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Resolvin D1 reverses chronic pancreatitis-induced mechanical allodynia, phosphorylation of NMDA receptors, and cytokines expression in the thoracic spinal dorsal horn.
BMC Gastroenterol. 2012 Oct 23; 12:148.BG

Abstract

BACKGROUND

We previously reported that immune activation in the spinal dorsal horn contributes to pain induced by chronic pancreatitis (CP). Targeting immune response in the CNS may provide effective treatments for CP-induced pain. Recent findings demonstrate that resolvin D1 (RvD1) can potently dampen inflammatory pain. We hypothesized that intrathecal injection of RvD1 may inhibit pain of CP.

METHODS

Rat CP model was built through intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). All the rats were divided into three groups: TNBS, sham, and naïve controls and were further divided for intrathecal RvD1 administration. Pain behavior of rats was tested with von Frey filaments. Anxiety-like behavior and free locomotor and exploration of rats were evaluated by open field test and elevated plus maze. Pancreatic histology was evaluated with hematoxylin and eosin staining. Phosphorylation of NMDA receptor and expression of inflammatory cytokines were examined with Western blot, real-time RT-PCR and ELISA.

RESULTS

Behavioral study indicated that compared to the vehicle control, RvD1 (100 ng/kg) significantly decreased TNBS-induced mechanical allodynia at 2 h after administration (response frequencies: 49.2 ± 3.7% vs 71.3 ± 6.1%), and this effect was dose-dependent. Neither CP nor RvD1 treatment could affect anxiety-like behavior. CP or RvD1 treatment could not affect free locomotor and exploration of rats. Western blot analysis showed that compared with that of naïve group, phosphorylated NR1 (pNR1) and pNR2B in TNBS rats were significantly increased in the spinal cord (pNR1: 3.87±0.31 folds of naïve control, pNR2B: 4.17 ± 0.24 folds of naïve control). Compared to vehicle control, 10 ng/kg of RvD1 could significantly block expressions of pNR1 (2.21 ± 0.26 folds of naïve) and pNR2B (3.31 ± 0.34 folds of naïve). Real-time RT-PCR and ELISA data showed that RvD1 (10 ng/kg) but not vehicle could significantly block expressions of TNF-alpha, IL-1beta and IL-6. In addition, RvD1 did not influence pain behavior, NMDA receptor phosphorylation or cytokines production in sham-operated rats.

CONCLUSIONS

These data highly suggest that RvD1 could be a novel and effective treatment for CP-induced chronic pain.

Authors+Show Affiliations

Xijing Hospital of Digestive Diseases, the Fourth Military Medical University, No, 127 West Changle Road, Xi'an, 710032, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

23092159

Citation

Quan-Xin, Feng, et al. "Resolvin D1 Reverses Chronic Pancreatitis-induced Mechanical Allodynia, Phosphorylation of NMDA Receptors, and Cytokines Expression in the Thoracic Spinal Dorsal Horn." BMC Gastroenterology, vol. 12, 2012, p. 148.
Quan-Xin F, Fan F, Xiang-Ying F, et al. Resolvin D1 reverses chronic pancreatitis-induced mechanical allodynia, phosphorylation of NMDA receptors, and cytokines expression in the thoracic spinal dorsal horn. BMC Gastroenterol. 2012;12:148.
Quan-Xin, F., Fan, F., Xiang-Ying, F., Shu-Jun, L., Shi-Qi, W., Zhao-Xu, L., Xu-Jie, Z., Qing-Chuan, Z., & Wei, W. (2012). Resolvin D1 reverses chronic pancreatitis-induced mechanical allodynia, phosphorylation of NMDA receptors, and cytokines expression in the thoracic spinal dorsal horn. BMC Gastroenterology, 12, 148. https://doi.org/10.1186/1471-230X-12-148
Quan-Xin F, et al. Resolvin D1 Reverses Chronic Pancreatitis-induced Mechanical Allodynia, Phosphorylation of NMDA Receptors, and Cytokines Expression in the Thoracic Spinal Dorsal Horn. BMC Gastroenterol. 2012 Oct 23;12:148. PubMed PMID: 23092159.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Resolvin D1 reverses chronic pancreatitis-induced mechanical allodynia, phosphorylation of NMDA receptors, and cytokines expression in the thoracic spinal dorsal horn. AU - Quan-Xin,Feng, AU - Fan,Feng, AU - Xiang-Ying,Feng, AU - Shu-Jun,Li, AU - Shi-Qi,Wang, AU - Zhao-Xu,Liu, AU - Xu-Jie,Zhang, AU - Qing-Chuan,Zhao, AU - Wei,Wang, Y1 - 2012/10/23/ PY - 2012/05/07/received PY - 2012/10/10/accepted PY - 2012/10/25/entrez PY - 2012/10/25/pubmed PY - 2013/6/15/medline SP - 148 EP - 148 JF - BMC gastroenterology JO - BMC Gastroenterol VL - 12 N2 - BACKGROUND: We previously reported that immune activation in the spinal dorsal horn contributes to pain induced by chronic pancreatitis (CP). Targeting immune response in the CNS may provide effective treatments for CP-induced pain. Recent findings demonstrate that resolvin D1 (RvD1) can potently dampen inflammatory pain. We hypothesized that intrathecal injection of RvD1 may inhibit pain of CP. METHODS: Rat CP model was built through intrapancreatic infusion of trinitrobenzene sulfonic acid (TNBS). All the rats were divided into three groups: TNBS, sham, and naïve controls and were further divided for intrathecal RvD1 administration. Pain behavior of rats was tested with von Frey filaments. Anxiety-like behavior and free locomotor and exploration of rats were evaluated by open field test and elevated plus maze. Pancreatic histology was evaluated with hematoxylin and eosin staining. Phosphorylation of NMDA receptor and expression of inflammatory cytokines were examined with Western blot, real-time RT-PCR and ELISA. RESULTS: Behavioral study indicated that compared to the vehicle control, RvD1 (100 ng/kg) significantly decreased TNBS-induced mechanical allodynia at 2 h after administration (response frequencies: 49.2 ± 3.7% vs 71.3 ± 6.1%), and this effect was dose-dependent. Neither CP nor RvD1 treatment could affect anxiety-like behavior. CP or RvD1 treatment could not affect free locomotor and exploration of rats. Western blot analysis showed that compared with that of naïve group, phosphorylated NR1 (pNR1) and pNR2B in TNBS rats were significantly increased in the spinal cord (pNR1: 3.87±0.31 folds of naïve control, pNR2B: 4.17 ± 0.24 folds of naïve control). Compared to vehicle control, 10 ng/kg of RvD1 could significantly block expressions of pNR1 (2.21 ± 0.26 folds of naïve) and pNR2B (3.31 ± 0.34 folds of naïve). Real-time RT-PCR and ELISA data showed that RvD1 (10 ng/kg) but not vehicle could significantly block expressions of TNF-alpha, IL-1beta and IL-6. In addition, RvD1 did not influence pain behavior, NMDA receptor phosphorylation or cytokines production in sham-operated rats. CONCLUSIONS: These data highly suggest that RvD1 could be a novel and effective treatment for CP-induced chronic pain. SN - 1471-230X UR - https://www.unboundmedicine.com/medline/citation/23092159/Resolvin_D1_reverses_chronic_pancreatitis_induced_mechanical_allodynia_phosphorylation_of_NMDA_receptors_and_cytokines_expression_in_the_thoracic_spinal_dorsal_horn_ L2 - https://bmcgastroenterol.biomedcentral.com/articles/10.1186/1471-230X-12-148 DB - PRIME DP - Unbound Medicine ER -