昆明山海棠离体胚培养的细胞学观察

首次报道了昆明山海棠离体胚的培养,诱导出愈伤组织、不定根、不定突起和丛芽,并进行了细胞学观察。指出:子叶上的愈伤组织起源于表皮及表皮下的叶肉细胞。不定根原基常来源于愈伤组织中散生分生组织或维管束。同时,对易分化形成不定根的愈伤组织的组织学特点进行了观察。     

雷公藤贝壳杉烯酸氧化酶基因的全长cDNA克隆与表达分析

贝壳杉烯酸氧化酶(kaurenoic acid oxidase)是二萜赤霉素生物合成途径上的关键酶,参与植物生长发育等重要生物学过程。该文根据雷公藤转录组数据设计特异性引物,采用PCR技术克隆得到贝壳杉烯酸氧化酶全长c DNA序列,并进行生物信息学分析;使用实时定量PCR(qRT-PCR)研究基因的诱导表达水平。克隆得到Tw KAO长度为1 874 bp,编码487个氨基酸,蛋白相对分子质量56.02 k Da,理论等电点8.89;经茉莉酸甲酯(Me JA)诱导后,Tw KAO基因相对表达量在12 h达到峰值;经植株组织表达分析证实,Tw KAO基因在雷公藤的叶中表达量最高,根中最低。该研究首次克隆得到雷公藤KAO基因,并分析其mRNA表达特征,为深入研究雷公藤生长发育以及萜类活性成分次生代谢研究奠定基础。     

不同地区不同药用部位雷公藤和昆明山海棠的总生物碱含量测定

本文用重量法测定了不同地区的雷公藤和昆明山海棠的不同药用部位的总生物碱含量。其根含总生物碱１％左右。实验结果，可供临床抗生育研究需要参考。     

抗生育剂量雷公藤对小鼠脾NK细胞活性的调节作用

采用银染和MTT的方法,分别观察不同剂量雷公藤对雄性小鼠的附睾尾精子变化和脾NK细胞活性的影响。结果显示:雷公藤实验组附睾尾精子多为头部异常,大部分出现头尾分离和折断现象,精子活率及密度均明显低于对照组。雷公藤对小鼠脾NK细胞活性存在着明显的剂量效应关系,多甙组和雷公藤糖浆大剂量组对NK细胞活性抑制较明显,而中剂量组和小剂量组则对NK细胞活性影响不明显。结果提示:雷公藤糖浆在有效抗生育剂量下对小鼠脾NK细胞活性无明显影响,为重新评价雷公藤的药用价值及今后的临床应用提供了有意义的实验数据。     

雷公藤配合温泉、理疗治疗类风湿性关节炎103例临床观察

本文报告雷公藤配合消炎痛、温泉浴、腊疗等治疗103例类风显性关节炎活动期的住院患者疗效,完全缓解22例(21％),明显改善47例(46％),轻度改善34例(33％)。     

Clinical Observation on Side Effects of Various Tripterygium Wilfordii Preparations

Ｔｒｉｐｔｅｒｙｇｉｕｍｗｉｌｆｏｒｄｉｉ（ＴＷ）ｉｓａＣｈｉｎｅｓｅｍｅｄｉｃｉｎａｌｈｅｒｂｗｉｔｈｃｌｅａｒｉｎｇａｗａｙＨｅａｔａｎｄｔｏｘｉｃｓｕｂｓｔａｎｃｅ，ｅｘｐｅｌｌｉｎｇＷｉｎｄａｎｄｒｅｍｏｖｉｎｇｏｂｓｔｒｕｃｔｉｏｎｉｎｃｏｌｌａｔｅｒａｌｓ，ｒｅｌａｘｉｎｇｔｈｅｔｅｎｄｏｎａｎｄａｃｔｉｖａｔｉｎｇｂｌｏｏｄｃｉｒｃｕｌａｔｉｏｎ，ｒｅｍｏｖｉｎｇＤａｍｐｎｅｓｓａｎｄｓｗｅｌｌｉｎｇ，ａｎｄｓｔｏｐｐｉｎｇｔｈｅｐａｉｎ．Ｃｕｒｒｅｎｔｌｙｉｔｈａｓｂｅｅｎｗｉｄ…     

昆明山海棠对小鼠IgE合成的调节

本文研究昆明山海棠对高lgE模型小鼠的影响。采用被动皮肤过敏试验、抗DNP-KLH lgE溶血空斑数测定、血球凝集及间接免疫荧光等技术检测结果表明,昆明山海棠使模型小鼠血清特异性IgE显著降低,脾细胞溶血空斑数较对照组明显减少,淋巴结T_H/Ts比例倒置,而对血清IgG及总抗体水平无显著影响。     

Effects of triptolide on hippocampal microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer’s disease

The principal pathology of Alzheimer's disease includes neuronal extracellular deposition of amyloid-beta peptides and formation of senile pl aques,which in turn induce neuroinflammation in the brain.Triptolide,a natural extract from the vine-like herb Tripterygium wilfordii Hook F,has potent anti-inflammatory and immunosuppressive efficacy.Therefore,we determined if triptolide can inhibit activation and proliferation of microglial cells and astrocytes in the APP/PS1 double transgenic mouse model of Alzheimer's disease.We used 1 or 5 μg/kg/d triptolide to treat APP/PS1 double transgenic mice(aged 4–4.5 months) for 45 days.Unbiased stereology analysis found that triptolide dose-dependently reduced the total number of microglial cells,and transformed microglial cells into the resting state.Further,triptolide(5 μg/kg/d) also reduced the total number of hippocampal astrocytes.Our in vivo test results indicate that triptolide suppresses activation and proliferation of microglial cells and astrocytes in the hippocampus of APP/PS1 double transgenic mice with Alzheimer's disease.     

雷公藤多甙并卡托普利治疗小儿肾病型紫癜性肾炎疗效分析

目的 观察雷公藤多甙并卡托普利对小儿肾病型紫癜性肾炎的治疗效果.方法 将101例诊断为肾病型紫癜性肾炎的患儿随机分为治疗组58例(口服雷公藤多甙和卡托普利)和对照组43例(口服单剂强的松),观察药物对两组患儿水肿、高血压、血尿、蛋白尿的疗效,采用SPSS10.0软件进行统计学分析.结果 治疗组治愈51例(88%),有效7例(12%);对照组治愈26例(61%),有效17例(39%),两组治愈率比较差异有统计学意义(P<0.01),对水肿、血尿、高血压的疗效比较差异有统计学意义(P<0.05或P<0.01),对蛋白尿的疗效比较差异亦有统计学意义(P<0.01).结论 雷公藤多甙并卡托普利治疗小儿肾病型紫癜性肾炎疗效优于单剂强的松,值得临床应用. Abstract： Objective To observed the efficacy of tripterygium wilfordii polyglycoside and captopril in the treatment of children with Henoch-Schonlein purpura nephritis kidney disease model. Methods One hundred and one children diagnosed with kidney-type purpura nephritis from May 1996 to June 2009 in our hospital, were respectively, randomly divided into treatment group (58 cases,oral tripterygium wilfordii polyglycoside and captopril) and the control group (43 patients, single-dose oral prednisone), observation of therapeutic effects of drugs in the two groups of children with edema, hypertension, hematuria, proteinuria efficacy, using SPSS10.0 software for statistical analysis. Results Fifty-one patients were cured (88%), effective in 7 patients (12%) in the treatment group, the control group cured 26 cases (61%), effective in 17 cases (39%), there was significant difference between the two groups (P<0.01). Pairs of edema, hematuria, hypertension were significantly different between the two groups(P<0.05 or P<0.01), and the efficacy of proteinuria was also significantly different (P<0.01). Conclusions Tripterygium wilfordii polyglycoside and captopril treatment of children with Henoch-Schonlein purpura nephritis kidney disease model is superior to single-dose prednisone, it is worth clinical application.     

Tripchlorolide protects against MPTP-induced neurotoxicity in C57BL/6 mice

Many current studies of Parkinson's disease (PD) suggest that inflammation is involved in the neurodegenerative process. Tripchlorolide (TW397), a traditional Chinese herbal compound with anti-inflammatory and immunosuppressive properties, has been shown to protect dopaminergic neurons against, and restore their function after, the neurotoxicity induced by 1-methyl-4-phenylpyridinium ions in vitro. This study was designed to investigate the effect of TW397 in vivo in the PD model of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned C57BL/6 mice. In the animals that received vehicle-only (i.e., no TW397) treatment with MPTP i.p. injection, the survival ratios of tyrosine hydroxylase-immunoreactive (TH-IR) neurons in the substantia nigra pars compacta and TH-IR fibres in the striatum were only 59 and 13%, respectively, compared with the normal controls. Intriguingly, in conjunction with MPTP, treatment with TW397, 1 microg/kg for 16 days, once per day, dramatically improved the survival rate of the TH-IR neurons and TH-IR fibres to 80 and 43% of the control. The treatment with TW397 also significantly improved the level of dopamine in the substantia nigra and striatum to 157 and 191%, respectively, of the MPTP- plus vehicle-treated group. In addition, in MPTP-treated animals the rota-rod performances of those treated with 0.5 or 1 microg/kg TW397 were significantly improved, by approximately 2- and 3-fold, respectively, relative to vehicle-treated animals. The neuroprotective effect of TW397 was coincident with an attenuated astroglial response within the striatum. These data demonstrate a neuroprotective action of TW397 in vivo against MPTP toxicity, with important implications for the treatment of PD.