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陈昺伃,张璐,卢冬雪,严晶,孙志广.基于TAS2R38探究黄连“苦寒败胃”的生物基础[J].湖南中医药大学学报,2021,41(2):224-229[点击复制] |
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| 基于TAS2R38探究黄连“苦寒败胃”的生物基础 |
| 陈昺伃,张璐,卢冬雪,严晶,孙志广 |
| (南京中医药大学第二附属医院, 江苏 南京 210000) |
| 摘要: |
| 目的 基于苦味受体38（bitter taste receptor，TAS2R38）探讨久服、误服黄连导致“苦寒败胃”的生物基础。方法 ICR小鼠随机分为5组，分别为空白对照组、黄连低（0.5 g/kg）/中（1.5 g/kg）/高（4.5 g/kg）剂量组和苯甲地那铵组（0.225 g/kg），每组12只。各组小鼠分别灌胃给予相应的药物，持续8周。于第2、4、8周处理动物，RT-qPCR检测小鼠胃肠TAS2R38 mRNA表达水平；观察小鼠胃排空、肠推进；ELISA测定小鼠胃泌素和胆囊收缩素；HE染色评估胃肠黏膜损伤程度。结果 与空白对照组相比：苯甲地那铵和黄连均显著增加TAS2R38 mRNA表达水平，其中黄连组呈剂量依赖性（P<0.01）；苯甲地那铵延缓胃排空（P<0.05），黄连在第2周时促进胃排空（P<0.01），但在第4、8周则延缓胃排空，特别是中、高剂量组（P<0.05）；苯甲地那铵与黄连均呈时间依赖性地抑制肠蠕动，尤以黄连高剂量组表现明显（P<0.01）；苯甲地那铵与黄连均抑制胃泌素的分泌、促进胆囊收缩素的分泌（P<0.05，P<0.01）；HE染色显示苯甲地那铵和黄连均可损伤胃肠组织。结论 长期使用黄连可通过激动TAS2R38，影响小鼠胃肠动力，调节胃肠激素分泌，加重胃肠组织损伤，可能是其“苦寒败胃”的生物基础之一。 |
| 关键词: TAS2R38 黄连 苦寒败胃 生物基础 |
| DOI：10.3969/j.issn.1674-070X.2021.02.012 |
| 投稿时间：2020-07-22 |
| 基金项目:国家自然科学基金项目（82074312）；江苏省研究生科研创新项目（KYCX20_1480）。 |
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| Exploring the Biological Basis of Huanglian (Coptidis Rhizoma) of “KuHanBaiWei” Based on TAS2R38 |
| CHEN Bingyu,ZHANG Lu,LU Dongxue,YAN Jin,SUN Zhiguang |
| (The Second Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, China) |
| Abstract: |
| Objective Based on the bitter taste receptor 38 (TAS2R38) to explore the biological basis of "KuHanBaiWei" caused by long-term or mistaken intake of Huanglian (Coptidis Rhizoma). Methods ICR mice were randomly divided into five groups, including the control group, the Huanglian (Coptidis Rhizoma) in low-dose group (0.5 g/kg), middle-dose group (1.5 g/kg), high-dose group (4.5 g/kg) and denatonium benzoate group (0.225 g/kg), with 12 mice in each group. All mice were treated with the corresponding drugs by gavage for 8 weeks. The mice were killed at 2nd, 4th, and 8th weeks, RT-qPCR was performed to examine the mRNA expression of TAS2R38 in gastrointestinal tract of mice; the gastric emptying and small intestinal propulsion of mice were observed; ELISA was used to detect gastrin and cholecystokinin in mice; HE staining was used to assess the gastrointestinal mucosal lesions. Results Denatonium benzoate group and Huanglian (Coptidis Rhizoma) group could significantly increase the mRNA expression of TAS2R38 in a dose-dependent manner compared with the control group (P<0.01); denatonium benzoate delayed gastric emptying (P<0.05); Huanglian (Coptidis Rhizoma) could promote gastric emptying at the 2nd week (P<0.01), and delay gastric emptying at the 4th and 8th week, especially in the middle-dose group and the high-dose group (P<0.05); both denatonium benzoate and Huanglian (Coptidis Rhizoma) inhibited intestinal peristalsis in a time-dependent manner, especially in the high-dose group (P<0.01); both denatonium benzoate and Huanglian (Coptidis Rhizoma) inhibited the secretion of gastrin and promoted the secretion of cholecystokinin (P<0.05, P<0.01); HE staining showed that both denatonium benzoate and Huanglian (Coptidis Rhizoma) could damage gastrointestinal tissue. Conclusion Long-term use of Huanglian (Coptidis Rhizoma) can affect gastrointestinal motility, regulate gastrointestinal hormone secretion and aggravate gastrointestinal injury in mice by activating TAS2R38, which may be one of the biological basis of "KuHanBaiWei". |
| Key words: TAS2R38 Huanglian (Coptidis Rhizoma) "KuHanBaiWei" biological basis |
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