Effect of Ethyl Pyruvate on Paclitaxel-Induced Neuropathic Pain in Rats.
10.3344/kjp.2013.26.2.135
- Author:
Seong Soo CHOI
1
;
Won Uk KOH
;
Jae Sik NAM
;
Jin Woo SHIN
;
Jeong Gill LEEM
;
Jeong Hun SUH
Author Information
1. Department of Anesthesiology and Pain Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. paindrsuh@gmail.com
- Publication Type:Original Article
- Keywords:
allodynia;
apoptosis;
dorsal root ganglion;
ethyl pyruvate;
paclitaxel
- MeSH:
Animals;
Apoptosis;
Caspase 3;
Compliance;
Diagnosis-Related Groups;
Ganglia, Spinal;
Glial Fibrillary Acidic Protein;
Hyperalgesia;
Myelin Sheath;
Neuralgia;
Neurons;
Paclitaxel;
Pyruvates;
Pyruvic Acid;
Rats
- From:The Korean Journal of Pain
2013;26(2):135-141
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Although paclitaxel is a widely used chemotherapeutic agent for the treatment of solid cancers, side effects such as neuropathic pain lead to poor compliance and discontinuation of the therapy. Ethyl pyruvate (EP) is known to have analgesic effects in several pain models and may inhibit apoptosis. The present study was designed to investigate the analgesic effects of EP on mechanical allodynia and apoptosis in dorsal root ganglion (DRG) cells after paclitaxel administration. METHODS: Rats were randomly divided into 3 groups: 1) a control group, which received only vehicle; 2) a paclitaxel group, which received paclitaxel; and 3) an EP group, which received EP after paclitaxel administration. Mechanical allodynia was tested before and at 7 and 14 days after final paclitaxel administration. Fourteen days after paclitaxel treatment, DRG apoptosis was determined by activated caspase-3 immunoreactivity (IR). RESULTS: Post-treatment with EP did not significantly affect paclitaxel-induced allodynia, although it tended to slightly reduce sensitivities to mechanical stimuli after paclitaxel administration. After paclitaxel administration, an increase in caspase-3 IR in DRG cells was observed, which was co-localized with NF200-positive myelinated neurons. Post-treatment with EP decreased the paclitaxel-induced caspase-3 IR. Paclitaxel administration or post-treatment with EP did not alter the glial fibrillary acidic protein IRs in DRG cells. CONCLUSIONS: Inhibition of apoptosis in DRG neurons by EP may not be critical in paclitaxel-induced mechanical allodynia.
