Subarnas A, Tadano T, Nakahata N, Arai Y, Kinemuchi H, Oshima Y, Kisara K, Ohizumi Y
Pharmaceutical Institute, Tohoku University, Sendai, Japan.
Life Sci. 1993;52(3):289-96. doi: 10.1016/0024-3205(93)90220-w.
A mechanism of antidepressant activity of beta-amyrin palmitate was studied using the forced swimming method in mice. Beta-amyrin palmitate (10 mg/kg) reduced the increase in the duration of immobility induced by tetrabenazine (100 and 200 mg/kg), but showed no effect on that in mice treated with alpha-methyl-para-tyrosine (500 mg/kg). Beta-amyrin palmitate (5 and 10 mg/kg) decreased the duration of immobility in mice treated with desipramine plus 6-hydroxy-dopamine (50 micrograms/mouse), but did not affect that induced by nomifensine plus 6-hydroxydopamine. The decreased immobility produced by desipramine (15 mg/kg) was not affected by beta-amyrin palmitate. A study of norepinephrine release in mouse brain synaptosomes indicated that beta-amyrin palmitate caused a release of [3H]norepinephrine. The results of the present study suggest that beta-amyrin palmitate might release norepinephrine from newly synthesized pools, and thus, it might activate noradrenergic activity.
采用小鼠强迫游泳法研究了棕榈酸β-香树脂醇的抗抑郁活性机制。棕榈酸β-香树脂醇（10毫克/千克）可减少丁苯那嗪（100和200毫克/千克）诱导的不动时间增加，但对用α-甲基对酪氨酸（500毫克/千克）处理的小鼠的不动时间无影响。棕榈酸β-香树脂醇（5和10毫克/千克）可缩短用去甲丙咪嗪加6-羟基多巴胺（50微克/只小鼠）处理的小鼠的不动时间，但不影响诺米芬辛加6-羟基多巴胺诱导的不动时间。去甲丙咪嗪（15毫克/千克）引起的不动时间减少不受棕榈酸β-香树脂醇的影响。对小鼠脑突触体中去甲肾上腺素释放的研究表明，棕榈酸β-香树脂醇可引起[3H]去甲肾上腺素的释放。本研究结果表明，棕榈酸β-香树脂醇可能从新合成的池中释放去甲肾上腺素，因此，它可能激活去甲肾上腺素能活性。
