目的明确雷公藤片和雷公藤多苷片发挥抗炎作用的剂量范围，比较其作用效果异同，为临床用药提供依据。方法给小鼠灌胃不同量的雷公藤片和雷公藤多苷片，连续3天，通过巴豆油混合致炎液致小鼠耳肿胀模型计算雷公藤片和雷公藤多苷片对抗急性炎症的半数有效量（ED50），探讨雷公藤片和雷公藤多苷片对小鼠急性炎症的抑制作用差异。结果雷公藤片和雷公藤多苷片发挥抗炎作用的ED50分别为17.753μg·kg-1和9.236mg·kg-1，折合成雷公藤甲素分别为17.753和8.922μg·kg-1，分别相当于临床70kg人临床日用量的20.30倍和10.21倍。结论雷公藤片、雷公藤多苷片均可拮抗巴豆油混合致炎液导致的急性炎症，且呈现良好的量效关系。抗炎作用强度为雷公藤多苷片〉雷公藤片。提示雷公藤甲素、雷公藤多苷均是雷公藤抗炎作用的物质基础。雷公藤抗炎作用机制有待于进一步研究。

Objective To explore the dose range of anti-inflammatory effect of Tripterygium wilfordii tablets (TWT) and Tripterygium wilfordii polyglycoside (TWP)tablets and compare with the results of them, so as to provide the basis for clinical medication. Methods Mice were respectively given the different doses of TWT and TWP for 3 consecutive days by gavage. The anti-inflammatory effects of TWT and TWP were explored according to the model of ear edema by mixture of compound croton oil we made. ED50 and ED95 of anti-inflammatory efficacy and LD50 and LD5 of acute toxicity test were calculated. Results ED50 and 95% confidence limit of TWT and TWP were respectively 17.753 (13.567~21.448)μg·kg-1, 9.236 (5.570~11.915) mg·kg-1, which were equal to triptolide of 17.753μg·kg-1, 8.922μg·kg-1. They were respectively equal to 20.30 and 10.21 times of 70 kg person''s daily dried medicine expenses. Conclusion TWT and TWP show good suppression on the acute inflammation caused by mixture of

目的：建立雷公藤中总生物碱的含量测定方法。方法：通过实验对雷公藤总生物碱提取方法、试剂及用量选择、浸泡时间、取样量等进行确定。结果：雷公藤总生物碱含量测定方法：超声提取仪提取，取样2 g，氯水5 mL，浸泡5 h。雷公藤样品含量测定：RSD为0.075%（n=6）。结论：利用滴定法测定雷公藤总生物碱含量，快速、准确，结果可靠。

Objective:To establish a method for content determination of alkaloids in tripterygium wilfordii. Method:The extract method,reagent and dosage choice,soaking time and sampling on alkaloids in tripterygium wilfordii were deter-mined by experiment. Results:The content determination method of alkaloids in tripterygium wilfordii were as follows:ex-tracting by ultrasonic extraction apparatus,sampling 2 g,chlorine water 5 mL,soaking 5 h. The RSD was 0.075%(n=6)in the content determination of tripterygium wilfordii sample. Conclusion:The content determination of alkaloids in triptery-gium wilfordii by titration method is rapid,accurate and the result is reliable.

研究凤尾草对雷公藤甲素的减毒作用以及免疫抑制和抗炎镇痛活性的影响。方法:通过比较雷公藤甲素单用及与凤尾草联用对小鼠急性毒性、肝组织形态和大鼠肝功能的影响来评价凤尾草对雷公藤甲素的减毒作用;采用噻唑兰(MTT)法测定雷公藤甲素单用及与凤尾草联用对小鼠T、B淋巴细胞增殖的影响;采用二甲苯致小鼠耳廓肿胀实验研究凤尾草对雷公藤甲素抗炎作用的影响;采用热板法和扭体法研究凤尾草对雷公藤甲素镇痛作用的影响。结果:雷公藤甲素联用凤尾草后LD50增大了约1倍,肝细胞损伤明显减轻,ALT和AST明显降低;雷公藤甲素单用及与凤尾草联用均能显著抑制小鼠T、B淋巴细胞的增殖和二甲苯致小鼠耳廓肿胀,并均有明显的镇痛作用,但两者作用效果差异无显著性。结论:联合运用凤尾草可降低雷公藤甲素毒性并基本保持其免疫抑制和抗炎镇痛活性。

OBJECTIVE To investigate the toxicities and activities of triptolide combined with Pteris multifida Poir..METHODS Toxicity of triptolide combined with Pteris multifida were evaluated with LD50,morphology of hepatic tissue and liver function.Activities of triptolide combined with Pteris multifida were evaluated with growth inhibiting effects of both T and B lymphocytes detected by MTT assay,swelling of mouse auricle caused by dimethyl benzene and analgesic effect detected by hot plate test and writhing method.RESULTS The LD_(50) of triptolide was significantly increased meanwhile ALT and AST were significantly decreased while combined with Pteris multifida.Both triptolide and triptolide combined with Pteris multifida can significantly inhibit the growth of T and B lymphocytes,swelling of mouse auricle caused by dimethyl benzene and alleviate pain inhot plate test of mouse.CONCLUSION Pteris multifida can reduce the toxicity of triptolide and maintain its immune suppression,antiinflarnmat

目的：探讨雷公藤甲素诱导鼻咽癌细胞凋亡的作用及机制。方法 MTT测定雷公藤甲素对CNE-2Z细胞的抑制作用；碘化丙啶（ propidium iodide, PI）染色测定雷公藤甲素对鼻咽癌细胞凋亡的影响；Western blot 测定葡萄糖调节蛋白78（glucose regulated protein78,GRP-78）、Akt的表达及Akt的磷酸化水平；ROS荧光探针-二氢乙啶测定细胞内活性氧（reactiveoxygenspecies,ROS）的水平。结果 MTT显示,雷公藤甲素对鼻咽癌细胞CNE-2Z的抑制作用随浓度增加及时间延长而增强；PI结果显示,雷公藤甲素能明显诱导鼻咽癌细胞的凋亡,25、50和100 nmol＆#183;L-1的雷公藤甲素作用细胞24 h, CNE-2Z 细胞的凋亡率分别为14.0%、26.9%和34.4%；Western blot显示,雷公藤甲素对CNE-2Z细胞GRP-78表达无明显影响,但可减弱Akt的表达及磷酸化水平；氧化应激实验结果表明,雷公藤甲素作用4h后,能增加鼻咽癌细胞CNE-2Z内ROS的水平。结论雷公藤甲素具有抑制鼻咽癌细胞CNE-2Z增殖的作用,且具有浓度与时间依赖性。其机制可能是雷公藤甲素通过诱导氧化应激,抑制细胞内Akt的表达及其磷酸化,调节下游的信号通路,进而促进CNE-2Z细胞的凋亡。

Aim Toexploretheinhibitioneffectof triptolide on nasopharynx cancer, and the mechanism. Methods Theinhibitionofcellproliferationwasde-tected by MTT assay;the cell apoptosis was analyzed by flow cytometry with propidium iodide staining. The ex-pressions of glucose regulated protein 78 ( GRP-78 ) , Akt and pAkt in cells were examined by Western blot;the effect of triptolide on reactive oxygen species ( ROS) accumulation was detected by ROS Fluorescent Probe-DHE.Results MTTassayshowedthatthe growth of nasopharynx cancer was inhibited by triptol-ide , and the inhibition occurred in a dose and time-de-pendent manner following triptolide treatment in CNE-2Z nasopharynx cancer cells. Propidium iodide staining revealed that the apoptosis of CNE-2 Z cells was in-duced remarkably by triptolide. After CNE-2Z cells treated with 25, 50,100 nmol·L-1 of triptolide for 24 h, the apoptosis rate was 14%,26. 9% and 34. 4% re-spectively. Western blot experiment showed that the expression of GRP-78 had no

目的：：观察雷公藤甲素对狗肾小管上皮细胞( MDCK细胞)的毒性作用,并初步探讨其对氧化应激的影响。方法：以马兜铃酸A为阳性对照,用0.5,5,50和500 nmol·L-1的雷公藤甲素与MDCK细胞共同孵育24 h后,MTT法检测细胞抑制率,乳酸脱氢酶( LDH)释放实验检测细胞膜损伤以及倒置显微镜观察雷公藤甲素对细胞形态的改变。用500 nmol·L-1雷公藤甲素分别与MDCK细胞作用30 min、1 h、2 h、4 h和6 h后,用2′,7′-二氯荧光黄双乙酸盐( DCFH-DA)荧光探针检测细胞的活性氧自由基(ROS)水平。结果：与阴性对照组比较,雷公藤甲素组的细胞抑制率明显升高(P<0.01)；LDH相对释放率明显增加(P<0.01)。雷公藤甲素处理组的细胞形态出现皱缩,呈现为球形,并有部分细胞脱落。雷公藤甲素与MDCK细胞作用30 min后ROS水平达到最高值,然后ROS逐渐减少(P<0.01)。结论：雷公藤甲素可诱导MDCK细胞的毒性作用,其毒性作用机制可能和氧化应激反应有关。

Objective:To study the nephrotoxicity induced by triptolide ( TP) on MDCK cell model and investigate its effect on oxidative stress. Methods:Aristolochic acid was chosen as the positive control. After the MDCK cells were incubated with 0. 5, 5, 50 and 500 nmol·L-1 TP for 24h, MTT method was used to observe the cell inhibiting rate and lactate dehydrogenase (LDH) release test was used to detect the cell membrane damage caused by TP. The cell morphology was observed under an inverted microscope. After the MDCK cells were incubated with 500 nmol·L-1 TP respectively for 30min, 1h, 2h, 4h and 6h, the level of reactive oxygen species ( ROS) was detected using 2′,7′-dichlorodihydro-fluorescein diacetate ( DCFH-DA) as the fluorescent probe. Results:Compared with those of the negative control group, the cell inhibiting rates and the relative LDH release rates in TP-treated group were increased sig-nificantly(P<0. 01). The cells in TP-treated group were creased, turned into the rou