电针“内关”预处理对心肌缺血再灌注损伤大鼠血清代谢物的影响

目的:基于核磁共振氢谱技术(1 H NMR)观察电针"内关"穴预处理对心肌缺血再灌注损伤(MIRI)大鼠血清代谢物及其代谢通路的影响,从代谢组学角度探讨电针预处理对MIRI大鼠产生保护作用的机制。方法:雄性SD大鼠48只随机分为正常组、模型组、电针内关组(内关组)、电针合谷组(合谷组),每组12只。采用结扎冠状动脉左前降支40min后恢复血流1h制备MIRI大鼠模型。两电针组造模前每天予电针相应穴位30min,连续7d。模型制备成功后,收集各组大鼠血清,利用~1 H NMR进行代谢物检测,利用最小二乘分析、正交偏最小二乘分析进行模式识别。结果:在造模后,模型组、电针组大鼠心电图均表现出T波高耸,R波与T波间无明显ST段。再灌注后T波下降超过0.2mV,无明显ST段。与正常组比较,模型组大鼠血清代谢模式发生明显改变,乙酰乙酸、乳酸、肌酸、丙三醇、葡萄糖升高,丙氨酸、谷氨酰胺、甘油磷酸胆碱、磷酸胆碱降低。与模型组比较,内关组大鼠血清代谢模式发生明显改变,表现为葡萄糖上升,亮氨酸、异亮氨酸、缬氨酸、三羟基丁酸、乳酸、醋酸盐、丙酮、乙酰乙酸、丙酮酸、谷氨酰胺、肌酸、丙三醇下降;合谷组与模型组代谢模式无显著差异。结论:电针"内关"预处理明显改变了MIRI大鼠糖代谢、丙酮酸代谢、氨基酸代谢、酮体代谢、能量代谢的模式,电针"内关"可能通过调节丙酮酸、氨基酸、酮体、能量等对MIRI大鼠起到一定的预保护作用。     

艾灸、电针预处理对急性胃黏膜损伤大鼠TGF-α、PCNA的影响

目的：对比观察艾灸预处理和电针预处理两种不同方法对急性胃黏膜损伤大鼠转化生长因子（TGF-α）和增殖细胞核抗原（PCNA）表达的影响差异。方法将40只SPF级的SD大鼠随机的分为4组（空白组、模型组、艾灸预处理组和电针预处理组）,艾灸预处理组和电针预处理组选取“足三里穴”、“中脘穴”分别行艾灸和电针预处理8 d后,除空白组外造模,选用无水乙醇灌胃的方法（0.5 mL/100 g）制成大鼠急性胃黏膜损伤模型。造模1 h后,用20%乌拉坦（0.6 mL/100 g）进行腹腔注射麻醉,再取材。在光镜下观察大鼠的胃黏膜组织形态学的改变,免疫组化法检测胃黏膜TGF-α、PCNA的表达。结果与空白组相比较,模型组胃黏膜中TGF-α、PCNA的表达明显升高（P<0.05或P<0.01）;与模型组相比较,艾灸预处理组和电针预处理组胃黏膜中TGF-α、PCNA的表达均有不同程度升高（P<0.05或P<0.01）;与艾灸预处理组相比较,电针预处理组胃黏膜中TGF-α的表达明显降低,具有统计学意义（P<0.05或P<0.01）,而胃黏膜中PCNA的表达则无明显差异（P>0.05）。结论艾灸预处理与电针预处理均可以减轻无水乙醇对胃黏膜造成的损伤,促进胃黏膜保护因子（TGF-α、PCNA）的表达,但艾灸预处理稍优于电针预处理。     

电针内关穴预处理对兔心肌缺血再灌注CK及心肌细胞活性的影响

目的观察电针内关穴预处理对心肌缺血再灌注损伤兔CK及心肌细胞活性的影响,为证实心包经穴位与心之间的相对特异性联系提供实验依据。方法将40只新西兰大耳白兔随机分为A组、B组、C组、D组和E组,每组8只。A组为假手术组;B组为缺血再灌注模型组,于左冠状动脉前降支阻断冠脉30 min,再灌注60 min;C组、D组和E组在造模前7 d,每日分别取内关、列缺及合谷给予电针刺激20 min。比较各组肌酸激酶(CK)及心肌formazan含量变化。结果 B组、C组、D组和E组血清CK及心肌formazan含量与A组比较,差异均具有统计学意义(P0.01,P0.05)。C组、D组和E组血清CK含量与B组比较,差异均具有统计学意义(P0.01)。C组心肌formazan含量与B组比较,差异具有统计学意义(P0.05)。D组和E组血清CK及心肌formazan含量与C组比较,差异均具有统计学意义(P0.01,P0.05)。结论电针内关穴能减轻心肌缺血再灌注对心肌细胞的损伤,从而对心脏产生保护作用。     

Effects of moxibustion pretreatment on extracellular signal-regulated kinase signaling transduction pathway in the gastric tissues of rats with gastric mucosal damage

Objective

To observe the effects of moxibustion pretreatment on the protein expressions of epidermal growth factor receptor (EGFR), phosphorylation extracellular signal-regulated kinase 1/2 (p-ERK1/2) and activated protein-1 (AP-1), the key factors of extracellular signal-regulated kinase signaling transduction pathway in gastric tissue of rats with stress-induced gastric mucosal damage, and to discuss the mechanisms of moxibustion therapy in promoting the restoration of damaged gastric mucosa.

Methods

Thirty Sprague-Dawley (SD) rats were randomly divided into a normal group, a model group, and a moxibustion group using the random digits table, 10 in each group. Except the rats in the normal group, rats in the other two groups were used to make stress-induced gastric mucosal damage model using restraint and cold stress. Before modeling, rats in the moxibustion group were alternately treated with moxibustion at Zusanli (ST 36) and Zhongwan (CV 12), or Pishu (BL 20) and Weishu (BL 21), once a day, for a total of 8 d. Histological changes of gastric mucosa were observed under the light microscopy, the expression of gastric tissue p-ERK1/2 was detected by immunohistochemistry assay, and the protein levels of EGFR and AP-1 were measured by Western blots.

Results

Compared with rats in the normal group, gastric mucosal damage was more serious, and protein expressions of gastric tissue EGFR, p-ERK1/2 and AP-1 increased in the model group (P<0.01, P<0.05, P<0.05). Compared with rats in the model group, gastric mucosal damage was milder, and protein expressions of gastric tissue EGFR, p-ERK1/2 and AP-1 increased in the moxibustion group (all P<0.01).

Conclusion

Moxibustion at Zusanli (ST 36), Zhongwan (CV 12), Pishu (BL 20) and Weishu (BL 21) could increase EGFR, p-ERK1/2 and AP-1 expression levels in gastric tissue of stress-induced gastric mucosal damage rats, maintain the information transfer function of ERK signaling transduction pathway, and promote restoration of gastric mucosal damage.