HPLC法测定香砂养胃丸（浓缩丸）中橙皮苷、厚朴酚及和厚朴酚含量

目的：建立香砂养胃丸中橙皮苷、厚朴酚及和厚朴酚的含量测定方法。方法：使用资生堂MGⅡC18（250mm×4．6mm,5μm）,乙腈-2％冰醋酸为流动相进行梯度洗脱,检测波长为294nm,流速1．0ml·min^-1,柱温35℃。结果：橙皮苷在0．15～4．15峙范围,厚朴酚在0．05～1．27μg范围和厚朴酚在0．02～0．67μg范围内进样量与色谱峰面积呈良好的线性关系（n=0．9999）,回收率分别为101．20％,103．29％,104．18％。结论：所建立的方法准确、简便、灵敏、可靠,可用于该制剂的质量控制。     

The mechanism of honokiol-induced and magnolol-induced inhibition on muscle contraction and Ca2+ mobilization in rat uterus

The effects of honokiol and magnolol extracted from the Magnolia officinalis on muscular contractile responses and intracellular Ca²⁺ mobilization were investigated in the non-pregnant rat uterus. Honokiol and magnolol (1–100 mol/l) were observed to inhibit spontaneous and uterotonic agonists (carbachol, PGF₂, and oxytocin)-, high K⁺-, and Ca²⁺ channel activator (Bay K 8644)-induced uterine contractions in a concentration-dependent manner. The inhibition rate of honokiol on spontaneous contractions appeared to be slower than that of magnolol-induced response. The time periods that were required for honokiol and magnolol, at 100 mol/l, to abolish 50% spontaneous contractions were approximately 6 min. Furthermore, honokiol and magnolol at 10 mol/l also blocked the Ca²⁺-dependent oscillatory contractions. Consistently, the increases in intracellular Ca²⁺ concentrations ([Ca²⁺]_i) induced by PGF₂ and high K⁺ were suppressed by both honokiol and magnolol at 10 mol/l. After washout of these treatments, the rise in [Ca²⁺]_i induced by PGF₂ and high K⁺ was still partially abolished. In conclusion, the inhibitory effects of honokiol and magnolol on uterine contraction may be mediated by blockade of external Ca²⁺ influx, leading to a decrease in [Ca²⁺]_i. Honokiol and magnolol may be considered as putative Ca²⁺ channel blockers and be of potential value in the treatment of gynecological dysfunctions associated with uterine muscular spasm and dysmenorrhea.     

厚朴酚对大鼠局灶性脑缺血再灌注损伤的保护作用与γ-氨基丁酸的关系

目的研究厚朴酚对大鼠局灶性脑缺血再灌注损伤的保护作用与γ-氨基丁酸(GABA)的关系。方法采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,用高效液相-荧光法测定大鼠脑组织谷氨酸(GLU)和GABA的含量。结果厚朴酚可以明显降低脑缺血再灌注后GLU含量,增加GABA的含量。结论厚朴酚对大鼠局灶性脑缺血再灌注损伤有明显的保护作用,该作用与其提高抑制性氨基酸GABA的含量,产生抑制性保护作用有关。     

HPLC法测定藿香正气口服液中橙皮苷、和厚朴酚、厚朴酚的含量

目的用HPLC法进行藿香正气口服液中几种有效成分的含量测定方法。方法采用DiamonsilTMC18柱（250×4.6mm,5μm）,以甲醇-水梯度洗脱,检测波长283nm,流速1mL.min-1,柱温25℃。结果橙皮苷、和厚朴酚、厚朴酚线性范围分别在0.1311～2.622μg、0.1728～3.4568μg、0.1751～3.5020μg。结论该测定方法简便可行,可用于藿香正气口服液中几种有效成分的含量测定。     

The effect of magnolol on Ca2+ homeostasis and its related physiology in human oral cancer cells

ObjectiveMagnolol, a polyphenol compound from herbal medicines, was shown to alter physiology in various cell models. However, the effect of magnolol on Ca²⁺ homeostasis and its related physiology in oral cancer cells is unclear. This study examined whether magnolol altered Ca²⁺ signaling and cell viability in OC2 human oral cancer cells.MethodsCytosolic Ca²⁺ concentrations ([Ca²⁺]_i) in suspended cells were measured by using the fluorescent Ca²⁺-sensitive dye fura-2. Cell viability was examined by 4-[3-[4-lodophenyl]-2-4(4-nitrophenyl)-2H-5-tetrazolio-1,3-benzene disulfonate] water soluble tetrazolium-1 (WST-1) assay.ResultsMagnolol at concentrations of 20–100 μM induced [Ca²⁺]_i rises. Ca²⁺ removal reduced the signal by approximately 50%. Magnolol (100 μM) induced Mn²⁺ influx suggesting of Ca²⁺ entry. Magnolol-induced Ca²⁺ entry was partially suppressed by protein kinase C (PKC) regulators, and inhibitors of store-operated Ca²⁺ channels. In Ca²⁺-free medium, treatment with the endoplasmic reticulum Ca²⁺ pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished magnolol-evoked [Ca²⁺]_i rises. Conversely, treatment with magnolol abolished BHQ-evoked [Ca²⁺]_i rises. Inhibition of phospholipase C (PLC) with U73122 partially inhibited magnolol-induced [Ca²⁺]_i rises. Magnolol at 20–100 μM decreased cell viability, which was not reversed by pretreatment with the Ca²⁺ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA/AM).ConclusionsTogether, in OC2 cells, magnolol induced [Ca²⁺]_i rises by evoking partially PLC-dependent Ca²⁺ release from the endoplasmic reticulum and Ca²⁺ entry via PKC-sensitive store-operated Ca²⁺ entry. Magnolol also caused Ca²⁺-independent cell death. Therefore, magnolol-induced cytotoxicity may not be involved in activation mechanisms associated with intracellular Ca²⁺ mobilization in oral cancer cells.     

RP-HPLC法测定香砂养胃软胶囊厚朴酚与和厚朴酚含量

目的:为控制香砂养胃软胶囊质量建立香砂养胃软胶囊含量测定方法.方法:RP-HPLC法测定样品厚朴酚、和厚朴酚含量,用Spherigel ODS C18(250 mm×4.6 mm,5μm)色谱柱分离厚朴酚与和厚朴酚,流动相:为乙腈-48 ml/L冰醋酸溶液(55∶45),检测波长:294 nm.结果:厚朴酚在0.120～0.960 μg范围内线性关系良好,r=0.999 9,平均回收率99.00%,RSD=1.06%(n=5);和厚朴酚在0.028～0.224 μg范围内线性关系良好,r=0.999 9,平均回收率98.56%,RSD=1.55%(n=5).结论:方法专属、灵敏、重现性好,为该制剂的质量控制提供有效的方法.     

蜂胶与厚朴酚混合物抑制变形链球菌生长的体外研究

目的 观察蜂胶与厚朴酚混合物对变形链球菌的生长抑制作用,以期为进一步开发利用复方中药防龋提供参考.方法 根据蜂胶、厚朴酚及二者混合液的最小抑菌浓度选择实验所需的质量浓度分别为:蜂胶250、125、62.5、31.25、15.625 g/L(蜂胶组),厚朴酚0.0625、0.0313、0.0156、0.0078、0.0039g/L(厚朴酚组),蜂胶与厚朴酚混合液A1(250 g/L蜂胶+0.0625 g/L厚朴酚)、A2(125g/L蜂胶+0.0313 g/L厚朴酚)、A3(62.5 g/L蜂胶+0.0156 g/L厚朴酚)、A4 (31.25 g/L蜂胶+0.0078 g/L厚朴酚)、A5(15.6 g/L蜂胶+0.0039 g/L厚朴酚)(混合组),另设0.95％乙醇组和菌液组作为对照,将蜂胶、厚朴酚及两者混合物分别倍比稀释至各浓度,采用纸片法观察各组对变形链球菌生长的影响.结果 蜂胶及厚朴酚组分别在质量浓度为62.5、0.0156 g/L时才出现明显的抑菌环,而混合组在蜂胶及厚朴酚最小质量浓度A5时即出现了明显的抑菌环;蜂胶组、厚朴酚组及混合组的抑菌作用均随质量浓度的增大而增强,3组分别在最小质量浓度时的抑菌环直径为(0.000±0.000)、(0.000±0.000)、(0.770±0.085) mm,在最大质量浓度时的抑菌环直径为(1.515±0.017)、(1.837±0.283)、(2.853±0.229) mm,且5种质量浓度下混合组的抑菌环直径均显著大于蜂胶组和厚朴酚组(P＜0.05).结论 蜂胶与厚朴酚混合物抑菌效果较二者单独作用时明显增强,提示复方中药防龋存在很大的开发潜力.