Effect of electro-acupuncture at Zusanli point on tumor necrosis factor-α induced-multiple organ dysfunction in rats with sepsis

AIM: To investigate the effect of electro-acupuncture (EA) at Zusanli (ST36) on proinflammatory factors induced-multiple organ dysfunction in rats with sepsis. METHODS: Sixty four male Wastar rats were used to develop the sepsis model by cecal ligation and puncture (CLP). The animals were randomly divided into 4 groups (n=16 in each group): CLP+EA (CLP/EA), CLP+sham EA (CLP/SEA), vagotomy+ CLP+SEA (VA/CLP/SEA) and vagotomy+CLP+EA (VA/CLP/EA). Zusanli point (ST36) was electroacupunctured with constant voltage (2-100 Hz, 2 mA for 0.5 h) 20 min after CLP surgery. Bilateral cervical vagotomies were performed in rats in VA/CL/SEA and VA/CLP/EA groups. Twelve hours after CLP, animals were sacrificed and liver, kidney and jejunum were harvested for evaluating the contents of tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO) and diamine oxidase (DAO). The rate of water content (WCR) of the organs was determined. At the same time, the plasma levels of alanine aminotransferase (ALT) and creatinine (Cr) in each group were also detected. RESULTS: The levels of ALT and Cr in plasma, as well as TNF-α, MPO and WCR in organ tissues were markedly lower, and the activity of DAO in jejunum tissue was obviously higher than that in CLP/SEA group at 12 h after CLP (all P<0.05). The levels of ALT, Cr, TNF-α, MPO and WCR in VA/CLP/SEA group and VA/CLP/EA group were significantly higher, the activity of DAO was obviously lower than that in CLP/SEA group (all P<0.05). No statistical difference in all above measurements between VA/CLP/EA group and VA/CLP/SEA group was observed (all P>0.05). CONCLUSION: The results indicate that EA at Zusanli point obviously decreases the levels of TNF-α in liver, kidney and jejunum tissues after CLP, and alleviates the tissue edema and dysfunction of those organs. Vagotomy decreases or eliminates the effects of EA, suggesting that activation of cholinergic anti-inflammatory pathway is one of the main mechanisms to induce the effects of EA at ST36 on CLP sepsis.