Capsaicin, a potent algogen, induces an itch-related behavior in the presence of inflammation. In this study, we tested whether bradykinin (BK) can evoke a similar response and investigated the potential mechanisms involved in this process. Local inflammation was induced by intradermal injection of complete Freund's adjuvant (CFA) into the back of the neck, left hind foot or left cheek of male C57BL/6J mice. BK was then injected intradermally into the same area on indicated days. Four days after CFA inflammation, BK treatment evoked scratching responses in a time- and dose-dependent manner. For BK receptor antagonist treatment, inflamed-mice were either given an intraperitoneal injection of B(1) receptor (B(1)R) or B(2) receptor (B(2)R) antagonist 30 min prior to BK administration, or an intradermal co-injection of antagonist and BK into the inflamed area. Our results indicate that B(1)R and B(2)R act in an opposite fashion during this process, as pretreatment with B(1)R antagonist by intraperitoneal injection significantly reduced BK-induced scratching behavior, whereas B(2)R antagonist treatment dramatically increased scratching behavior. Moreover, combined injection of BK and B(2)R antagonist enhanced BK-induced scratching activity in CFA-inflamed mice. In addition, pretreatment or co-injection with B(2)R antagonist dramatically reduced the pain-related licking behavior induced by BK injection. The data suggest that BK-induced scratching responses in CFA-inflamed mouse skin occur via activation of B(1)R. Furthermore, B(1) and B(2) receptors play different roles in modulating BK-induced itch-related behavior in CFA-inflamed mice.

The aim of the present study was to explore the feasibility of real-time monitoring and quantitative guiding the repair of enamel white spot lesions (WSLs) with resin infiltration by optical coherence tomography (OCT). Seven New Zealand rabbits were treated with 37% phosphoric acid etchant for 15 min to establish the model of enamel demineralization chalk spots of upper incisors, which were repaired by Icon resin infiltrant. OCT, stereo microscope (SM) imaging, scanning electron microscope (SEM) imaging and hematoxylin eosin (HE) staining were used to image each operation step. The changes of WSLs of enamel before and in the process of restoration with resin infiltrant showed specific performance in OCT images, which were consistent with the corresponding results of stereomicroscope and SEM. OCT can non-invasively and accurately image the whole process of repairing enamel demineralization layer with resin infiltration real-time, which can effectively guide the clinical use of resin infiltrant to repair enamel WSLs and be used as an imaging tool to evaluate the process and effect of restoration with resin infiltrant at the same time.

Intrathecal administration of the CCC inhibitor furosemide had antinociceptive effects in rats with incisional pain. Furosemide may be a novel treatment for postoperative pain.

Accumulating evidence has demonstrated that the sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 have a role in the modulation of pain transmission at the spinal level through chloride regulation in the pain pathway and by effecting neuronal excitability and pain sensitization. The present study aimed to investigate the analgesic effect of the specific sodium-potassium-chloride co-transporter 1 inhibitor bumetanide, and the change in spinal sodium-potassium-chloride co-transporter 1 and potassium-chloride co-transporter 2 expression in a rat model of incisional pain. Results showed that intrathecal bumetanide could decrease cumulative pain scores, and could increase thermal and mechanical pain thresholds in a rat model of incisional pain. Sodium-potassium-chloride co-transporter 1 expression increased in neurons from dorsal root ganglion and the deep laminae of the ipsilateral dorsal horn following incision. By contrast, potassium-chloride co-transporter 2 expression decreased in neurons of the deep laminae from the ipsilateral dorsal horn. These findings suggest that spinal sodium-potassium-chloride co-transporter 1 expression was up-regulated and spinal potassium-chloride co-transporter 2 expression was down-regulated following incision. Intrathecal bumetanide has analgesic effects on incisional pain through inhibition of sodium-potassium-chloride co-transporter 1.