Sakumoto Hitoshi, Yokota Yumiko, Ishibashi Gakushi, Maeda Shouta, Hoshi Chihiro, Takano Haruyo, Kobayashi Miki, Yahagi Tadahiro, Ijiri Soichiro, Sakakibara Iwao, Hara Akiyoshi
Department of Pharmaceutical Science, International University of Health and Welfare, 2600-1, Kitakanemaru, Ohtawara, Tochigi, 324-8501, Japan.
J Nat Med. 2015 Jul;69(3):441-8. doi: 10.1007/s11418-015-0907-7. Epub 2015 Apr 4.
The effects of the water extract of Sinomeni Caulis et Rhizoma (SCR-WE) and its major constituents, sinomenine (SIN) and magnoflorine (MAG), on moderate hemolysis induced by lysophosphatidylcholine (LPC) were investigated in rat erythrocytes and compared with the anti-hemolytic effects of lidocaine (LID) and propranolol (PRO) as reference drugs. LPC caused hemolysis at concentrations above the critical micelle concentration (CMC), and the concentration of LPC producing moderate hemolysis (60 %) was approximately 10 μM. SCR-WE at 1 ng/mL-100 μg/mL significantly inhibited the hemolysis induced by LPC. SIN and MAG attenuated LPC-induced hemolysis in a concentration-dependent manner from very low to high concentrations (1 nM-100 μM and 10 nM-100 μM, respectively). In contrast, the inhibiting effects of LID and PRO on LPC-induced hemolysis were observed at higher concentrations (1-100 μM) but not at lower concentrations (1-100 nM). Neither SIN nor MAG affected micelle formation of LPC, nor, at concentrations of 1 nM-1 μM, did they attenuate the hemolysis induced by osmotic imbalance (hypotonic hemolysis). Similarly, SCR-WE also did not modify micelle formation or hypotonic hemolysis, except at the highest concentration. These results suggest that SIN and MAG potently protect the erythrocyte membrane from LPC-induced damage and contribute to the beneficial action of SCR-WE. The protective effects of SIN and MAG are mediated by some mechanism other than prevention of micelle formation or protection of the erythrocyte membrane against osmotic imbalance.
研究了青风藤水提取物（SCR-WE）及其主要成分青藤碱（SIN）和木兰碱（MAG）对大鼠红细胞中溶血磷脂酰胆碱（LPC）诱导的中度溶血的影响，并与作为参考药物的利多卡因（LID）和普萘洛尔（PRO）的抗溶血作用进行了比较。LPC在高于临界胶束浓度（CMC）的浓度下引起溶血，产生中度溶血（60%）的LPC浓度约为10μM。1 ng/mL至100μg/mL的SCR-WE显著抑制LPC诱导的溶血。SIN和MAG以浓度依赖性方式从非常低到高浓度（分别为1 nM至100μM和10 nM至100μM）减弱LPC诱导的溶血。相比之下，LID和PRO对LPC诱导的溶血的抑制作用在较高浓度（1至100μM）下观察到，但在较低浓度（1至100 nM）下未观察到。SIN和MAG均不影响LPC的胶束形成，在1 nM至1μM的浓度下，它们也不减弱渗透失衡诱导的溶血（低渗溶血）。同样，SCR-WE除了在最高浓度外，也不改变胶束形成或低渗溶血。这些结果表明，SIN和MAG有效地保护红细胞膜免受LPC诱导的损伤，并有助于SCR-WE的有益作用。SIN和MAG的保护作用是通过防止胶束形成或保护红细胞膜免受渗透失衡以外的某种机制介导的。
