蒙药材地梢瓜的质量标准研究

目的修订并完善蒙药材地梢瓜的质量标准,着重建立地梢瓜对照药材的薄层色谱鉴别方法。方法依据中国药典2010年版一部附录药品标准研究方法对10批蒙药材地梢瓜进行显微、理化和薄层色谱鉴别;对水分、总灰分、酸不溶性灰分和浸出物含量进行检查。结果修订了蒙药材地梢瓜原质量标准中的显微和理化鉴别,并建立了其对照药材的薄层色谱鉴别方法;水分、总灰分、酸不溶性灰分检查分别≤7.13%、5.42%、0.71%,浸出物≥19.25%。结论修订和完善了蒙药材地梢瓜的质量标准,并为其对照药材及薄层色谱鉴别方法的设立提供了依据。     

荔枝草的质量标准建立与探讨

目的 完善中药材荔枝草的质量标准。方法 采用显微鉴别、薄层鉴别、水分、总灰分、浸出物、含量测定等项目对荔枝草的质量进行考察。结果 荔枝草显微鉴别特征明显;薄层鉴别斑点清晰,易于识别;质量标准为：水分≤12.0%,总灰分≤10.0%,醇溶性浸出物≥20.0%;含量测定原儿茶酸在1.068~106.8 μg·mL^-1内呈良好的线性关系(r=0.999 7),其含量≥70 μg·g^-1。结论 荔枝草药材的显微鉴别、薄层鉴别、水分、总灰分、浸出物、含量测定研究可为该药材质量标准的修订、提高提供参考依据。     

苍耳草的生药学鉴别及浸出物的测定

目的 提高苍耳草药材的质量控制标准.方法采用生药学常规方法进行性状鉴别、显微鉴别,建立薄层色谱鉴别方法;按《中国药典》一部附录方法,检查水分、总灰分、酸不溶性灰分、测定浸出物的含量.结果找到了苍耳草药材性状和显微鉴别特征;薄层色谱鉴别专属性强,重复性好;暂定苍耳草水分不得过14%,总灰分不得过17%,酸不溶性灰分不得超...     

川产兔耳风质量标准初步研究

目的:建立川产兔耳风药材质量标准.方法:通过组织学研究建立兔耳风药材显微鉴别方法;测定其水分、总灰分、酸不溶性灰分以及浸出物含量并建立薄层色谱鉴别方法.结果:川产兔耳风显微鉴别特征性较强,易于鉴别.水分不得过9.68%,总灰分不得过21.75%,酸不溶性灰分不得过14.23%,浸出物不得少于6.31%.薄层色谱鉴定专属性强,重现性较好.结论:所建立的方法能初步评价川产兔耳风的质量.     

彝药水指甲药材的质量标准研究

目的:建立彝药水指甲药材的质量标准。方法:分别对水指甲药材进行性状鉴别和粉末显微鉴别,再以β-谷甾醇为对照品进行薄层色谱(TLC)鉴别;采用《中国药典》方法测定不同产地水指甲药材的水分、总灰分、酸不溶性灰分、醇溶性浸出物并制定其限度。结果:样品性状和显微鉴别特征明显,TLC特征斑点清晰,水分、总灰分、酸不溶性灰分、醇溶性浸出物的平均百分含量分别为9.5%、12.9%、2.6%、22.5%。结论:所建标准可用于水指甲药材的质量控制。     

山枝仁质量标准初步研究

目的:建立山枝仁的质量标准.方法:按照相关文献资料进行了药材性状、显微、薄层鉴别方法研究,测定了10批山枝仁药材的水分、灰分、酸不溶性灰分、浸出物含量.结果:对山枝仁药材的性状和粉末显微特征进行了描述,建立了其薄层鉴别方法.初步拟定了山枝仁药材常规检查项下的限量标准:水分不得过14.0%,总灰分不得过5.0%、酸不溶性灰分不得过1.0%,50%乙醇浸出物不得少于16.0%.结论:初步建立了山枝仁药材的质量标准规范,为山枝仁的临床安全合理用药提供科学依据.     

瑶药小马胎药材质量标准初探

目的 建立瑶药小马胎的质量标准。方法 采用显微观察、薄层色谱法对产自广西不同地区的瑶药小马胎进行性状鉴别,按2020年版《中国药典（四部）》通则测定瑶药小马胎浸出物、总灰分、酸不溶性灰分和水分。结果 与对照药材比较,瑶药小马胎的形态特征,根茎、茎横切面及粉末显微特征无显著差异,甲醇提取物薄层色谱主要特征斑点无显著差异。瑶药小马胎的总灰分为5.16%～13.19%,酸不溶性灰分为0.83%～5.73%,70%乙醇浸出物为11.74%～19.18%,水分为7.91%～13.32%。结论 所建立的瑶药小马胎质量标准可行,拟订其总灰分不得过14.0%,酸不溶性灰分不得过6.0%,70%乙醇浸出物不得少于11.0%,水分不得过14.0%。     

维药材欧绵马的质量标准研究

目的研究新疆产维药材欧绵马的质量标准,为该植物资源的开发利用提供科学依据。方法采用性状鉴别、显微鉴别、薄层色谱法、紫外可见分光光度法对新疆不同产地的10批欧绵马药材进行研究,对其水分、总灰分、酸不溶灰分、浸出物和总间苯三酚的含量进行测定。结果对新疆产欧绵马药材的性状、显微特征进行了描述,建立了TLC定性鉴别方法,制订了维药材欧绵马的质量标准:水分、灰分、酸不溶灰分分别不得超过12.0%,15.0%和6.0%;醇溶性浸出物、总间苯三酚含量分别不少于20.0%和5.0%。结论建立的方法简便、快速、重复性好,适用于欧绵马药材的质量控制。     

畲药十二时辰的质量标准研究

目的 建立畲药十二时辰的质量标准,为其质量控制和开发提供参考。方法 对十二时辰进行性状、显微特征、薄层色谱鉴别;参照《中华人民共和国药典》2020年版相关规定,对十二时辰水分、灰分、浸出物进行测定;以齐墩果酸为对照物质,采用高效液相色谱法对其含量进行检测。结果 十二时辰药材在性状、显微和TLC鉴别方面均有专属性特征;6批不同采收期的十二时辰水分平均值为11.79%,总灰分平均值为3.16%,酸不溶性灰分平均值为0.34%,热浸法水溶性浸出物含量为31.46%;含量测定齐墩果酸平均质量分数为1.72%。结论 该研究结果可为畲药十二时辰的质量标准的制定提供依据,暂定本品水分不得超过14.0%,总灰分不得超过4.00%,酸不溶性灰分不得超过0.40%,浸出物含量不得低于25.00%。     

蜀漆质量标准研究

目的:开展蜀漆药材质量标准的研究,确保用药的安全有效.方法:采用中国药典附录的方法对蜀漆药材的性状、显微、鉴别、浸出物含量及杂质限度进行研究.结果:确定了蜀漆药材性状、显微特征;建立了薄层色谱法鉴别的方法;根据测定结果拟定蜀漆药材浸出物不得少于7.0%、水分不得过12.0%、总灰分不得过13.0%、酸不溶性灰分不得过1.0%.结论:完善了蜀漆药材质量控制方法并建立该药材质量标准.     

Trichloroethylene. I. Carcinogenicity of trichloroethylene.

Trichloroethylene (TCE) as an industrial pollutant may damage human health and can be considered as carcinogen. TCE has been detected in the environment and in various human organs, e.g., liver, kidney and brain etc. There are histological alterations such as depletion of glycogen and hydropic degeneration in the liver, however, other signs of TCE effects can be found in various organs as well. TCE and its metabolites, e.g., trichlorethanol, trichloro-acetic acid and epoxides were recently identified as strong mutagens in Ames mutagenicity test inducing frameshift and base-substitution mutations. TCE induced predominantly hepatocellular carcinoma after long term administration in mice. In these animals, kidneys and liver were supposed to be primary target organs with low epoxy-hydrolase activity. A high level of mitotic gene conversion (or gene rearrangement) was indicated by the metabolism of TCE after repeated administration. Purified TCE by was a weak mutagen in the presence of S9 microsomal fraction of rats and as a consequence, the carcinogenic activity was low in the kidney of rats. However, a dose related increase of Leydig cell tumors was found in male rats.     

Trichloroethylene. II. Mechanism of carcinogenicity of trichloroethylene.

The cancer inducing effect of trichloroethylene (TCE) was studied by various methods. DNA complexing activity and apoptosis inhibition were found to be the key elements of the carcinogenicity of TCE and its metabolites. The ability of TCE to interact with DNA was low, but its incorporation into the RNA and DNA of the brain, testis, pancreas, kidney, liver, lung and spleen, cannot be excluded. Exposure to TCE and its metabolites provides a selective growth advantage to spontaneously occurring mutations in some K- and H-ras oncogenes (as non specific results of secondary DNA or RNA damage). The amount of DNA-TCE adducts was higher in mouse hepatocytes than in rat hepatocytes. These differences may explain the species difference in carcinogenicity of TCE, which was dose dependent (due to metabolism) in mice but independent in rats. The blood level kinetics of TCE confirmed the faster metabolic rate in mice, including peroxisome proliferation and induction in hepatocytes. Dichloroacetic- and trichloroacetic acid were found to be hepatic carcinogens in mice, and the specificity depends on peroxisome proliferation induction. Possibly, TCE and related compounds down regulated apoptosis in mouse liver, and the reduced ability to remove initiated cells by apoptosis could be responsible for liver cancer induction by TCE.     

Studies in antifertility agents. 11. Secosteroids. 5. Synthesis of 9,11-secoestradiol.

9,11-Secoestradiol (9) and 11-hydroxy-9,11-secoestradiol (12) have been synthesized starting from 17-acetoxyestradiol 3-methyl ether (1) and found to possess significant antifertility activity in rats. 3-Methoxy-9,11-seco-9-oxo-17beta-acetoxyestra-1,3,5(10)-trien-11-oic acid (2), prepared by CrO3 oxidation of 1, on hydrogenolysis gave methyl 17beta-hydroxy-3-methoxy-9,11-secoestra-1,3,5(10)-triene-11-carboxylate (3). The 17-O-THP derivative of 3 was treated with LiAlH4 to give 17beta-(O-tetrahydropyranyl)-3-methoxy-11-hydroxy-9,11-secoestra-1,3,5(10)-triene (5). The 11-O-mesylate of 5 on LiAlH4 reduction followed by mild acid treatment and demethylation under alkaline conditions gave 9. LiAlH4 reduction of 3 gave 9,11-seco-11-hydroxyestradiol 3-methyl ether (11) which on demethylation gave 9,11-seco-11-hydroxyestradiol (12).     

Metabolism of benzothiazole. I. Identification of ring-cleavage products.

1. The metabolic fate of benzothiazole in guinea pig has been investigated following i.p. administration at a dose of 30 mg/kg. 2. Five ring-cleavage products were identified in urinary extracts by g.l.c.-mass spectra. By reference to authentic compounds the three major metabolites were shown to be 2-methylmercaptoaniline (I), 2-methylsulphinylaniline (II) and 2-methylsulphonylaniline (III). On the basis of the mass spectrometric evidence the remaining two metabolites were postulated to be 2-methylsulphinylphenylhydroxylamine (IV) and 2-methylsulphonylphenylhydroxylamine (V). 3. I, II and III were present in conjugated and unconjugated forms; IV and V were identified only after hydrolysis with sulphatase.