文章摘要
刘嘉宝,金舒文,康朝霞,等.电针足三里对功能性消化不良大鼠十二指肠半胱氨酸蛋白酶-1和消皮素D的影响[J].中华物理医学与康复杂志,2022,44(12):1057-1063
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电针足三里对功能性消化不良大鼠十二指肠半胱氨酸蛋白酶-1和消皮素D的影响
  
DOI:10.3760/cma.j.issn.0254-1424.2022.12.001
中文关键词: 功能性消化不良  电针  细胞焦亡  半胱氨酸蛋白酶-1  消皮素D
英文关键词: Functional dyspepsia  Electroacupuncture  Pyroptosis  Caspase-1  Dermatin D
基金项目:国家自然科学基金青年项目(82060897);湖北省自然科学基金项目(2021CFB548);湖北省武汉市中医药科研项目青年项目(WZ22Q34);湖北中医药大学“青苗计划”资助项目(2021zzx009)
作者单位
刘嘉宝 湖北中医药大学针灸骨伤学院武汉 430061 
金舒文 湖北中医药大学针灸骨伤学院武汉 430061 
康朝霞 贵州中医药大学针灸推拿学院贵阳 550025 
刘译茗 湖北中医药大学针灸骨伤学院武汉 430061 
周丽 武汉市中西医结合医院武汉 430022 
沈峰 湖北中医药大学针灸骨伤学院武汉 430061 
徐派的 湖北中医药大学针灸骨伤学院武汉 430061 
张红星 湖北中医药大学针灸骨伤学院武汉 430061 
潘小丽 湖北中医药大学针灸骨伤学院武汉 430061 
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中文摘要:
      目的 探讨电针足三里对功能性消化不良(FD)大鼠十二指肠细胞焦亡的影响和可能的作用机制。 方法 将24只7日龄Sprague-Dawley(SD)大鼠按照随机数字表法分为空白组、模型组、电针组,每组8只。模型组和电针组采用多因素诱导法(碘乙酰胺灌胃法+夹尾刺激法)制备FD大鼠模型。造模成功后,电针组大鼠给予针刺“足三里”穴后连接韩式穴位神经刺激仪治疗2周,空白组和模型组不予任何干预。于基线期、造模后、电针干预7 d和14 d后记录3组大鼠的体重,于电针干预结束后检测3组大鼠的胃排空率和小肠推进率,并采用酶联免疫法(ELISA)检测其血清白介素-1β(IL-1β)和白介素-6(IL-6)的表达水平,采用实时荧光定量聚合酶链式反应检测3组大鼠十二指肠IL-1β和IL-6转录水平,采用免疫印迹法检测3组大鼠十二指肠半胱氨酸蛋白酶-1(caspase-1)p20和消皮素D(GSDMD)蛋白表达水平。 结果 造模成功后,模型组和电针组大鼠的平均体重与空白组造模成功后比较,差异均有统计学意义(P<0.01);电针干预7 d和14 d后,模型组和电针组大鼠的平均体重与空白组同时间点比较,差异均有统计学意义(P<0.05),且电针组电针干预7 d和14 d后的平均体重与模型组同时间点比较,差异均有统计学意义(P<0.05)。电针干预结束后,电针组大鼠胃内残留率和小肠推进率与模型组比较,差异均有统计学意义(P<0.01),而模型组大鼠胃内残留率和小肠推进率与空白组比较,差异均有统计学意义(P<0.01)。电针干预结束后,模型组和电针组大鼠血清中IL-1β和IL-6表达水平、十二指肠组织IL-1β和IL-6 mRNA的表达水平和十二指肠组织GSDMD、caspase-1 p20蛋白表达水平与空白组比较,差异均有统计学意义(P<0.01),且电针组大鼠血清中IL-1β和IL-6表达水平、十二指肠组织IL-1β和IL-6 mRNA的表达水平和十二指肠组织GSDMD、caspase-1 p20蛋白表达水平与模型组比较,差异均有统计学意义(P<0.05)。 结论 电针足三里可显著降低FD大鼠十二指肠的细胞焦亡水平,改善十二指肠低度炎症,进而减轻FD临床症状,其作用机制可能与电针足三里可下调caspase-1 p20、GSDMD-N蛋白的表达水平,降低IL-1β和IL-6等炎性因子的表达水平,以及缓解FD大鼠十二指肠的低度炎症有关。
英文摘要:
      Objective To explore any effect of electroacupuncture (EA) at the Zusanli point on the scorch death of duodenal cells in rats with functional dyspepsia (FD) and possible mechanisms. Methods Twenty-four 7-day-old Sprague-Dawley rats were randomly divided into a blank group, a model group and an EA group, each of 8. FD was induced in both the model and EA group rats using iodoacetamide gavage with tail-clip stimulation. After successful modeling the EA group was given acupuncture at the Zusanli point and then connected with a Korean acupuncture point nerve stimulator for 2 weeks. The other 2 groups were not given any intervention. The rats′ body weight was recorded before and after the modeling, as well as 7 and 14 days later. The gastric emptying rate and the small intestine propulsion rate of the three groups were detected right after the EA intervention, and the serum expression levels of interleukin-1β (IL-1β) and interleukin-6 (IL-6) were measured using enzyme-linked immunoassays. Real-time fluorescence quantitative polymerase chain reactions were used to detect the transcription levels of IL-1β and IL-6 in the rats′ duodenums, while western blotting was employed to assess the expression of caspase-1 P20 and dermatin D (GSDMD) in their duodenums. Results After successful modeling, the average body weight of the rats in the model and EA groups was significantly different from that in blank group, and after 7 and 14 days the average body weight of the former groups was significantly different from that of the blank group, with significant differences between the two groups as well. After the EA intervention significant differences were observed in gastric reside and small intestine propulsion rate between the EA group and the model group, as well as between the model and the blank group. After the intervention, there were significant differences between the blank group and the other two groups in the average expression of IL-1β and IL-6 in serum, IL-1β and IL-6 mRNA in the duodenum, as well as the GSDMD and caspase-1 p20 proteins in the duodenum. There were significant differences between the model and EA groups in all of the above measurements. Conclusions EA at the Zusanli point can significantly reduce the level of scorch death in the duodenum of FD rats, as well as relieve low-grade duodenal inflammation and the clinical symptoms of FD. Its mechanism may be related to the down-regulation of the expression of caspase-1 P20 and GSDMD-N protein, and of inflammatory factors such as IL-1β and IL-6, relieving low-grade duodenal inflammation.
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