The time-course and RNA interference of TNF-alpha, IL-6, and IL-1beta expression on neuropathic pain induced by L5 spinal nerve transection in rats.
10.4097/kjae.2015.68.2.159
- Author:
Byung Moon CHOI
1
;
Soo Han LEE
;
Sang Mee AN
;
Do Yang PARK
;
Gwan Woo LEE
;
Gyu Jeong NOH
Author Information
1. Department of Anesthesiology and Pain Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. nohgj@amc.seoul.kr
- Publication Type:Original Article
- Keywords:
Cytokine;
Neuropathic pain;
RNA interference
- MeSH:
Animals;
Catheters;
Cytokines;
Hyperalgesia;
Interleukin-6*;
Neuralgia*;
Neuroglia;
Rats*;
RNA Interference*;
RNA, Messenger;
RNA, Small Interfering;
Spinal Nerves*;
Tumor Necrosis Factor-alpha*
- From:Korean Journal of Anesthesiology
2015;68(2):159-169
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: The objective of this study was to investigate the time-course of the expression of TNF-alpha, IL-6, and IL-1beta after L5 spinal nerve transection (SNT), and to determine the effect of small interfering RNA (siRNA) targeting these cytokines on neuropathic pain. METHODS: Rats received control siRNA (CON group, n = 80) or a cocktail of siRNAs targeting these cytokines (COCK group, n = 70). The siRNAs were given via intrathecal catheter 1 d prior to SNT, on the operation day, and 1, 2 and 3 d postoperatively. Behavioral tests and levels of the cytokine mRNAs and proteins as well as glial cell activity were following the L5 SNT. RESULTS: In the CON group, TNF-alpha and IL-1beta mRNA levels increased immediately after SNT and remained high for 6 d, while IL-6 transcripts only began to increase after 12 h. TNF-alpha and IL-1beta mRNA levels in the COCK group were lower than in the CON group at all time points (P < 0.05). In the behavioral tests, allodynia and hyperalgesia were significantly lower in the COCK group from 2 d after SNT (P < 0.05). CONCLUSIONS: The time courses of TNF-alpha, IL-6 and IL-1beta mRNA expression after L5 SNT differ. RNA interference may be a method of reducing the development of mechanical allodynia and hyperalgesia in response to nerve injury.
