Objective To observe the effects of cyclovirobuxinum D(Cvb-D)on the myocardium cell apoptosis of myocardial ischemia rats.Methods The rats were given Cvb-D 0.55,1.1 and 2.2 mg/kg orally per day for 21 days respectively.The myocardial ischemia model was induced by isoprenaline intraperitoneal injection.Myocardium tissue was observed under light microscope and end labelling TUNEL method was used to determine the cell apoptosis.Then the average percentage of apoptosis cell was figured out to evaluate the effect of Cyb-D.Results Cvb-D obviously lightened isoprenaline-induced myocardial pathological changes such as turbulence of myocardial fiber,plasmolysis of necrotic cell,inflammatory cell infiltration of necrotic interstitial region.Cvb-D remarkably inhibited myocardium cell apoptosis of myocardial ischemia rats caused by isoprenaline.Conclusion Cvb-D has the action of ameliorating myocardium cell apoptosis caused by myocardial ischemia.

Objective To observe the effects of color retention treatment on the preservation of medicinal plant herbariums, film-cover specimens and resin specimens. Methods Seven kinds of medicinal plants with different characters after color retention treatment were made into herbariums, film-cover specimens and resin specimens, and then the preservation results for the above three kinds of medicinal plant specimens with or without color retention treatment were compared. Results Resin and film-cover specimens without color retention treatment had better preservation results than herbariums. All of the three kinds of specimens with color retention treatment had better preservation results for the original color and shape than the specimens without color retention treatment. Conclusion Color retention treatment for the medicinal plants results into higher preservation quality of the herbariums and longer preservation period.

AIM　To investigate the relationship between sinomenine distribution and its organic toxicology in rats so as to give some pharmacological data for clinical application of sinomenine. METHODS　Three kinds of administration plans were designed in the experiment, ie sinomenine was ip administered at the dosage of l50 mg*kg-1 per day, repreat-dosed for 6 wk and suspended the drug for 1 wk after 6wk repeat-doses．At the end of the each administration plan，the animals were sacrificed and their blood and their main internal organs were collected for the purpose of measurement of sinomenine concentration in each sample by HPLC. Meanwhile，the histopathological and serological examinations were also done in the experiments. RESULTS　The sinomenine concentration in rats internal organs were in order of liver, heart, lung and brain either in single-dosed treated animals or in repeat-dosed treated animals for 6 wk. However，the concentration of sinomenine could not be detected by HPLC after l wk drug-suspension，the histopathological examination showed that sinomenine at the dosage of l50 mg*kg-l per day for 6wk treatment could slightly damage liver ce11s, dominant1y caused the cell edema，but no any influence on the sero1ogy of liver and kidney. Sinomenine ip could also cause a mild hyperaemia of the rats heart tissues but no any histopathological changes had been observed. In testis tissues no sinomenine had beed detected although the animals were treated by repeat treatment for 6 wk and no any histopathological changes had been found yet. However, Sinomenine could partialy inhibit the sperm vitalities and amount of the dead sperms were a1so augmented. It was similar to in vitro eperiments. These influences of sinomenine on testis could be quickly recovered by drug suspension. CONCLUSION　Sinomenine concentration were in order of liver, heart, kidney, lung and brain either in treatment by single dose or by repeat-dose administration. The histopathological changes were only abserved in liver cells of the animals which indicates that it should be in consideration of the liver functions during treatment course of the drug.

AIM To investigate the relationship between sinomenine distribution and its organic toxicology in rats so as to give some pharmacological data for clinical application of sinomenine. METHODS Three kinds of administration plans were designed in the experiment, ie sinomenine was ip administered at the dosage of l50 mg?kg -1 per day, repreat dosed for 6 wk and suspended the drug for 1 wk after 6wk repeat doses.At the end of the each administration plan,the animals were sacrificed and their blood and their main internal organs were collected for the purpose of measurement of sinomenine concentration in each sample by HPLC. Meanwhile,the histopathological and serological examinations were also done in the experiments. RESULTS The sinomenine concentration in rats internal organs were in order of liver, heart, lung and brain either in single dosed treated animals or in repeat dosed treated animals for 6 wk. However,the concentration of sinomenine could not be detected by HPLC after l wk drug suspension,the histopathological examination showed that sinomenine at the dosage of l50 mg?kg -l per day for 6wk treatment could slightly damage liver ce11s, dominant1y caused the cell edema,but no any influence on the sero1ogy of liver and kidney. Sinomenine ip could also cause a mild hyperaemia of the rats heart tissues but no any histopathological changes had been observed. In testis tissues no sinomenine had beed detected although the animals were treated by repeat treatment for 6 wk and no any histopathological changes had been found yet. However, Sinomenine could partialy inhibit the sperm vitalities and amount of the dead sperms were a1so augmented. It was similar to in vitro eperiments. These influences of sinomenine on testis could be quickly recovered by drug suspension. CONCLUSION Sinomenine concentration were in order of liver, heart, kidney, lung and brain either in treatment by single dose or by repeat dose administration. The histopathological changes were only abserved in liver cells of the animals which indicates that it should be in consideration of the liver functions during treatment course of the drug.