Effect of compound K on spinal Toll-like receptor 4 expression during morphine-induced hyperalge-sia in rats
10.3760/cma.j.issn.0254-1416.2015.12.008
- VernacularTitle:人参皂苷Compound K对吗啡诱发大鼠痛觉过敏时脊髓TLR4表达的影响
- Author:
Li LI
;
Yi CHEN
;
Yonghao YU
- Publication Type:Journal Article
- Keywords:
GINSENOSIDE;
Morphine;
Hyperalgesia;
Toll-like receptor 4;
Spinal cord
- From:
Chinese Journal of Anesthesiology
2015;(12):1443-1445
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the effect of compound K ( CK) on spinal Toll?like receptor 4 ( TLR4) expression during morphine?induced hyperalgesia in rats. Methods Thirty?six healthy male Spra?gue?Dawley rats in which intrathecal catheters were successfully implanted were randomly divided into 3 groups ( n=12 each) using a random number table: control group ( group C) , morphine?induced hyperal?gesia group ( group M) , and morphine + CK group ( group M+CK) . Starting from 5 days after successful implantation, normal saline 10 μl, morphine 10 μg, and morphine 10 μg + CK 10 μg were injected in?trathecally twice a day for 7 consecutive days. Tail?flick latency ( TFL) to a thermal nociceptive stimulus was measured at 1 day before administration ( T0 , baseline) and at 30 min after the initial administration on 1st, 3rd, 5th and 7th days (T1?4), and the percentage of maximum possible effect (MPE) was calculated. The rats were sacrificed after the last measurement of tail?flick latency, and the lumbar segment ( L3?5 ) of the spinal cord was removed for determination of the expression of TLR4 by Western blot. Results MPE was significantly lower at T3,4 than at T1 in M and M+CK groups ( P<0?05) . Compared with group C, MPE was significantly lower at T2?4 , and the expression of TLR4 was up?regulated in M and M+CK groups ( P<0?05). Compared with group M, MPE was significantly increased at T1?4, and the expression of TLR4 was down?regulated in group M+CK ( P<0?05 ) . Conclusion The mechanism by which CK alleviates mor?phine?induced hyperalgesia is associated with down?regulation of TLR4 expression in rats.
