Effects of ginsenosides on Ca channels and membrane capacitance in rat adrenal chromaffin cells

We investigated the effects of ginseng total saponins (GTS) and five ginsenosides on voltage-dependent Ca²⁺ channels and membrane capacitance using rat adrenal chromaffin cells. In this study, cells were voltage-clamped in a whole-cell recording mode and a perforated patch-clamp technique was used. The inward Ca²⁺ currents (I_Ca) was elicited by depolarization and the change in cell membrane capacitance (ΔC_m) was monitored. The application of GTS (100 μg/ml) induced rapid and reversible inhibition of the Ca²⁺ current by 38.8 ± 3.6% (n = 16). To identify the particular single component that seems to be responsible for Ca²⁺ current inhibition, the effects of five ginsenosides (ginsenoside Rb₁, Rc, Re, Rf, and Rg₁) on the Ca²⁺ current were examined. The inhibitions to the Ca²⁺ current by Rb₁, Rc, Re, Rf, and Rg₁ were 15.3 ± 2.2% (n = 5); 36.9 ± 2.4% (n = 7); 28.1 ± 1.9% (n = 12); 19.0 ± 2.5% (n = 10); and 16.3 ± 1.6% (n = 15), respectively. The order of inhibitory potency (100 μM) was Rc > Re > Rf > Rg₁ > Rb₁. A software based phase detector technique was used to monitor membrane capacitance change (ΔC_m). The application of GTS (100 μg/ml) induced inhibitory effects on ΔC_m by 60.8 ± 9.7% (n = 10). The inhibitions of membrane capacitance by Rb₁, Rc, Re, Rf, and Rg₁ were 35.3 ± 5.5% (n = 7); 41.8 ± 7.0% (n = 8); 40.5 ± 5.9% (n = 9); 51.2 ± 7.6% (n = 9); and 35.9 ± 5.1% (n = 10), respectively. The inhibitory potencies of the ginsenosides on ΔC_m were Rf > Rc > Re > Rg₁ > Rb₁. Therefore, we found that GTS and ginsenosides exerted inhibitory effects on both Ca²⁺ currents and ΔC_m in rat adrenal chromaffin cells. These results suggest that ginseng saponins regulate catecholamine secretion from adrenal chromaffin cells and this regulation could be the cellular basis of antistress effects induced by ginseng.     

人参茎叶皂甙及其单体对大鼠脑内B型单胺氧化酶活性的影响

本文用体外法研究了人参茎叶皂甙(GSLS)及其单体Rg_1,Rg_2,Re和Rh_1大鼠脑内B型单胺氧化酶(MAO-B)活性的影响。结果表明,GSLS和Rh_1可加强MAO-B的活性。Rg_1和Rg_2可抑制MAO-B的活性,其抑制强度与3.3×10~(-5)mg/ml优降宁相当。抑制特征曲线表明Rg_1和Rg_2对MAO-B的抑制作用均属竞争性抑制。     

人参芦头脂溶性成分的研究

从人参（ＰａｎａｘＧｉｎｓｅｎｇＣ．Ａ．Ｍｅｙｅｒ）芦头的醚溶性成分中，用硅胶柱层析法，分得４种单体化合物。经ＩＲ，ＭＳ，ＮＭＲ，ＧＣ及化学降解等方法分别鉴定为二十九烷（１）、三棕榈酸甘油酯（２）、人参萜醇（３）及β－谷甾醇（４），其中化合物（１），（２），（３）为首次从人参芦头中分离得到的已知成分。     

人参果胶的结构研究

人参果胶是一酸性杂多糖混合物,经分离纯化获均一的S_A-1,它含半乳糖、半乳糖醛酸、阿拉伯糖、鼠李糖基摩尔比为3.7:1.7:1.8:1。S_A-1的结构分析用高碘酸氧化、Smith降解、甲基化等方法,在S_A-1中的羧基用Taylor与Conrad方法较原·来自S_A-1甲基化与乙酰化水解物的乙酰化衍生物用G.C.与G.C.—MS联用鉴定。结果表明S_A-1为多分支结构,分子主干由β(1-3)D-半乳糖基组成,部分半乳糖基C₆位有支链,尚有部分半乳糖基以(1-6)键连接。分子的支链由半乳糖醛酸基(1-4),鼠李糖基(1-3或1-2,4),阿拉伯糖基(1-5或1-3,5)组成。     

人参多糖降血糖和肝糖原作用的研究

给小鼠一次ⅳ人参多糖(GH_1)50、100mg/kg,可明显降低血糖和肝糖原含量,但对血总脂和蛋白质含量无明显影响。同时使大鼠肝组织氧消耗增加,并增强腺苷酸环化酶(AC)活性,使cAMP含量增加,提示GH_1降血糖作用可能是由于促进了糖的氧化利用,而降低肝糖原作用可能与其增加cAMP浓度有关。     

救脱一号注射液对家兔肠系膜上动脉夹闭型休克脑、肝、肾组织超微结构的影响

救脱一号注射液是由枳实、丹参、人参、麦冬制备而成的中医急救用药,中医临床研究表明,该注射液对感染性及失血性休克均有明显的疗效;对肠系膜上动脉夹闭型及晚期失代偿性失血性休克家兔的病理状态均有明显的改善作用。救脱一号注射液(1.0 g生药/kg iv.2.0 g生药/kg 50 ml生理盐水静脉点滴),能明显减轻肠系膜上动脉夹闭型休克家兔脑、肝、肾组织线粒体损伤,阻抑溶酶体的蜕变及肝糖元的耗竭。多巴胺(0.15 mg/kg 50 ml生理盐水静脉点滴)与救脱一号注射液效应大体一致,但未观察到多巴胺减轻休克家兔肾组织线粒体损伤的作用。     

~3H—人参皂甙单体Rg~1、Rb~1、Rb~2在小鼠体内分布的整体放射自显影研究

以~3H标记的人参皂甙单体R_(g1)、R_(b1)、R_(b2)为示踪剂分别在三只雄性昆明种小鼠中经灌胃或尾静脉注射给于500uci,2h后乙醚麻醉致死,进行整体切片自显影。结果表明,三种皂甙单体都有肝、肾、心、肺、脾、胃、肠、胆囊、膀胱分布;R_(g1)和R_(b1)还可通过血脑屏障进入脑组织,特别是R_(g1);R_(b1)在毛囊、肾上腺和眼内有明显分布;Rb_2在造血红骨髓(如脊柱)、毛囊、肾上腺中的分布有其特点,提示三种单体均有胆-肠和肾-膀胱排泄,Rb_1以后者为主。     

人参地鼠害综合防制技术

笔者对吉林省人参地害鼠的种类和数量及其对人参的危害进行了调查。结果表明,参地害鼠有鼢鼠、花鼠、大林姬鼠等8种,并进行了综合防制试验,即以提高参地卫生水平和布放毒饵为主要手段,防治效果在90%以上。     

人参总皂甙对犬肾自体移植再灌注损伤中氧自由基的清除作用

为了解人参总皂甙对肾移植再灌注损伤中氧自由基（ＯＦＲ）的清除作用，采用犬肾移植模型观察再灌注后２４小时肾组织中超氧化物歧化酶（ＳＯＤ）和丙二醛（ＭＤＡ）含量的变化及移植前后不同时期内生肌酐清除值。结果发现，在肾缺血和再灌注损伤过程中肾组织ＳＯＤ活性下降，ＭＤＡ含量异常增高。给人参总皂甙后能显著减少肾组织中ＭＤＡ含量，提高ＳＯＤ活性及内生肌酐清除值。结果提示，人参总皂甙能清除肾脏再灌注损伤产生的ＯＦＲ，保护内源性ＳＯＤ活性，减轻肾脂质过氧化损伤。     

生脉散口服液中人参皂甙的薄层扫描

生脉散由人参、麦冬、五味子三味中药组成。其口服液为单糖浆液。有关人参制剂中人参皂甙的含量测定方法有重量法、比色法、薄层层析-比色法、薄层扫描法等。本文采用柱层析法提取人参总皂甙,然后利用二次展开成功地将总皂甙与糖完全分离并用薄层扫描法测定其含量,方法简单可靠。