苦楝皮的化学成分

目的对中药苦楝皮(Melia azedarachL.Sied.)体积分数为95%的乙醇提取物的乙酸乙酯部位化学成分进行研究。方法采用硅胶柱色谱、Sephadex LH-20柱色谱等方法进行分离,利用理化性质和1H-NMR1、3C-NMR等谱学技术,对分离得到的化合物进行结构鉴定。结果从中分离得到6个化合物,其结构鉴定为羽扇豆醇(lupeol,1)、α-菠甾酮(-αspinasterone,2)、丁香树脂酚双葡萄糖苷(syringaresinol-di-O--βD-glucoside,3)、阿魏酸(ferulic acid,4)、β-谷甾醇(-βsitosterol,5)、胡萝卜苷(daucosterol,6)。结论化合物2、3和4均为首次从楝属植物中分离得到的已知化合物。     

苗药水黄花化学成分的分离与鉴定(Ⅱ)

目的研究水黄花(Euphorbia chrysocomaLévi.et Vant.)地上部分的化学成分。方法运用硅胶柱色谱、RP-18柱色谱、Sephadex LH-20、制备薄层色谱等多种色谱手段和方法分离纯化化合物,采用核磁共振、质谱等现代波谱技术和理化性质鉴定化合物的结构。结果从水黄花地上部分体积分数75%乙醇提取物的乙酸乙酯萃取部位中分离得到6个化合物,分别为没食子酸甲酯(methylgallate,1)、5-羟甲基糠醛(5-hydroxymethyl furaldehyde,2)、大黄酚(chrysophanol,3)、大黄素甲醚(physcion,4)、东莨菪内酯(scopoletin,5)和七叶内酯(aesculetin,6)。结论化合物1~6均为首次从水黄花中分离得到。     

野独活茎化学成分的分离与鉴定

目的更好地开发利用野独活(Miliusa balansae Fin. et Gag.)药用植物资源。方法用质量分数为80%的乙醇提取,用硅胶柱色谱、羟丙基葡聚糖凝胶LH-20柱色谱分离纯化;通过NMR谱和薄层色谱等鉴定化合物的结构。结果分离鉴定了10个化合物,分别为尿囊素(allantion,1)、(+)-衡州乌药碱(coclaurine,2)、1-N-甲基乌药碱(1-N-methylcoclaurine,3)、鹅掌揪碱(liriodenine,4)、腺嘌呤核苷(adenine riboside,5)、尿嘧啶核苷(uridine,6)、蔗糖(sucrose,7)、葡萄糖(glucose,8)、β-谷甾醇(β-sitosterol,9)、胡萝卜苷(daucosterol,10)。结论除化合物4外,其他化合物均为首次从野独活属植物中分离得到。     

青风藤化学成分的分离与鉴定

目的对青风藤(Sinomenium auctum (Thunb.) Rehd.et Wils.)化学成分进行分离、鉴定。方法适量干燥青藤茎用10倍量体积分数为70%的乙醇水溶液提取,减压回收乙醇,所得干浸膏研成细粉后,分别用环己烷、氯仿、甲醇超声溶取;采用ODS中低压柱色谱、制备型HPLC方法进行分离,并通过1H-NMR、13C-NMR、ESI-MS等谱学技术对化合物进行结构鉴定。结果分离得到5个化合物,分别鉴定为穆坪马兜铃酰胺(N-trans-feruloyl tyramine,1)、syringaresinol mono-β-D-glucoside(2)、1,2,4/3,5-cyclohexanepentol(3)、3-methoxy-6-hydroxy-17-methylmorphinane(4)、青藤碱(sinomenine,5)。结论化合物1~4为首次从防己属中分离得到。     

大理卫矛乙醇提取物的化学成分研究

目的:研究大理卫矛的化学成分。方法:采用硅胶柱色谱、凝胶柱色谱、薄层色谱、半制备高效液相色谱对大理卫矛乙醇提取物进行分离纯化,根据理化性质和波谱数据(质谱、氢谱和碳谱)分析鉴定化合物结构。结果:从大理卫矛乙醇提取物中分离得到10个化合物,分别鉴定为蒲公英赛醇(1)、槐二醇(2)、蒲公英萜酮(3)、Sorghumol(4)、十七烷酸(5)、十八烷酸(6)、β-谷甾醇(7)、胡萝卜苷(8)、表木栓醇(9)、木栓酮(10)。结论:上述10个化合物均为首次从大理卫矛中分离得到,化合物1、2、4、5、6为首次从卫矛属植物中分离得到。该研究为大理卫矛的质量评价奠定了一定基础。     

费菜茎叶化学成分的分离与鉴定(Ⅱ)

目的对费菜(Sedum aizoon L.)茎叶的化学成分进行研究。方法采用硅胶柱色谱、ODS柱色谱、Sephadex LH-20柱色谱和HPLC色谱分离纯化,依据理化性质和光谱数据确定化合物的化学结构。结果从费菜茎叶体积分数为70%的乙醇提取物的乙酸乙酯萃取物中分离得到8个化合物,分别鉴定为:熊果苷(arbutin,1)、picein(2)、丁香酸葡萄糖苷(glucosyringic acid,3)、杨梅素-3-O-β-D-葡萄糖苷(myricetin-3-O-β-D-glucopyranoside,4)、杨梅素-3'-O-β-D-葡萄糖苷(myricetin-3'-O-β-D-glucopyranoside,5)、pyroside(6)、p-hydroxybenzoyl arbutin(7)和koaburaside(8)。结论化合物2、5、6和8为首次从景天属植物中分离得到。     

朝鲜淫羊藿的化学成分

目的研究朝鲜淫羊藿(Epimedium koreanumNakai)中的化学成分。方法朝鲜淫羊藿干燥地上部分用水回流提取后,经大孔吸附树脂柱色谱分离,用水及不同体积分数的乙醇洗脱;50%乙醇洗脱部分的浸膏用硅胶柱色谱分离,用氯仿甲醇梯度洗脱,得到的第5、8、10流份用羟丙基葡聚糖凝胶柱色谱分离、十八烷基键合硅胶柱色谱分离、制备型HPLC纯化后得到化合物1~8;根据化合物的理化性质和核磁共振氢谱、碳谱数据对所得化合物进行结构鉴定,分析确定化学结构。结果从朝鲜淫羊藿水提取物中分离得到8个化合物:淫羊藿苷(icariin,1)、宝藿苷Ⅰ(baohuosideⅠ,2)、箭藿苷B(sagittatoside B,3)、宝藿苷Ⅱ(baohuosideⅡ,4)a、stragalin(5)、3,5,7三羟基4′甲氧基8异戊烯基黄酮3OαL鼠李吡喃糖基(1→2)α鼠李吡喃糖苷(6)、1,2,3,4 tetrahy-dro 3,7 dihydroxy 1(4 hydroxy 3 methoxyphenyl)6 methoxy 2,3 naphthalenedimethanol(7)、朝藿定C(epimedin C,8)。结论化合物7为首次从该属植物中分离得到,化合物8为首次从该种植物中分离得到。     

山楂叶化学成分的分离与鉴定

目的对蔷薇科山楂属植物山楂(Crataegus pinnatifida Bge.)叶的化学成分进行研究。方法运用硅胶柱色谱﹑Sephadex LH-20柱色谱﹑ODS柱色谱、制备HPLC等分离手段进行化学成分的分离纯化,根据理化性质及波谱数据鉴定其结构。结果从山楂叶体积分数80%乙醇水溶液的提取物中分离得到7个化合物,分别鉴定为α-tetrahydrobisabolen-2,5,6-triol(1)、10,11-dihydroxynero-lidol(2)、3,5,4'-三甲氧基-4-羟基-联苯(3,5,4'-trimethoxy-4-hydroxyl-biphenyl,3)、(+)-7R,8S-5-methoxy dihydrodehydroconiferyl alcohol(4)、5,4'-二甲氧基-联苯-4-羟基-3-O-β-D-葡萄糖苷(5,4'-dimethoxy-biphenyl-4-ol-3-O-β-D-glucoside,5)、槲皮素(quercetin,6)、牡荆素(vitexin,7)。结论化合物1为新天然产物,化合物2～4为首次从山楂属植物中分离得到。     

板栗种皮化学成分的分离与鉴定

目的研究板栗种皮的化学成分。方法采用硅胶柱色谱、凝胶柱色谱、氧化铝柱色谱和重结晶等多种分离方法对板栗种皮的体积分数为75%的乙醇提取物进行分离,通过化合物理化性质、谱学数据分析鉴定化合物结构。结果分离得到8个化合物,分别鉴定为软脂酸-1-甘油单酯(hexa-decanoic acid-2,3-dihydroxypropyl ester,1)、滨蒿内酯(scoparone,2)、异泽兰黄素(eupatilin,3)、5,7,4′-三羟基-6,3′-二甲氧基黄酮(jaceosidin,4)、5,7,4′-三羟基-6,3′,5′-三甲氧基黄酮(5,7,4′-trihy-droxy-6,3′,5′-methoxyflavone,5)、clovane-2,9-diol(6)、β-谷甾醇(β-sitosterol,7)、胡萝卜苷(dau-costerol,8)。结论化合物3~6为首次从栗属植物中分离得到。     

鹅绒藤地上部位化学成分研究

目的研究鹅绒藤(Cynanchum chinense R.Br.)地上部位的化学成分。方法采用AB-8大孔树脂柱,硅胶柱色谱,LX2000树脂柱,Sephadex LH-20柱色谱等方法分离纯化;利用核磁共振波谱技术鉴定化合物结构。结果从鹅绒藤地上部位70%乙醇提取物中分离得到9个化合物,分别鉴定为十六烷酸(Ⅰ)、水杨酸(Ⅱ)、β-谷甾醇(Ⅲ)、β-胡萝卜苷(Ⅳ)、芹菜素(Ⅴ)、山奈酚(Ⅵ)、山奈酚-3-O-β-D-吡喃葡萄糖苷(Ⅶ)、小麦黄素(Ⅷ)、小麦黄素-7-O-β-D-葡萄糖醛酸苷(Ⅸ)。结论化合物Ⅴ、Ⅷ、Ⅸ为首次从本属植物中分离得到;化合物Ⅰ、Ⅱ、Ⅴ～Ⅸ为首次从本植物中分离得到。     

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.