Effect of acupoint catgut embedding on p38 MAPK pathway in the lung tissue of asthmatic rats

Zhen Ci Yan Jiu. 2024 Jan 25;49(1):23-29. doi: 10.13702/j.1000-0607.20221221.
[Article in English, Chinese]

Abstract

Objectives: To observe the effect of catgut embedding at "Feishu"(BL13), "Dingchuan" (EX-B1) and "Danzhong" (CV17) on expression of phosphorylated p38 mitogen activated protein kinase (p-p38 MAPK), interleukin-4 (IL-4), interferon-γ (IFN-γ) and changes of airway epithelial cells (AEC) in the lung tissue of bronchial asthma (BA) rats, so as to explore its mechanisms underlying improvement of BA.

Methods: Forty male Wistar rats were randomly and equally divided into blank control, model, dexamethasone (DEX) and catgut embedding groups. The BA model was established by intraperitoneal injection of suspension of ovalbumin and aluminum hydroxide. Rats of the DEX group received intraperitoneal injection of DEX (1.5 mg/kg), once daily for 2 weeks, and those of the catgut embedding group received catgut embedding at BL13, EX-B1 and CV17 only one time. The rats' sneezing times per miniute in each group were recorded. H.E. staining was used to observe the histopathological changes of the lung tissue under light microscope. A transmission electron microscope (TEM) was used to observe the ultrastructural changes of AEC in the lung tissue, including the thickness of bronchial wall and bronchial smooth muscle by using an image analysis software. The protein expressions of p-p38 MAPK, IL-4 and INF-γ in the lung tissue were determined using Western blot.

Results: Morphological observation revealed that in the model group, light microscope showed deformed and swollen bronchial tube wall with increased folds and thickened bronchial smooth muscle;and TEM showed a large number of autophagy vesicles containing swollen and deformed organelles in the AEC, and apparent reduction of intracellular mitochondria, these situations were obviously milder in both DEX and catgut embedding groups. Compared with the blank control group, the sneezing times, thickness of bronchial wall and bronchial smooth muscle in the model group were significantly increased (P<0.01), and the expressions of p-p38 MAPK and IL-4 in lung tissue were significantly increased (P<0.01), while the expression of IFN-γ was significantly decreased (P<0.01) in the model group. In comparison with the model group, the sneezing times, thickness of bronchial wall and bronchial smooth muscle, protein expressions of p-p38 MAPK and IL-4 were significantly decreased (P<0.01), while the expression of IFN-γ was obviously increased (P<0.01) in both the DEX and catgut embedding groups.

Conclusions: Acupoint catgut embedding can reduce the expression of IL-4 and increase the expression of IFN-γ by inhibiting p38 MAPK signal pathway of lung tissues in BA rats, which may contribute to its effect in alleviating the degree of airway epithelial cells damage.

目的: 观察穴位埋线对支气管哮喘(BA)大鼠肺组织磷酸化p38丝裂原活化蛋白激酶(p-p38 MAPK)、白细胞介素-4(IL-4)、γ-干扰素(IFN-γ)和气道上皮细胞(AEC)的影响,探讨穴位埋线治疗BA的作用机制。方法: Wistar大鼠随机分为空白组、模型组、地塞米松组和穴位埋线组,每组10只。采用卵蛋白和氢氧化铝混悬液腹腔注射制备BA模型。穴位埋线组予“肺俞”“定喘”和“膻中”埋线治疗1次。地塞米松组予地塞米松磷酸钠(1.5 mg/kg)腹腔注射治疗,每日1次,治疗2周。记录各组大鼠每分钟打喷嚏次数;HE染色法观察大鼠肺组织病理形态学的变化;透射电镜观察大鼠肺组织中AEC超微结构的变化,测量支气管壁和支气管平滑肌的厚度;Western blot法检测大鼠肺组织中p-p38 MAPK、IL-4和INF-γ的表达水平。结果: 模型组大鼠支气管变形明显,AEC内出现大量自噬泡结构,线粒体减少;地塞米松组和穴位埋线组大鼠支气管变形缓解,AEC内空泡结构减少,线粒体数量增加。与空白组比较,模型组大鼠每分钟打喷嚏次数、支气管壁厚度、支气管平滑肌厚度明显增加(P<0.01),肺组织中p-p38 MAPK和IL-4表达水平明显升高(P<0.01),IFN-γ的表达水平明显降低(P<0.01)。与模型组比较,地塞米松组和穴位埋线组大鼠治疗后打喷嚏次数、支气管壁厚度、支气管平滑肌厚度明显减少(P<0.01),肺组织中p-p38 MAPK和IL-4的表达水平明显降低(P<0.01),IFN-γ的表达水平明显升高(P<0.01)。结论: 穴位埋线可通过抑制p38 MAPK信号通路,降低IL-4的表达、升高IFN-γ的表达,从而缓解BA大鼠AEC受损的程度。.

Keywords: Acupoint catgut embedding; Airway epithelial cell; Asthma; Phosphorylated p38 mitogen-activated protein kinase.

MeSH terms

  • Acupuncture Points
  • Animals
  • Asthma* / genetics
  • Asthma* / therapy
  • Catgut
  • Interleukin-4* / genetics
  • Lung
  • Male
  • Rats
  • Rats, Wistar
  • Sneezing
  • p38 Mitogen-Activated Protein Kinases / genetics

Substances

  • Interleukin-4
  • p38 Mitogen-Activated Protein Kinases