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Evidence-Based Complementary and Alternative Medicine
Volume 2014, Article ID 451674, 8 pages
http://dx.doi.org/10.1155/2014/451674
Research Article

Electrical Stimulation at the ST36 Acupoint Protects against Sepsis Lethality and Reduces Serum TNF Levels through Vagus Nerve- and Catecholamine-Dependent Mechanisms

1Medical Research Unit on Immunochemistry, Specialties Hospital, National Medical Centre “Siglo XXI,” Mexican Social Security Institute (IMSS), 06720 Mexico City, DF, Mexico
2Universidad Autónoma Benito Juarez de Oaxaca (UABJO), 68120 Oaxaca de Juárez, OAX, Mexico
3National School of Medicine and Homeopathy, National Polytechnic Institute, 07320 Mexico City, DF, Mexico
4Immunobiology Laboratory, Mexico’s Juarez Hospital, Ministry of Health, 07760 Mexico City, DF, Mexico

Received 12 February 2014; Revised 21 May 2014; Accepted 28 May 2014; Published 26 June 2014

Academic Editor: Alvin J. Beitz

Copyright © 2014 Albino Villegas-Bastida et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Electrical vagus nerve (VN) stimulation during sepsis attenuates tumor necrosis factor (TNF) production through the cholinergic anti-inflammatory pathway, which depends on the integrity of the VN and catecholamine production. To characterize the effect of electroacupuncture at ST36 (EA-ST36) on serum TNF, IL-6, nitrite, and HMGB1 levels and survival rates, based on VN integrity and catecholamine production, a sepsis model was induced in rats using cecal ligation and puncture (CLP). The septic rats were subsequently treated with EA-ST36 (CLP+ST36), and serum samples were collected and analyzed for cytokines levels. The serum TNF, IL-6, nitrite, and HMGB1 levels in the CLP+ST36 group were significantly lower compared with the group without treatment, the survival rates were significantly higher ( ), and the acute organ injury induced by CLP was mitigated by EA-ST36; however, when subdiaphragmatic vagotomy was performed, the serum levels of TNF in the CLP+ST36 group did not show a significant difference compared with the group without electrostimulation, and, similarly, no significant difference in serum TNF levels was found under the pharmacological blockade of catecholamines. These results suggest that in rats with CLP sepsis models EA-ST36 reduces serum TNF levels through VN- and atecholamine-dependent mechanisms.