Journal of the Formosan Medical Association = Taiwan yi zhi · 2013
Attenuation of neuropathic pain by sodium butyrate in an experimental model of chronic constriction injury in rats.
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Kukkar Ankesh, Singh Nirmal, Jaggi Amteshwar Singh
Аннотация
BACKGROUND/PURPOSE: The present study was designed to investigate the potential of sodium butyrate, a histone deacetylase (HDAC) inhibitor, in chronic constriction injury (CCI)-induced neuropathic pain in rats.
METHODS: Neuropathic pain was induced by placing four loose ligatures around the sciatic nerve. Acetone drop, Von frey hair, pin prick and hot plate tests were performed to assess cold allodynia, mechanical allodynia, and mechanical and heat hyperalgesia, respectively. The level of tumor necrosis factor (TNF)-α was measured in the sciatic nerve as an inflammatory marker.
RESULTS: CCI was associated with the development of cold allodynia, mechanical allodynia, and mechanical and heat hyperalgesia, along with an increase in TNF-α level. Administration of sodium butyrate (200 and 400 mg/kg, oral) for 14 days in CCI-subjected rats significantly attenuated behavior related to injury-induced pain and the increase in TNF-α level.
CONCLUSION: It may be concluded that the anti-inflammatory actions mediated by sodium butyrate are responsible for its beneficial effects in neuropathic pain in rats.
METHODS: Neuropathic pain was induced by placing four loose ligatures around the sciatic nerve. Acetone drop, Von frey hair, pin prick and hot plate tests were performed to assess cold allodynia, mechanical allodynia, and mechanical and heat hyperalgesia, respectively. The level of tumor necrosis factor (TNF)-α was measured in the sciatic nerve as an inflammatory marker.
RESULTS: CCI was associated with the development of cold allodynia, mechanical allodynia, and mechanical and heat hyperalgesia, along with an increase in TNF-α level. Administration of sodium butyrate (200 and 400 mg/kg, oral) for 14 days in CCI-subjected rats significantly attenuated behavior related to injury-induced pain and the increase in TNF-α level.
CONCLUSION: It may be concluded that the anti-inflammatory actions mediated by sodium butyrate are responsible for its beneficial effects in neuropathic pain in rats.