Kim H J, Woo D S, Lee G, Kim J J
Department of Urology, Dankook University College of Medicine, Cheonan, Chungnam, Korea.
Br J Urol. 1998 Nov;82(5):744-8. doi: 10.1046/j.1464-410x.1998.00811.x.
To determine whether crude extracts of ginseng saponin (GCS), containing the active ingredients from Panax ginseng and used as an aphrodisiac in oriental countries, relax corpus cavernosal smooth muscle in the rabbit.
Corpus cavernosal strips were prepared from rabbit penises. Isometric tension changes, recorded with a pressure transducer, in response to various drugs and electrical stimulation were assessed in an organ chamber, after active muscle tone had been induced by 10 micromol/L phenylephrine.
GCS (0.2-8.0 mg) relaxed the smooth muscle of rabbit corpus cavernosum (SMRCC) pre-contracted with phenylephrine in a dose-dependent manner. GCS at 0.75 mg significantly enhanced the relaxation of SMRCC induced by electrical field stimulation. The relaxation induced by 0.2-8.0 mg GCS was significantly attenuated by atropine (1 micromol/L), methylene blue (100 micromol/L) and N-omega-nitro-L-arginine methyl ester (L-NAME, 10 micromol/L). However, there was no significant difference in the attenuation of GCS-induced relaxation of SMRCC by adding vasoactive intestinal peptide antagonists or indomethacin. In addition, the decreasing rate of GCS-induced relaxation of SMRCC by methylene blue and L-NAME was greater than that by atropine. L-arginine (10 mmol/L) reversed the inhibitory effect induced by L-NAME (1 mmol/L) on the attenuation of GCS-induced relaxation.
These data suggest that GCS, as a nitric oxide donor, induces the relaxation of SMRCC through the L-arginine/nitric oxide pathway. For the clinical application of ginseng saponin, further studies are required to clarify the active subfraction(s) of GCS.
确定人参皂苷粗提物（GCS），其含有来自人参的活性成分且在东方国家用作壮阳药，是否能使兔海绵体平滑肌松弛。
从兔阴茎制备海绵体条。在由10微摩尔/升去氧肾上腺素诱导产生主动肌张力后，在器官浴槽中用压力换能器记录等长张力变化，以评估对各种药物和电刺激的反应。
GCS（0.2 - 8.0毫克）以剂量依赖方式使预先用去氧肾上腺素收缩的兔海绵体平滑肌（SMRCC）松弛。0.75毫克的GCS显著增强电场刺激诱导的SMRCC松弛。0.2 - 8.0毫克GCS诱导的松弛被阿托品（1微摩尔/升）、亚甲蓝（100微摩尔/升）和N-ω-硝基-L-精氨酸甲酯（L-NAME，10微摩尔/升）显著减弱。然而，添加血管活性肠肽拮抗剂或吲哚美辛对GCS诱导的SMRCC松弛减弱作用无显著差异。此外，亚甲蓝和L-NAME对GCS诱导的SMRCC松弛减弱作用的降低率大于阿托品。L-精氨酸（10毫摩尔/升）逆转了L-NAME（1毫摩尔/升）对GCS诱导松弛减弱的抑制作用。
这些数据表明，GCS作为一氧化氮供体，通过L-精氨酸/一氧化氮途径诱导SMRCC松弛。对于人参皂苷的临床应用，需要进一步研究以阐明GCS的活性亚组分。
