4.3 Article

Protective effects of the calcium-channel blocker flunarizine on crush injury of sciatic nerves in a rat model

Journal

NEUROLOGY INDIA
Volume 58, Issue 4, Pages 530-536

Publisher

MEDKNOW PUBLICATIONS & MEDIA PVT LTD
DOI: 10.4103/0028-3886.68665

Keywords

c-fos; crush injury; dorsal root ganglion; flunarizine; nerve conduction velocity; sciatic nerve

Categories

Funding

  1. Medical Research Council [Natural Science of Jiangsu Province] [BK2001116]
  2. Medical Research Council [Changzhou Board of Health] [2002-202-17, 2004-182-01]
  3. Medical Research Council [Jintan Science and Technology Bureau] [2002-28-25]

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Background: Neural damage can be mitigated by calcium-channel blockers (CCBs). However, the mechanism of action of CCBs is not yet fully understood. Objective: To investigate the mechanism of action and efficacy of CCB, flunarizine in restoring neural function after crush injury to the nerves Materials and Methods: The sciatic nerves of rats were crushed using pincers to establish the model for crush injury. Two hundred and eighty-eight Sprague-Dawley (SD) rats were randomly divided into sham-operated, saline, and low-dose flunarizine and high-dose flunarizine (FI and FII) groups. The expression of the protein c-fos in the dorsal root ganglia (DRG) after crush injury to the sciatic nerves was investigated by using reverse transcription-polymerase chain reaction (RT-PCR) and Western blot. The effect of flunarizine on c-fos expression and its efficacy in restoring neural function was evaluated. Results: The c-fos messenger ribonucleic acid (mRNA) and protein expression in FI and FII groups was significantly lower than in the saline group and was the least in the FII group. Nerve-conduction velocity was increased in the order of: saline < FI< FII< sham-operated. There was no significant difference in the nerve-conduction velocity in the sham-operated and FII groups (P>.05). Conclusions: When administered after crush injury to peripheral nerves, flunarizine may protect neurons with lesions from further damage and improve neural function by downregulating c-fos expression.

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