病大鼠早期，胃底神经源性收缩反应紊乱主要与胆碱能和氮能神经功能障碍有关。BBR主要通过影响钙通道促进ACh释放，从而改善胃底神经功能障碍。
