Acupuncture has long been used for pain relief. Although recent studies have shown that acupuncture can reduce neuropathic pain, the mechanism of this effect is not clear and little information is available regarding proteins that are involved in the development of neuropathic pain and the effects of acupuncture. We have developed an animal model for neuropathic pain using young adult male Sprague-Dawley rats. The model was confirmed by behavioral tests. Electroacupuncture (EA) treatment was applied to Zusanli (ST36) of neuropathic pain model to examine the analgesic effect of EA. The protein expression profile of the hypothalamus in both neuropathic pain and EA treatment models was analyzed using two-dimensional electrophoresis-based proteomics. We detected thirty-six proteins that were differentially expressed in the neuropathic pain model compared with normal rats and that restored to normal expression levels after EA treatment. Twenty-one of these proteins were identified in the MS-FiT database and are involved in a number of biological processes, including inflammation, enzyme metabolism and signal transduction. Potential applications of our results include the identification and characterization of signaling pathways involved in EA treatment and further exploration of the role of selected identified proteins in the animal model.

Human LZIP is a transcription factor that is involved in leukocyte cell mobility. Expression of LZIP is known to differentially regulate monocyte cell migration induced by CCR1-dependent chemokines. However, its transcriptional regulation has not been characterized. Our results indicate that Lkn-1 induces LZIP expression in a time-and dose-dependent manner, and the induction of LZIP shows an immediate early response to Lkn-1. We identified and cloned ϳ1.4 kb of the LZIP promoter from a human genomic DNA. To identify regulatory elements controlling restricted expression of LZIP, deletion mutants were constructed from the 1469-bp LZIP promoter region (؊1219/؉251) linked to the luciferase reporter gene. Maximal promoter activity was contained within 613 bp from the tentative transcription initiation site and was sharply reduced in a truncated construct (؊338/؉251). This promoter sequence contained consensus NF-B-and Sp-1-binding sites. Results from an inhibitor assay showed that NF-B is involved in Lkn-1-induced LZIP expression, but Sp-1 is not. We also demonstrated that NF-B binds to the LZIP promoter and that the binding is specific, as revealed by an electrophoretic mobility shift assay and a mutation analysis. Chemotaxis analysis showed that LZIP expression because of the NF-B subfamily is specifically involved in Lkn-1-induced chemotaxis. Our findings suggest that transcription factor NF-B plays an important role in regulation of LZIP expression, and LZIP expression regulates the monocyte cell migration induced by Lkn-1.The human leucine zipper protein LZIP binds to canonical cAMP-responsive elements (CREs) 2 and can activate transcription from CRE-containing reporter genes (1-3). LZIP also binds to the CCAAT enhancer-binding protein element (1). LZIP is known to be involved in the regulation of cell growth by binding to the human host cell factor, which is involved in cell proliferation (4). It has also been suggested that LZIP serves a novel cellular tumor suppressor function that is targeted by the hepatitis C virus core protein (4). We have recently reported that LZIP associates with CC chemokine receptor 1 (CCR1) and up-regulates leukotactin-1 (Lkn-1)-induced chemotactic activity, indicating that LZIP functions as a positive regulator in leukocyte cell migration induced by chemokines (5). However, the exact biological roles and the natural target genes of LZIP remain to be characterized.The human LZIP gene is located on chromosome 9p and consists of nine exons and eight introns. Sequence analysis of the 5Ј-flanking region of the LZIP gene has revealed that LZIP promoter has potential binding sites for transcription factors involved in inflammatory processes and regulation of the immune system, including nuclear factor B (NF-B), nuclear factor of activated T-cells, specific protein-1 (Sp-1), and activator protein-2 (AP-2) (6). However, the regulatory mechanism of the transcriptional activation of LZIP is still obscure.Chemokines are a large family of chemotactic cytokines that provide key signals for traff...