目的:建立黄杨宁中环维黄杨星 D 含量测定和有关生物碱检查的 HPLC 方法。方法:以氨丙基硅烷键合硅胶为填充剂(Lichrospher-NH_2),乙腈-0.4%的磷酸氢二钾溶液(70:30)为流动相,在柱温、流速和检测波长分别为40℃、1 mL·min^(-1)和21...目的:建立黄杨宁中环维黄杨星 D 含量测定和有关生物碱检查的 HPLC 方法。方法:以氨丙基硅烷键合硅胶为填充剂(Lichrospher-NH_2),乙腈-0.4%的磷酸氢二钾溶液(70:30)为流动相,在柱温、流速和检测波长分别为40℃、1 mL·min^(-1)和210nm 的条件下,对黄杨宁进行直接 HPLC-UV 分析测定。结果:黄杨宁中环维黄杨星 D 与其有关生物碱 HPLC 分离良好,环维黄杨星 D 色谱峰面积与其浓度在0.020～1.00 mg·mL^(-1)范围,具有良好线性响应。结论:建立的氨丙基硅烷键合硅胶柱正相高效液相色谱法能准确、快速地测定黄杨宁中环维黄杨星 D 含量,同时适用于环维黄杨星 D 和黄杨宁制剂中有关生物碱的检查。展开更多
Objective： To investigate the underlying mechanisms of cyclovirobuxinum D（Cvb-D） on alleviating cardiac hypertrophy in rats. Methods： Sprague-Dawley rats were randomly divided into 5 groups： control group; levoth...Objective： To investigate the underlying mechanisms of cyclovirobuxinum D（Cvb-D） on alleviating cardiac hypertrophy in rats. Methods： Sprague-Dawley rats were randomly divided into 5 groups： control group; levothyroxine-induced cardiac hypertrophy group（model）; levothyroxine-induced cardiac hypertrophy ＋ Cvb-D group（Cvb-D）; levothyroxine-induced cardiac hypertrophy ＋ captopril group（captopril）; levothyroxine-induced cardiac hypertrophy ＋ SB203580 group（SB203580）, n=10 for each group. Rats were daily administered the respective drugs continuously for14 days by gastric gavage. A rat model of cardiac hypertrophy was established by intraperitoneal injection of levothyroxine to investigate whether Cvb-D protects against cardiac hypertrophy by inhibiting the p38 mitogen-activated protein kinase（MAPK） signaling pathway and preventing apoptosis of cardiac cells. Results： Treatment with Cvb-D significantly deceased left ventricle hypertrophy, improved the histopathology, hemodynamic conditions, and cardiac function in rats with cardiac hypertrophy. Compared with the normal control group, in rats with cardiac hypertrophy, expression of bax in the heart and phospho-p38 MAPK protein levels were significantly up-regulated（P〈0.01 or 0.05）, whereas the bcl-2 protein level was downregulated（P〈0.01）. In contrast, Cvb-D treatment reversed the changes in bax and phospho-p38 MAPK protein levels but increased the bcl-2 protein level（P〈0.01 or 0.05）, and these effects were similar to those of captopril and SB203580（a specific p38 MAPK inhibitor） treatment. Furthermore, both Cvb-D, captopril and SB203580 reduced m RNA expression of p38α, p38β, c-fos, and c-jun m RNA, and Cvb-D had a stronger effect（P〈0.01）. Conclusion： These results demonstrate that Cvb-D protects against cardiac hypertrophy, which is possibly mediated by prevention of cardiac cell apoptosis and inhibition of the p38 MAPK signaling pathway.展开更多
文摘目的:建立黄杨宁中环维黄杨星 D 含量测定和有关生物碱检查的 HPLC 方法。方法:以氨丙基硅烷键合硅胶为填充剂(Lichrospher-NH_2),乙腈-0.4%的磷酸氢二钾溶液(70:30)为流动相,在柱温、流速和检测波长分别为40℃、1 mL·min^(-1)和210nm 的条件下,对黄杨宁进行直接 HPLC-UV 分析测定。结果:黄杨宁中环维黄杨星 D 与其有关生物碱 HPLC 分离良好,环维黄杨星 D 色谱峰面积与其浓度在0.020～1.00 mg·mL^(-1)范围,具有良好线性响应。结论:建立的氨丙基硅烷键合硅胶柱正相高效液相色谱法能准确、快速地测定黄杨宁中环维黄杨星 D 含量,同时适用于环维黄杨星 D 和黄杨宁制剂中有关生物碱的检查。
基金Supported by the State Administration of Traditional Chinese Medicine of Guangdong Province,China(No.2009231)
文摘Objective： To investigate the underlying mechanisms of cyclovirobuxinum D（Cvb-D） on alleviating cardiac hypertrophy in rats. Methods： Sprague-Dawley rats were randomly divided into 5 groups： control group; levothyroxine-induced cardiac hypertrophy group（model）; levothyroxine-induced cardiac hypertrophy ＋ Cvb-D group（Cvb-D）; levothyroxine-induced cardiac hypertrophy ＋ captopril group（captopril）; levothyroxine-induced cardiac hypertrophy ＋ SB203580 group（SB203580）, n=10 for each group. Rats were daily administered the respective drugs continuously for14 days by gastric gavage. A rat model of cardiac hypertrophy was established by intraperitoneal injection of levothyroxine to investigate whether Cvb-D protects against cardiac hypertrophy by inhibiting the p38 mitogen-activated protein kinase（MAPK） signaling pathway and preventing apoptosis of cardiac cells. Results： Treatment with Cvb-D significantly deceased left ventricle hypertrophy, improved the histopathology, hemodynamic conditions, and cardiac function in rats with cardiac hypertrophy. Compared with the normal control group, in rats with cardiac hypertrophy, expression of bax in the heart and phospho-p38 MAPK protein levels were significantly up-regulated（P〈0.01 or 0.05）, whereas the bcl-2 protein level was downregulated（P〈0.01）. In contrast, Cvb-D treatment reversed the changes in bax and phospho-p38 MAPK protein levels but increased the bcl-2 protein level（P〈0.01 or 0.05）, and these effects were similar to those of captopril and SB203580（a specific p38 MAPK inhibitor） treatment. Furthermore, both Cvb-D, captopril and SB203580 reduced m RNA expression of p38α, p38β, c-fos, and c-jun m RNA, and Cvb-D had a stronger effect（P〈0.01）. Conclusion： These results demonstrate that Cvb-D protects against cardiac hypertrophy, which is possibly mediated by prevention of cardiac cell apoptosis and inhibition of the p38 MAPK signaling pathway.
