Mechanical injuries of peripheral nerves disturb the reciprocal fast and slow communication between periphery and central nervous system and may lead to variety of clinical pain syndromes, including the hyperalgesia, allodynia and spontaneous pain. An...
Mechanical injuries of peripheral nerves disturb the reciprocal fast and slow communication between periphery and central nervous system and may lead to variety of clinical pain syndromes, including the hyperalgesia, allodynia and spontaneous pain. And then, the effective animal models which mimic most developed to investigate the mechanisms and the control responsible for human neuropathic pain. One of the effective animal models used for this study is the "chronic constriction injury (CCI)" method, described by Bennett and Xie, that is ligated loosely with the chromic gut (4-0) around the left sciatic nerve of the rats. After the surgery of the CCI method, the behavioral evidences of neuropathic pain that seen in patients produced for a long time ; mechanical and thermal allodynia, thermal hyperalgesia and spontaneous pain.
The extract of Korean red gingseng (Panax ginseng C.A Meyer) has been known to produce a vatiety of effects mediated by central nervous system. Especially, they showed the inhibitory effects on the tolerance and the dependence of morphine, and the decreased effects on the serotonin release from the brain stem. Recent studies suggested that the extract show clearly the analgesic and the hypothermic effects in the rat at relatively high doses, and these effects were not mediated via endogenous opiates or opiate receptors since the effects were not antagonized by naltrexone. This study was undertaken to determine the effects and their mechanisms of a standard Korean red ginseng extract on peripheral neuropathic pain induced by the CCI method. The hind paw withdrawal responses as a indicator of pain were determined by the mechanical (von Frei filaments : 0.8 gm and 4.2 gm), thermal (5℃, 30℃ and 44℃) and acetone stimuli to compare with both effects before and after the intraperitoneal injection of ginseng extract(200 mg/kg). And morphine (5 mg/kg, i.m.), ketamine (3 mg/kg, i.m.) and guanethidine (30 mg/kg, i.p.) were treated to the animal pain model after injection of ginseng extract or not for investigating the pain mechanisms or the action mechanism of ginseng extract.
The results of the present study were summarized as follows :
1. Ginseng extract did not show a significant analgesic effect on the mechanical allodynia and thermal hyperalgesia and allodynia.
2. Ginseng extract showed the evidence to increase the hind paw sensitivity of the injured opposite side to some kinds of the stimuli.
3. Ginseng extract produced significantly an inhibitory effect on the hind paw withdrawal responses to acetone stimuli.
4. Morphine, opioid analgesia, showed the inhibitory effects on the responses to noxious cold, acetone, and noxious heat stimuli. The effects of morphine, however, were antagonized significantly by the ginseng extract.
5. Ketamine, non-competitive antagonist of N-methyl-D-aspartate, showed significantly the inhibitory effects to noxious cold and acetone stimuli.
6. Guanethidine, chemical sympathetic blocker, showed no significant effects on the responses to noxious cold and heat stimuli, and acetone stimuli.
These results suggested that the ginseng extract showed the partially analgesic effect on disorders of pain sensation, and the hyperesthesia produced in this animal pain model was not dependent to the chemical sympathectomy. This effect may be resulted from the depression of both the dorsal horn neurons in the spinal cord or the nociceptors sensitized by continous impulse discharges at the nerve injury sites, and may be produced via a non-opioid mechanism.