Tee Bae Huey, Hoe See Ziau, Cheah Swee Hung, Lam Sau Kuen
Department of Physiology, Faculty of Medicine, University of Malaya, Kuala Lumpur, Malaysia.
Med Princ Pract. 2017;26(3):258-265. doi: 10.1159/000464363. Epub 2017 Feb 22.
This study was conducted to investigate the mechanisms of action of Eurycoma longifolia in rat corpus cavernosum.
Tincture of the roots was concentrated to dryness by evaporating the ethanol in vacuo. This ethanolic extract was partitioned into 5 fractions sequentially with hexane, dichloromethane (DCM), ethyl acetate, butanol, and water. The corpus cavernosum relaxant activity of each fraction was investigated. The DCM fraction which showed the highest potency in relaxing phenylephrine-precontracted corpora cavernosa was purified by column chromatography. The effects of the most potent DCM subfraction in relaxing phenylephrine-precontracted corpora cavernosa, DCM-I, on angiotensin I- or angiotensin II-induced contractions in corpora cavernosa were investigated. The effects of DCM-I pretreatment on the responses of phenylephrine-precontracted corpora cavernosa to angiotensin II or bradykinin were also studied. An in vitro assay was conducted to evaluate the effect of DCM-I on angiotensin-converting enzyme activity.
Fraction DCM-I decreased the maximal contractions (100%) evoked by angiotensin I and angiotensin II to 30 ± 14% and 26 ± 16% (p < 0.001), respectively. In phenylephrine-precontracted corpora cavernosa, DCM-I pretreatment caused angiotensin II to induce 82 ± 27% relaxation of maximal contraction (p < 0.01) and enhanced (p < 0.001) bradykinin-induced relaxations from 47 ± 8% to 100 ± 5%. In vitro, DCM-I was able to reduce (p < 0.001) the maximal angiotensin-converting enzyme activity to 78 ± 0.24%.
Fraction DCM-I was able to antagonize angiotensin II-induced contraction to cause corpus cavernosum relaxation via inhibition of angiotensin II type 1 receptor and enhance bradykinin-induced relaxation through inhibition of angiotensin-converting enzyme.
本研究旨在探讨长叶淫羊藿对大鼠海绵体的作用机制。
通过真空蒸发乙醇将根酊浓缩至干。将该乙醇提取物依次用己烷、二氯甲烷（DCM）、乙酸乙酯、丁醇和水分为5个部分。研究了每个部分的海绵体舒张活性。通过柱色谱法纯化在舒张去氧肾上腺素预收缩海绵体方面显示出最高效力的DCM部分。研究了在舒张去氧肾上腺素预收缩海绵体方面最有效的DCM亚组分DCM-I对海绵体中血管紧张素I或血管紧张素II诱导的收缩的影响。还研究了DCM-I预处理对去氧肾上腺素预收缩海绵体对血管紧张素II或缓激肽反应的影响。进行体外试验以评估DCM-I对血管紧张素转换酶活性的影响。
DCM-I部分分别将血管紧张素I和血管紧张素II引起的最大收缩（100%）降低至30±14%和26±16%（p<0.001）。在去氧肾上腺素预收缩的海绵体中，DCM-I预处理使血管紧张素II诱导的最大收缩舒张82±27%（p<0.0），并将缓激肽诱导的舒张从47±8%增强至100±5%（p<0.001）。在体外DCM-I能够将最大血管紧张素转换酶活性降低至78±0.24%（p<0.001）。
DCM-I部分能够通过抑制1型血管紧张素II受体拮抗血管紧张素II诱导的收缩，从而使海绵体舒张，并通过抑制血管紧张素转换酶增强缓激肽诱导的舒张。
