Effect of Intrathecal Ginsenosides on Mechanical Allodynia in a Neuropathic Rat Model.
- Author:
Myung Ha YOON
1
;
Hyung Kon LEE
;
Woong Mo KIM
;
Ji Hoon PARK
;
Yeo Ok KIM
;
Lan Ji HUANG
Author Information
1. Department of Anesthesiology and Pain Medicine, Medical School, Chonnam National University, Gwangju, Korea. mhyoon@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
analgesia;
ginsenosides;
neuropathic pain;
spinal cord
- MeSH:
Analgesia;
Animals;
Catheters;
Ginsenosides;
Humans;
Hyperalgesia;
Ligation;
Male;
Neuralgia;
Panax;
Rats;
Rats, Sprague-Dawley;
Spinal Cord;
Spinal Nerves;
Subarachnoid Space
- From:Anesthesia and Pain Medicine
2008;3(3):205-209
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: Traditionally, ginseng has been widely used to manage various types of diseases. In particular, the analgesic effect of ginsenosides has been reported for inflammatory pain. However, the effect of ginsenosides on neuropathic pain has not been determined. The aim of this study was to examine the effect of ginsenosides on neuropathic pain in the spinal cord. METHODS: Neuropathic pain was induced by ligation of the lumbar 5, 6 spinal nerves in male Sprague-Dawley rats. Intrathecal catheters were placed into the subarachnoid space of rats that presented with mechanical allodynia. Mechanical allodynia was evaluated by measuring the withdrawal threshold to a von Frey filament applied to the plantar surface of rats. The analgesic effect of intrathecal ginsenosides was observed at 15, 30, 60, 90, 120, 150 and 180 min after delivery of the ginsenosides. RESULTS: After nerve ligation, the paw withdrawal threshold was significantly decreased at the ligated site. At the doses used in this study, intrathecal ginsenosides did not alter the withdrawal threshold in the ligated paw during the entire observation period. However, a dose of intrathecal ginsenosides greater than 1,500microg caused motor impairment. CONCLUSIONS: These results suggest that ginsenosides may not have a direct modulatory role in the transmission of neuropathic pain at the spinal level.
