Background： Our previous studies have demonstrated that the levels of 5-hydroxytryptamine （5-HT） and 5-HT 2A receptor （5-HT2AR） in serum and platelet were associated with depression and myocardial infarction （MI...Background： Our previous studies have demonstrated that the levels of 5-hydroxytryptamine （5-HT） and 5-HT 2A receptor （5-HT2AR） in serum and platelet were associated with depression and myocardial infarction （MI）, and pretreatment with ginseng fruit saponins （GFS） before MI and depression had an effect on the 5-HT system. In this study, the effects of GFS on the 5-HT system in the Sprague-Dawley （SD） rats with MI, depression, and MI ＋ depression were evaluated. Methods： A total of eighty SD rats were allocated to four groups： MI, depression, MI ＋ depression, and control groups （n = 20 in each group）. Each group included two subgroups （n = 10 in each subgroup）： Saline treatment subgroup and GFS treatment subgroup. The levels of 5-HT, 5-HT2AR, and serotonin transporter （SERT） were quantified in serum, platelet lysate, and brain tissue through the enzyme-linked immunosorbent assay method, respectively. Results： Compared with those in the saline treatment subgroups, the levels of 5-HT in serum and platelet lysate statistically significantly increased in the GFS treatment subgroups of MI, depression, and MI ＋ depression groups （serum： all P = 0.000; platelet lysate： P = 0.002, 0.000, 0.000, respectively）. However, the 5-HT levels in brain homogenate significantly decreased in the GFS treatment subgroups compared with those in the saline treatment subgroups in MI and depression groups （P = 0.025 and 0.044 respectively）, and no significant difference was observed between saline and GFS treatment subgroups in MI ＋ depression group （P = 0.663）. Compared with that in GFS treatment subgroup of control group, the 5-HT2AR levels in the platelet lysate significantly decreased in GFS treatment subgroups of MI, depression, and MI ＋ depression groups （all P = 0.000）. Compared to those in the saline treatment subgroups, the serum SERT levels significantly decreased in the GFS treatment subgroups in MI, depression, and MI ＋ depression groups （P = 0.009, 0.038, and P = 0.001, respectively）, while the SERT levels of platelet lysate significantly decreased in GFS treatment subgroup of MI group （P = 0.000）, significantly increased in GFS treatment subgroup of depression group （P = 0.019）, and slightly changed in GFS treatment subgroup of MI ＋ depression group （P = 0.219）. No significant changes for SERT levels in brain homogenate could be found between the saline and GFS treatment subgroups in MI, depression, and MI ＋ depression groups （P = 0.421, 0.076 and P = 0.642）. Conclusions： This study indicated that GFS might inhibit the reuptake of 5-HT from serum to platelet according to decreased 5-HT2AR in platelet and SERT in serum and platelet. The change of 5-HT in serum after GFS treatment was inconsistent with that in the brain. It seemed that GFS could not pass through the blood-brain barrier to affect the central serotonergic system.展开更多
文摘Background： Our previous studies have demonstrated that the levels of 5-hydroxytryptamine （5-HT） and 5-HT 2A receptor （5-HT2AR） in serum and platelet were associated with depression and myocardial infarction （MI）, and pretreatment with ginseng fruit saponins （GFS） before MI and depression had an effect on the 5-HT system. In this study, the effects of GFS on the 5-HT system in the Sprague-Dawley （SD） rats with MI, depression, and MI ＋ depression were evaluated. Methods： A total of eighty SD rats were allocated to four groups： MI, depression, MI ＋ depression, and control groups （n = 20 in each group）. Each group included two subgroups （n = 10 in each subgroup）： Saline treatment subgroup and GFS treatment subgroup. The levels of 5-HT, 5-HT2AR, and serotonin transporter （SERT） were quantified in serum, platelet lysate, and brain tissue through the enzyme-linked immunosorbent assay method, respectively. Results： Compared with those in the saline treatment subgroups, the levels of 5-HT in serum and platelet lysate statistically significantly increased in the GFS treatment subgroups of MI, depression, and MI ＋ depression groups （serum： all P = 0.000; platelet lysate： P = 0.002, 0.000, 0.000, respectively）. However, the 5-HT levels in brain homogenate significantly decreased in the GFS treatment subgroups compared with those in the saline treatment subgroups in MI and depression groups （P = 0.025 and 0.044 respectively）, and no significant difference was observed between saline and GFS treatment subgroups in MI ＋ depression group （P = 0.663）. Compared with that in GFS treatment subgroup of control group, the 5-HT2AR levels in the platelet lysate significantly decreased in GFS treatment subgroups of MI, depression, and MI ＋ depression groups （all P = 0.000）. Compared to those in the saline treatment subgroups, the serum SERT levels significantly decreased in the GFS treatment subgroups in MI, depression, and MI ＋ depression groups （P = 0.009, 0.038, and P = 0.001, respectively）, while the SERT levels of platelet lysate significantly decreased in GFS treatment subgroup of MI group （P = 0.000）, significantly increased in GFS treatment subgroup of depression group （P = 0.019）, and slightly changed in GFS treatment subgroup of MI ＋ depression group （P = 0.219）. No significant changes for SERT levels in brain homogenate could be found between the saline and GFS treatment subgroups in MI, depression, and MI ＋ depression groups （P = 0.421, 0.076 and P = 0.642）. Conclusions： This study indicated that GFS might inhibit the reuptake of 5-HT from serum to platelet according to decreased 5-HT2AR in platelet and SERT in serum and platelet. The change of 5-HT in serum after GFS treatment was inconsistent with that in the brain. It seemed that GFS could not pass through the blood-brain barrier to affect the central serotonergic system.
