3 years ago

Protective effect of electroacupuncture preconditioning at zúsānlĭ (足三里 ST36) on mitochondria in the intestinal ischemia/reperfusion injury

Zheng Huang, Yong-ming Han, Xiao-ping Hong, Yan-jun Duan, Tao Chen, Jiao-rong Chen

Publication date: Available online 29 August 2018

Source: World Journal of Acupuncture - Moxibustion

Author(s): Zheng HUANG, Yong-ming HAN, Xiao-ping HONG, Yan-jun DUAN, Tao CHEN, Jiao-rong CHEN


The study explored the effect of applying electroacupuncture (EA) preconditioning at ST 36 on mitochondria in rats with intestinal ischemia/reperfusion injury.


Forty SD rats were divided into four sets: sham operation group (sham group); intestinal ischemia/reperfusion group (I/R group); EA preconditioning at ST 36 followed by intestinal ischemia/reperfusion injury (ST 36 + I/R group); EA preconditioning at the lateral site away from ST36 0.5 cm followed by intestinal ischemia/reperfusion injury (N + I/R group). For the sham group, the rats were opened abdominal cavity for 3 h and 20 min and their abdominal cavities were covered with wet gauze avoiding drying and kept on the thermostat at 37 °C. For the ischemia/reperfusion (I/R) group, rats were anaesthetised and their abdominal cavities were opened to expose jejunum segments. The segment's collateral blood supply was restricted by bilateral ligation of the intestine. Next, one of the branches of a mesenteric artery was occluded with a thread for 20 min and then the thread was released after such ischemia conditions, keeping reperfusion for 3 h. For the ST36 + I/R group, the electroacupuncture at ST36 was first performed, then the intestinal ischemia/reperfusion model was constructed. For the N + I/R group, electroacupuncture at non ST36 acupoint, which is away from ST36 about 0.5 cm, and then the intestinal ischemia/reperfusion model was performed. Measurements of the levels of inflammatory markers tumour necrosis factor α (TNFα) and interleukin-1 beta (IL-1β), cytochrome c (CYCS), and the mitochondrial membrane pro-apoptotic protein (BAX), anti-apoptotic protein Bcl-2 were performed.


Compared to I/R group, the intensity of cytoplasmic CYCS in intestinal tissues was significantly decreased in the ST 36 + I/R group (1.65 vs. 0.18, p < 0.05). Compared to N + I/R group, the intensity of cytoplasmic CYCS in intestinal tissues was also dramatically declined in the ST 36 + I/R group (1.37 vs. 0.18, p < 0.05). The level of CYCS in mitochondria in rats in the ST 36 + I/R group were appreciably increased than those of rats in the I/Rgroup (1.42 vs. 0.06, p < 0.05), and CYCS in mitochondria was also largely expressed in ST36 + I/R group than N + I/R group (1.42 vs. 0.08, p < 0.05). Bcl-2 was shown to be elevated in the ST 36 + I/R group than I/R group (1.01 vs. 0.10) and N + I/R group (1.01 vs. 0.09, all p < 0.05), whereas BAX expression was greatly decreased in the ST36 + I/R group than I/R group (0.11 vs. 0.78 ) and N + I/R group (0.11 vs. 0.87, all p < 0.05).


The results suggest the EA intervention has a protective effect upon mitochondria, preventing CYCS release and the subsequent activation of downstream apoptosis pathway. It is proposed that patients due to undergo gastrointestinal surgery get benefit from EA preconditioning at ST 36.

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