Background: Chrysin is a natural bioactive compound belonging to the flavonoid group. The pain-relieving effects of chrysin have been reported in several studies; however, the molecular mechanism underlying its analgesic properties remains unknown. In the present study, the analgesic effect of chrysin was investigated on the hypothalamic Calcitonin Gene-Related Peptide (CGRP) and Tachykinin 1 (Tac1) gene expression in a formalin-induced pain model.
Methods: Twenty male rats weighing 200 ± 10 g were divided into four groups. Pain was induced by injecting 50 μl of formalin into the hind paw. The control and formalin groups received saline. In addition, 20 or 40 µg of chrysin was injected into pain-induced rats via the third cerebral ventricle. After 30 minutes, a behavioral test was conducted. Hypothalamus samples were then dissected, and real-time polymerase chain reaction (PCR) was performed to measure gene expression.
Results: The mRNA levels of CGRP and Tac1 significantly increased in the formalin-treated rats compared to the control group. In contrast, the mRNA levels of CGRP and Tac1 were significantly reduced in the chrysin-treated groups compared to the formalin group. Furthermore, the pain score was significantly lower in the chrysin-treated groups compared to the formalin group.
Conclusion: The pain-relieving effects of chrysin were mediated through the downregulation of hypothalamic CGRP and Tac1 in the pain model rats.
نوع مقاله:
تحقیقی |
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علوم مولکولی دریافت: 1402/12/1 | پذیرش: 1403/2/16 | انتشار: 1404/2/31