Abstract
IntroductionLutein is a dietary constituent known to inhibit inflammation; however, its effect on nociceptive neuron-associated hyperalgesia remains to be determined. The present study therefore investigated under in vivo conditions whether administration of lutein attenuates the inflammation-induced hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) neurons that is associated with mechanical hyperalgesia.ResultsComplete Freund’s adjuvant (CFA) was injected into the whisker pads of rats to induce inflammation, and then mechanical stimulation was applied to the orofacial area to assess the threshold of escape. The mechanical threshold was significantly lower in inflamed rats compared to uninjected naïve rats, and this lowered threshold was returned to control levels by 3 days after administration of lutein (10 mg/Kg, i.p.) Also the lutein administration, inflammation-induced thickness of edema was returned to control levels. The mean increased number of cyclooxygenase-2 (Cox-2)-immunoreactive cells in the whisker pads of inflamed rats was also returned to control levels by administration with lutein. The mean discharge frequency of SpVc wide-dynamic range (WDR) neurons to both nonnoxious and noxious mechanical stimuli in inflamed rats was significantly decreased after lutein administration. In addition, the increased mean spontaneous discharge of SpVc WDR in inflamed rats was significantly decreased after lutein administration. Similarly, lutein significantly diminished noxious pinch-evoked mean after discharge frequency and occurrence in inflamed rats. Finally, lutein restored the expanded mean size of the receptive field in inflamed rats to control levels.ConclusionThese results together suggest that administration of lutein attenuates inflammatory hyperalgesia associated with hyperexcitability of nociceptive SpVc WDR neurons via inhibition of the peripheral Cox-2 signaling cascade. These findings support the proposed potential of lutein as a therapeutic agent in complementary alternative medicine strategies for preventing inflammatory mechanical hyperalgesia.
Highlights
Lutein is a dietary constituent known to inhibit inflammation; its effect on nociceptive neuron-associated hyperalgesia remains to be determined
Administration of lutein inhibits inflammation-induced edema The edematous area of whisker pad in the inflamed rats was increased in thickness compared to that in naïve rats, from one day to three days (P < 0.05), with the day 2 thickness of naïve vs. inflamed at 6.0 ± 0.1 mm vs. 8.1 ± 0.5 mm, n = 8 (Fig. 2)
Administration of lutein attenuates trigeminal inflammatory hyperalgesia The present study produced the following main findings: (i) the threshold of escape from mechanical stimulation applied to the orofacial area in inflamed rats was significantly lower than that in naïve rats, as described previously [8, 17]; (ii) from one to three days after inflammation, the lowered mechanical threshold in the inflamed rats tended toward control levels following daily administration of lutein (10 mg/kg, i.p); (iii) the reduced escape threshold from mechanical stimulation in inflamed rats increased to control levels with lutein at day 3 of inflammation; (iv) inflammation-induced edema was significantly decreased to control levels with lutein at 2 days inflammation
Summary
Lutein is a dietary constituent known to inhibit inflammation; its effect on nociceptive neuron-associated hyperalgesia remains to be determined. The present study investigated under in vivo conditions whether administration of lutein attenuates the inflammation-induced hyperexcitability of trigeminal spinal nucleus caudalis (SpVc) neurons that is associated with mechanical hyperalgesia. Since graded noxious stimuli applied to receptive fields produce increased firing frequency of SpVc WDR neurons in proportion to stimulus intensity, it can be assumed that WDR neurons are important for encoding stimulus intensity. Chronic pathological conditions such as tissue inflammation can change the properties of somatic sensory pathways, leading to hyperalgesia [4]. SpVc neurons have been implicated in the mechanism of hyperalgesia and/or referred pain associated with dental pain [2, 3, 9]
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