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Inhibition of prostaglandins synthesis in the inflamed site results in opioid-mediatedhypoalgesia in rats

HUANG Jian, WU Jian, YANG Huai-Zu, HONG Yanguo^*

College of Life Sciences, Fujian Normal University, Fujian Key Laboratory of Developmental and Neurological Biology, Fuzhou350117, China

Abstract

This study was designed to investigate the contribution of prostaglandins to the maintenance of inflammatory pain. Inflammation was induced by intraplantar (i.pl.) injection of carrageenan in right hindpaw in rats. Indomethacin (non-selective COX inhibitor) was administered i.pl. 1 h after the carrageenan injection, and paw withdrawal latency (PWL) responding to noxious heat was measured. β-endorphin (β-END) and μ-opioid receptor (MOR) expressed in the inflamed site were examined by using immunocytochemistry, ELISA and RT-PCR techniques. The results showed that indomethacin dose-dependently increased PWL to the levels that were above the baseline on the day 2 and 3, referred to as hypoalgesia. The hypoalgesia was abolished by a local injection of the non-selective opioid receptor inhibitor naloxone methiodide. The number of β-END-positive cells, the content of β-END and the expression of MOR mRNA in the inflammatory site of inflammation model rats were all significantly increased by indomethacin. These results reveal a novel mechanism of prostaglandins for the inhibition of inflammation-induced endogenous opioid activity. Thisstudy provides further evidence that inhibition of prostaglandins in inflamed site could be a promising therapy for inflammatory pain.

Key words: prostaglandins; inflammatory pain; endogenous opioid mechanism; hypoalgesia

Received: 　　Accepted:

Corresponding author: 洪炎国　　E-mail: yhong@fjnu.edu.cn

Citing This Article：

HUANG Jian, WU Jian, YANG Huai-Zu, HONG Yanguo. Inhibition of prostaglandins synthesis in the inflamed site results in opioid-mediatedhypoalgesia in rats. Acta Physiol Sin 2016; 68 (3): 241-248 (in Chinese with English abstract).