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Lidocaine attenuates the development of diabetic-induced tactile allodynia by inhibiting microglial activation.
Anesth Analg. 2011 Oct; 113(4):941-6.A&A

Abstract

BACKGROUND

Lidocaine is used clinically for tactile allodynia associated with diabetes-induced neuropathy. Although the analgesic effect of lidocaine through suppression of microglial activation has been implicated in the development of injury-induced neuropathic pain, its mechanism of action in diabetes-induced tactile allodynia has not yet been completely elucidated.

METHODS

To evaluate the effects of lidocaine on microglial response in diabetic neuropathy, streptozotocin (STZ)-injected mice received a continuous infusion of lidocaine (vehicle, 2, or 10%) from day 14 to day 21 after STZ injection. On day 21, microglial accumulation and p38 mitogen-activated protein kinase activation in the dorsal horn were evaluated. In vitro, the effects of lidocaine on cell viability, chemotactic response to monocyte chemotactic protein-1, and induction of proinflammatory mediators were examined in interferon (IFN)-γ-stimulated primary microglial cells.

RESULTS

Continuous systemic administration of lidocaine in the early progression of tactile allodynia produced long-lasting analgesic effects in STZ-treated mice. Lidocaine significantly reduced accumulation and p38 phosphorylation of microglial cells in the dorsal horn. In vitro, lidocaine down-regulated IFN-γ-induced gene induction of inducible oxide synthase and interleukin-1β. Pretreatment with lidocaine significantly reduced chemotactic response to monocyte chemotactic protein-1 of IFN-γ-activated microglial cells.

CONCLUSION

Lidocaine alleviates STZ-induced tactile allodynia, possibly by modulating the p38 pathway in spinal microglial cells. Inhibiting microglial activation by lidocaine treatment early in the course of diabetes-induced neuropathy represents a potential therapeutic strategy for tactile allodynia.

Authors+Show Affiliations

Department of Anesthesiology and Pain Medicine, Juntendo University School of Medicine, 2-1-1 Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21788310

Citation

Suzuki, Naoko, et al. "Lidocaine Attenuates the Development of Diabetic-induced Tactile Allodynia By Inhibiting Microglial Activation." Anesthesia and Analgesia, vol. 113, no. 4, 2011, pp. 941-6.
Suzuki N, Hasegawa-Moriyama M, Takahashi Y, et al. Lidocaine attenuates the development of diabetic-induced tactile allodynia by inhibiting microglial activation. Anesth Analg. 2011;113(4):941-6.
Suzuki, N., Hasegawa-Moriyama, M., Takahashi, Y., Kamikubo, Y., Sakurai, T., & Inada, E. (2011). Lidocaine attenuates the development of diabetic-induced tactile allodynia by inhibiting microglial activation. Anesthesia and Analgesia, 113(4), 941-6. https://doi.org/10.1213/ANE.0b013e31822827a2
Suzuki N, et al. Lidocaine Attenuates the Development of Diabetic-induced Tactile Allodynia By Inhibiting Microglial Activation. Anesth Analg. 2011;113(4):941-6. PubMed PMID: 21788310.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lidocaine attenuates the development of diabetic-induced tactile allodynia by inhibiting microglial activation. AU - Suzuki,Naoko, AU - Hasegawa-Moriyama,Maiko, AU - Takahashi,Yoshika, AU - Kamikubo,Yuji, AU - Sakurai,Takashi, AU - Inada,Eiichi, Y1 - 2011/07/25/ PY - 2011/7/27/entrez PY - 2011/7/27/pubmed PY - 2012/7/17/medline SP - 941 EP - 6 JF - Anesthesia and analgesia JO - Anesth Analg VL - 113 IS - 4 N2 - BACKGROUND: Lidocaine is used clinically for tactile allodynia associated with diabetes-induced neuropathy. Although the analgesic effect of lidocaine through suppression of microglial activation has been implicated in the development of injury-induced neuropathic pain, its mechanism of action in diabetes-induced tactile allodynia has not yet been completely elucidated. METHODS: To evaluate the effects of lidocaine on microglial response in diabetic neuropathy, streptozotocin (STZ)-injected mice received a continuous infusion of lidocaine (vehicle, 2, or 10%) from day 14 to day 21 after STZ injection. On day 21, microglial accumulation and p38 mitogen-activated protein kinase activation in the dorsal horn were evaluated. In vitro, the effects of lidocaine on cell viability, chemotactic response to monocyte chemotactic protein-1, and induction of proinflammatory mediators were examined in interferon (IFN)-γ-stimulated primary microglial cells. RESULTS: Continuous systemic administration of lidocaine in the early progression of tactile allodynia produced long-lasting analgesic effects in STZ-treated mice. Lidocaine significantly reduced accumulation and p38 phosphorylation of microglial cells in the dorsal horn. In vitro, lidocaine down-regulated IFN-γ-induced gene induction of inducible oxide synthase and interleukin-1β. Pretreatment with lidocaine significantly reduced chemotactic response to monocyte chemotactic protein-1 of IFN-γ-activated microglial cells. CONCLUSION: Lidocaine alleviates STZ-induced tactile allodynia, possibly by modulating the p38 pathway in spinal microglial cells. Inhibiting microglial activation by lidocaine treatment early in the course of diabetes-induced neuropathy represents a potential therapeutic strategy for tactile allodynia. SN - 1526-7598 UR - https://www.unboundmedicine.com/medline/citation/21788310/Lidocaine_attenuates_the_development_of_diabetic_induced_tactile_allodynia_by_inhibiting_microglial_activation_ L2 - https://doi.org/10.1213/ANE.0b013e31822827a2 DB - PRIME DP - Unbound Medicine ER -