Khadijeh Haghighat; Fariba Mahmoudi; Homayoun Khazali
Abstract
Stress is one of the most prevalent mental health disorders. Chrysin, a phytochemical compound, is known for its anti-stress effects; however, the molecular mechanisms underlying its anxiolytic properties are not well understood. The present study aimed to investigate the effects of chrysin on the gene ...
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Stress is one of the most prevalent mental health disorders. Chrysin, a phytochemical compound, is known for its anti-stress effects; however, the molecular mechanisms underlying its anxiolytic properties are not well understood. The present study aimed to investigate the effects of chrysin on the gene expression of hypothalamic phoenixin and nesfatin-1 in a rat model of acute restraint stress. In the study, twenty male Wistar rats weighing 200 ± 10 g were split up into four groups (n=5). A cannula was surgically implanted into the third cerebral ventricle. Following a one-week recovery period, the rats were exposed to a two-hour acute restraint stress protocol. While the control and stress groups received saline, two additional experimental groups subjected to stress were administered either 20 µg or 40 µg of chrysin via the third cerebral ventricle. Hypothalamic samples were removed. Then, RNA was extracted. In the next step, cDNA was synthesized. Finally, relative gene expression was assessed by a real-time polymerase chain reaction (PCR). The findings revealed a significant upregulation of nesfatin-1 mRNA in the stressed rat relative to the control group. The mRNA level of nesfatin-1 in the chrysin-treated group was significantly reduced compared to the stressed group. Furthermore, the stressed rats showed a significant decrease in mRNA levels of phoenixin in comparison to the control group. There was no significant increase in the mRNA level of phoenixin between the stressed group and the group receiving chrysin. In conclusion, downregulation of the hypothalamic nesfatin may be involved in mediating the anti-anxiety effects of chrysin.
