Pain: Causes, Concerns and Consequences

The Ameliorative Potential of 7-Hydroxy- 4-Methylcoumarin in Acrylamide Induced Neuropathic Pain via Improving of Mitochondrial Function in Rat

Author(s): Jaspreet Kaur, Arunachalam Muthuraman and Muthusamy Ramesh

Pp: 161-187 (27)

DOI: 10.2174/9781681083711116010009

* (Excluding Mailing and Handling)


The present study was designed to investigate the analgesic potential of 7- hydroxy-4-methylcoumarin (HMC) in acrylamide induced neuropathic pain in rats. Acrylamide (30 mg/kg, i.p.; once in three days, for 24 consecutive days) was administered for inducing neuropathic pain. The acrylamide induced nociceptive pain sensation, i.e., acetone drop, plantar, hot plate, Von Frey Hair and tail immersion tests have been assessed at different time intervals, i.e., 0, 6, 12, 18 and 24th day. Furthermore, the biochemical estimation, i.e., thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH), total calcium, cytochrome c oxidase activity and ATP content levels were estimated from the sciatic nerve tissue sample on 24th day. The HMC (10 and 20 mg/kg, p.o.) and cyclosporin A (CsA, 50 μM/kg; p.o.) was administered for 24 consecutive days, one hour before each injection of acrylamide. The treatment of acrylamide resulted in significant (P < 0.05) changes of behavioral and biochemical changes. Pretreatment of HMC ameliorate the acrylamide induced changes of behavioral and biochemical parameters in a dose dependent manner. These results are similar to that of CsA treated group. Based on these findings, it may conclude that, HMC possesses the potential ameliorative effect against acrylamide induced neuropathic pain, it may be because of its therapeutic potential of anti-oxidant, anti-lipidperoxidative, calcium ion regulatory and mitochondrial permeability transition pore inhibitory action.

Keywords: 7-hydroxy-4-methylcoumarin, Acrylamide, Adenosine triphosphate, Allodynia, Calcium, Cyclosporin A, Cytochrome c oxidase, Electron transport chain, Hyperalgesia, Mitochondrial dysfunction.

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