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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 574629, 14 pages
Research Article

Huang Qi Jian Zhong Pellet Attenuates TNBS-Induced Colitis in Rats via Mechanisms Involving Improvement of Energy Metabolism

1Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330004, China
2Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing 100191, China
3Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, China
4Department of Anatomy, School of Basic Medical Sciences, Peking University, Beijing 100191, China
5Key Laboratory of Microcirculation, State Administration of Traditional Chinese Medicine, Beijing 100191, China
6Department of Internal Medicine, Keio University School of Medicine, Tokyo 160-8582, Japan
7Key Laboratory of Modern Preparation of TCM, Ministry of Education, Jiangxi University of TCM, 18 Yunwan Road, Nanchang, Jiangxi 330004, China

Received 13 March 2013; Revised 17 May 2013; Accepted 20 May 2013

Academic Editor: Zhaoxiang Bian

Copyright © 2013 Duan-Yong Liu 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.


Huang Qi Jian Zhong Pellet (HQJZ) is a famous Chinese medicine formula for treatment of various gastrointestinal tract diseases. This study investigated the role of HQJZ in 2,4,6-trinitrobenzene sulfonic acid- (TNBS-) induced colitis and its underlying mechanism. Colonic mucosal injury was induced by TNBS in the Sprague-Dawley rats. In the HQJZ treatment group, HQJZ was administered (2 g/kg) for 14 days starting from day 1 after TNBS infusion. Colonic mucosal injury occurred obviously 1 day after TNBS challenge and did not recover distinctively until day 15, including an increase in macro- and microscopic scores, a colonic weight index, a decrease in colonic length, a number of functional capillaries, and blood flow. Inverted intravital microscopy and ELISA showed colonic microcirculatory disturbances and inflammatory responses after TNBS stimulation, respectively. TNBS decreased occludin, RhoA, and ROCK-I, while increasing Rac-1, PAK-1, and phosphorylated myosin light chain. In addition, ATP content and ATP5D expression in colonic mucosa decreased after TNBS challenge. Impressively, treatment with HQJZ significantly attenuated all of the alterations evoked by TNBS, promoting the recovery of colonic injury. The present study demonstrated HQJZ as a multitargeting management for colonic mucosal injury, which set in motion mechanisms involving improvement of energy metabolism.