邻苯二甲酸酯类对大鼠睾丸支持细胞毒性作用

目的探讨大鼠睾丸支持细胞间紧密连接结构能否作为邻苯二甲酸酯类(PAE)毒性作用效应的标志物。方法建立大鼠睾丸支持细胞原代双室培养模型,通过光镜、跨上皮电阻测定及免疫荧光定位方法研究PAE对大鼠支持细胞及支持细胞间紧密连接结构的影响。结果PAE染毒后,支持细胞单层破坏、细胞间的嵴线消失、跨上皮电阻值下降、紧密连接相关蛋白ZO-1、F-肌动蛋白和闭锁蛋白表达降低;600μmol·L-1浓度下,单乙基己基邻苯二甲酸酯(MEHP)对睾丸支持细胞的毒性大于单丁基邻苯二甲酸酯(MBP)。结论MEHP和MBP可破坏睾丸支持细胞间的紧密连接结构,跨上皮电阻值可作为PAE睾丸毒作用敏感的效应标志物。

大鼠肺泡Ⅱ型上皮细胞的体外培养及内毒素攻击模型的建立

目的探讨大鼠肺泡Ⅱ型上皮细胞（ATⅡ）体外培养的方法及建立脂多糖（LPS）攻击ATⅡ的模型模拟内毒素性肺损伤。方法分离、纯化、鉴定得到大鼠ATⅡ，分别用01、1、10μg／ml的LPS刺激ATⅡ，并利用细胞增殖／毒性检测试剂在刺激2、4、6h后分别检测ATⅡ的抑制率，从而探索内毒素性肺损伤细胞模型中最适的LPS浓度和刺激时间。结果用碱性磷酸酶染色及电镜观察进行细胞纯度判断，未用差异贴壁去除成纤维细胞和IgG免疫黏附去除巨噬细胞纯化前，纯度达（70．4±4．8）％，纯化后可提高至（90．2±3．4）％；而用LPS干预ATⅡ，ATⅡ出现明显的细胞抑制。其中刺激浓度为1μg／ml时与其他3个实验组相比，细胞毒性反应最大（P〈0．01），且在各个浓度的不同刺激时间里，4h时，细胞毒性反应最大（P〈0．01）。结论细胞分离后采用差异贴壁法和免疫黏附法进行纯化可使细胞纯度提高18％左右l细胞培养时接种密度达到1X107／ml以上有利于细胞的贴壁和生长，而用1μg／ml LPS刺激体外培养的大鼠ATⅡ4h能建立较为合理的内毒素性肺损伤细胞模型。

Constituents from Ranunculus sieboldii Miq.

Aim To investigate the chemical composition of Ranunculus sieboldii Miq..Methods Repeated column chromatography over silica gel, polyamide and RP-18 followed by gelfiltration on sephadex LH-20 were used to isolate chemical constituents, and their structures wereelucidated by extensive spectroscopic methods (UV, IR, MS, ~1H NMR, ^(13)C NMR) including 2D NMR(COSY, HMQC, HMBC, NOESY) techniques and by direct comparing spectral data with those reported inliterature. Results Five flavonoid glycosides named apigenin-4'-O-α-L-rhamnopyranoside (1),apigenin-7-O-β-D-glucopyranosyl-4'-O-α-L-rhamnopyranoside (2), apigenin-8-C-α-L-arabinopyranoside(3), apigenin-8-C-β-D-ga-lactopyranoside (4) , tricin-7-O-β-D-glucopyranoside (5), together withtricin (6), luteolin (7), scopoletin (8), esculetin (9), scoparone (10), ferulic acid (11),protocatechuic acid (12) , and tematolide (13) were isolated from the 95% etha-nolic extract of itswhole plant, and their cytotoxic activities were preliminarily tested. Conclusion Compounds 1-12were obtained from this genus and compound 13 from this species for the first time. Furthermore,compound 1 was for the first time isolated from nature while the ^(13)C NMR data of compounds 2 and3 are reported for the first time. The bioassay revealed that compound 1 was active against BEL-7407and A549 cell lines (IC_(45) 43, 77 μg·mL^(-1)), 8 and 10 showed inhibitory activities on KB celllines (IC_(50) 78, 44 μg·mL^(-1)) and HL-60 cell lines (Ic_(50) 85, 85 μg·mL^(-1)), while 7exerted moderate cytotoxic activities on KB, BFL-7407, A549 and HL-60 cell lines with their IC_(50)being 51, 55, 44 and 10 μg·mL^(-1) , respectively.

Polyhydroxylated Steroidal Sapogenins from Tupistra wattii

Two novel polyhydroxylated steroidal sapogenins, wattigenin B ((25R)-spirost-1beta, 2beta, 3beta, 4beta, 5beta, 6beta, 7alpha-heptol, 1) and wattigenin C ((25S)-spirost-1beta, 2beta, 3beta, 4beta, 5beta, 7alpha-hexalrydroxyl-6-one, 2), together with two known sapogenins, kitigenin (3) and convallagenin B (4), were isolated froth the fresh rhizomes of Tupistra wattii Hook. f. The structures of the compounds were determined on the basis of spectroscopic analysis. The four sapogenins were evaluated for the cytotoxicities on the cancer cell line K562 and A2780a in vitro. Compounds 1 - 4 were obtained from the plant for the first time.

Binding tendency with oligonucleotides and cell toxicity of cetyltrimethyl ammonium bromide-coated single-walled carbon nanotubes

Functionalized carbon nanotubes （CNTs） were made for the delivery of genes and drugs and CNT-based biosensors. The basis of CNTs is for binding with biomolecules in biomedical applications. The binding tendency with small interfering RNA oligonucleotides and cytotoxicity of cetyltrimethyl ammonium bromide （CTAB）-coated single-walled carbon nanotubes （SWNTs） were studied. The field emission scanning electron microscopy and transmission electron microscopy results show that a SWNT suspension in CTAB solution was well-dispersed and stable. CTAB is the cross-linker between SWNTs and oligonucleotides. The CTAB-coated SWNTs have less cytotoxicity to human umbilical vein endothelial cells than single SWNTs and the cytotoxicity of CTAB-coated SWNTs depended on the concentration of CTAB-coated SWNTs.

Effects of chitosan coating on biocompatibility of Mg-6%Zn-10%Ca_3(PO_4)_2 implant

A Mg?6%Zn?10%Ca3(PO4)2 composite with a chitosan coating was prepared to study its in vivo biodegradation properties. The chitosan dissolved in a 0.2% acetic acid solution was applied on the surface of Mg?6%Zn?10%Ca3(PO4)2 composite specimens and solidified at 60 °C for 30 min to form the coating. The cytotoxicity evaluation of chitosan coated specimens is at level 0, which indicates that such coating is safe for cellular applications. The in vivotests of chitosan coated composite show that the concentration of metal ions from the composite measured in the venous blood of Zelanian rabbits is less than that from the uncoated composite specimens. The chitosan coating impedes the in vivo degradation of the composite after surgery. The in vivo testing also indicates that the chitosan coated composite is harmless to important visceral organs, including the heart, kidneys and liver of the rabbits. The new bone formation surrounding the chitosan coated composite implant shows that the composite improves the concrescence of the bone tissues. And the chitosan coating is an effective corrosion resistant layer that reduces the hydrogen release of the implant composite, thereby decreasing the subcutaneous gas bubbles formed.

Purification and Characterization of Cytotoxins from Agkistrodon acutus Venom and Their Anticancer Activity

Aim To investigate the anticancer activity of two new cytotoxins from thevenom of Agkistrodon acutus. Methods The venom was isolated by FPLC column chromatography consistingof DEAE Sepharose FF and Source 30S. The cytotoxic activity on tumor cells was detected by MITmethod. Purity and molecular weight were determined by SDS-PAGE (silver staining). Their stabilitiesto temperature and pH were also detected. Results Two pure cytotoxins named ACTX-6 and ACTX-8 wereobtained. Their molecular weights are 98 kDa and 27 kDa, respectively. ACTX-6 consists of twosubunits bonded together by disulfide bonds. Conclusion ACTX-6 and ATCX-8 have highest inhibitoryactivity on lung cancer cell A549. ACTX-6 is stable to heat while ACTX-8 not. ACTX-6 is stablebetween pH 7-9 and ACTX-8 between pH 6 - 9.

Role of Antivirus Therapy in Treatment of Hepatocellular Carcinoma with Chronic Hepatitis B Infection

Objective： To observe the recurrence and prognosis of hepatocellular carcinoma （HCC） patients coexisting with chronic hepatitis B infection with active virus replication after receiving antivirus therapy using lamivudine and thymosin α1 （Tα1） postoperatively. Methods： From Jan. 2000 to Dec. 2003, 70 patients with HCC coexisting chronic hepatitis B infection with active virus replication were prospectively divided into two groups： control group （n=35） received hepatectomy only; treatment group （n=35） received hepatectomy and lamivudine plus Tα1 therapy postoperatively. The suppression of HBV-DNA, HBeAg seroconverted rate, tumor recurrent rate and the median survival for the two groups were observed and calculated. Results： In treatment group and control group, the 2-year HBV-DNA suppression rate was 100% vs. 4% （P=0.0000）; HBeAg seroconverted rate was 73.0% vs. 7.5% （P〈0.05）; the recurrent rate was 10.0 vs 6.5 months （P=0.0032）; the median survival time was 12.5 vs. 6.0 months （P=0.0023）, respectively. Conclusion： Antivirus therapy using lamivudine and Tα1 postoperatively may suppress the HBV reaction, delay the recurrent time and prolong the survival for HCC patients coexisting chronic HBV infection with active virus replication.

Study on Flavonoids from the Methanol Extracts of Tephrosia purpurea Leaves

[Objective] The aim was to determine flavonoids from the MeOH extracts of Tephrosia purpurea leaves and their cytotoxicitives against the ovarian cells from Sprodenia litura （SL cells）.[Method] The compounds were isolated with column chromatography and their structures were established on the basis of various spectroscopic analysis （including UV,1D and 2D NMR analyses as well as HR-ESRMS）.The cytotoxicity against the SL cells was evaluated by using MTT method.[Result] Six known flavonoids,6-methoxykaempferol （1）,6-methoxykaempferol 7-O-α-rhamnopyranoside （2）,6-methoxykaempferol 3-O-α-rhamnopyranosyl（1→2）[α-rhamno-pyranosyl（1→6）]-β-galactopyranoside （3）,6-methoxykaempferol 3-O-α-rhamnopyranosyl （1 →2）[α-rhamnopyranosyl （1 →6）]-β-galactopyranoside-7-O-α-rhamnopyranoside （4）,pongachin （5）,5,7-dimethoxy-8-（3-hydroxy-3-methylbut-1Z-enyl） flavanone （6） were isolated and determined.Except compound 5,the others were isolated from T.purpurea for the first time.For the cytotoxicity compound 5 had significant activity with the IC50 value of 4.4 mg/L while compound 1 and 3,whose cytotoxicity exceeded rotenone,also showed moderate activity.[Conclusion] Of all the compounds from T.purpurea leaves,the content of 6-methoxykaempferol compounds was considerable.The profiles of these compounds against SL cells suggested that compounds 1,3 and 5,whose cytotoxicity exceeded rotenone,were worth further research.

Fixed-Tumor Vaccine: A Practical Formulation with Cytokine-Microspheres for Protective and Therapeutic Antitumor Immunity

Objective: To study the protective and therapeutic antitumor immunity against hepatocellular carcinoma (HCC) with the fixed-tumor vaccine.Methods: A tumor vaccine consisting of fixed tumor cells or fixed tumor fragments combined with sustained-releasers of cytokines and a non-toxic adjuvant was developed. C57BL/6J mice were immunized intra-dermally with the vaccine on day 0 and 7, followed by intrahepatic challenge with live Hepa 1–6 cells.Results: All of 15 nonimmunized control mice developed the hepatoma. Protection of mice immunized with fixed Hepa 1–6 cells and both of IL-2/GM-CSF microspheres or further mixed with TiterMax Gold reached 80% and 87%, respectively. Mass growth of the established tumors, vaccinated twice at 5 mm in diameter, the tumor of control animals continued to grow. However, 7–10 days after the second injection of the tumor vaccine, the tumor growth was suppressed in 9 of 10 mice and then markedly reduced. Complete tumor regression was observed in 60% (6/10) of mice. Splenocytes from the control mice were not able to lyse target Hepa 1–6 cells and other tumor cells. In contrast splenocytes from the vaccinated mice exhibited a 41% lytic activity against the Hepa 1–6 cells tested at an effector/target (E/T) ratio of 5, whereas they did not exhibited such activity against the melanoma cells (B16-F1), Lewis lung carcinoma cells (LLC), renal carcinoma cells (Renca), and bladder carcinoma cells (MBT-2). The cytotoxic activity was inhibited by the treatment with anti-CD3, anti-CD8, and anti-MHC-class I monoclonal antibodies but not with anti-CD4 and anti-MHC-class II antibodies. In the Phase-I clinical trial, vaccination of HCC patients with the autologous vaccine is a well-tolerated treatment and induces fixed tumor fragment-specific immunity.Conclusion: Fixed HCC vaccination elicited protective and therapeutic antitumor immunity against HCC. The tumor vaccine elicited antigen specific CTL response lysis of the target HCC was mediated by the typical MHC-class I restricted CD8+ T cells. Key words cancer vaccine - cytotoxic T lymphocyte - immunotherapy - hepatoma

Reversal of Multidrug Resistance by Neferine in Adriamycin Resistant Human Breast Cancer Cell Line MCF-7/ADM

Objective: To study the reversal effect of neferine on adriamycin (ADM) resistant human breast cancer cell line MCF-7/ADM. Methods: The cytotoxic effect of Nef or ADM was determined by 3-[4, 5-dimethylthiazol-2.-yl], 5-diphenyl tetraxolium bromid (MTT) assay. Apoptosis and the expression of P-glycoprotein (P-gp) were detected by flow cytometry (FCM). The intracellular ADM concentration was measured by HPLC. Results: Nef at 1, 5, 10 mol/L decreased the IC50 of ADM to MCF-7/ADM from 11.63 g/mL to 4.59, 2.44, 0.27 g/mL respectively. MCF-7/ADM could resist the apoptosis induced by ADM while Nef (1-10 mol/L) could augment ADR-mediated apoptosis. Nef (10 mol/L) increased the accumulation of ADM up to 2.88 fold in MCF-7/ADM but not in sensitive cells MCF-7/S and reduced the expression of P-gp in MCF-7/ADM cells. Conclusion: Nef can circumvent multidrug resistance (MDR) of MCF-7/ADM cells and the mechanism was associated with the increase of intracellular accumulation of ADM and the reduced expression of P-gp in MCF-7/ADM cells.

Ascorbic Acid Promotes Arsenic-induced Cytotoxicity in Human Hepatocarcinoma Cells and Their Underlying Mechanisms

Objective: To study synergistic effect with Ascorbic acid(AA) on arsenic trioxide inducing human Hepatocarcinoma cell apoptosis, and provide theoretical basis for promoting human Hepatocarcinoma cell apoptosis induced by arsenic trioxide(AT). Methods: Human Hepatocarcinoma cell line BEL-7402 being cultured in vitro, the effect of AT and (or) AA on its growth inhibition and its two intracellular signal molecules was evaluated separately using MTT and Western blot. Results: AT at a few μmol/L concentration could suppress abnormal proliferation of human hepatocarcinoma cells, and initiate their apoptosis by activation of caspase-3, and activate extracellular-signal regulated kinases (ERKs), which were dependent on the dosage of AT conspicuously. The effect of AA on BEL-7402 was not significant; However, AA could effectively enhance AT-induced hepatocarcinoma cell apoptosis and lesion severity through activation of caspase-3 but not ERKs. Conclusion: Caspase-3 and ERKs proteins could involve in arsenic-induced hepatocarcinoma cell apoptosis and differentiation respectively as intracellular signaling molecules; The effect between AT and AA on hepatocarcinoma is synergistic, which further inhibits cell growth and induces apoptosis in human hepatocarcinoma cells through activation of caspase-3 but not ERKs.

Advances in Toxicology of Nε-(carboxymethyl)-lysine(CML)

Advanced glycation end-products （AGEs） are products of non-enzymatic glycation of proteins, lipids or nucleic acids and other macromolecules. To be spe- cific, Nε-（carboxymethyl）-Iysine （CML） is one of the most important components of AGEs, which is wildly distributed in the body and can be formed in vivo or in food processing and heating processes. Previous studies have shown that CML is a ma- jor immunological epitope in AGEs and plays an important role in diabetes and its complications, as well as in the development and progression of aging. This review summarized recent advances in major source, toxicological hazard and control mea- sures of CML.

Corrosion degradation behavior of Mg-Ca alloy with high Ca content in SBF

The corrosion degradation behavior of a Mg-Ca alloy with high Ca content aiming for a potential bone repair material in the simulated body fluid（SBF） was investigated.The microstructure and phase constitution of the pristine Mg-30%Ca（mass fraction） alloy were characterized with scanning electron microscopy（SEM） and X-ray diffraction（XRD）.The Mg-30%Ca alloy samples were immersed in the SBF for 90 d,and the morphology,composition and cytotoxicity of the final corrosion product were examined.It is found that Mg-30%Ca alloy is composed of α-Mg and Mg2 Ca phases.During the corrosion process in the SBF,the Mg2 Ca phase acts as an anode and the α-Mg phase acts as a cathode.The final corrosion product of the Mg-30%Ca alloy in SBF includes a small amount of black precipitates and white suspended particles.The white suspended particles are Mg（OH）2 and the black particles are believed to have a core-shell structure.The cytotoxicity experiments indicate that these black precipitates do not induce toxicity to cells.

Alterations of red blood cell immunoadherence function in hepatitis B patients

AIMS To investigate the alterations of RBC immunoadherence function in patients with various hepatitis B. METHODS RBCC3bRR,RBCICRR and serum CIC levels were measured in 42 patients with acute and chronic hepatitis B at ac- tive and convalescence stages. RESULTS RBCC3bRRs at the active/acute stage of various hepatitis were decreased.They were 13,54%±5,23% in AH, 7.61%±4.12% in AFH,and 16.18%±6.10% in CH, respectively,all of which were lower than those in normal persons (18.12%±3.91% ).At the quiescent/recovery stage of various hepatitis,the RBCC3bRRs were increased significantly.The changes of RBCICRR and serum CIC level were contrary to those of RBCC3bRR. CONCLUSIONS RBC immunoadherence function is decreased in acute and chronic hepatitis.The decrease is in direct proportion to the severity of the diseases.

Overexpression of lentivirus-mediated glial cell line-derived neurotrophic factor in bone marrow stromal cells and its neuroprotection for the PC12 cells damaged by lactacystin

Objective To construct recombinant lentiviral vectors for gene delivery of the glial cell line-derived neurotropnic factor （GDNF）, and evaluate the neuroprotective effect of GDNF on lactacystin-damaged PC12 cells by transfecting it into bone marrow stromal cells （BMSCs）. Methods pLenti6/V5-GDNF plasmid was set up by double restriction enzyme digestion and ligation, and then the plasmid was transformed into Top10 cells. Purified pLenti6/V5-GDNF plasmids from the positive clones and the packaging mixture were cotransfected to the 293FT packaging cell line by Lipofectamine2000 to produce lentivirus, then the concentrated virus was transduced to BMSCs. Overexpression of GDNF in BMSCs was tested by RT-PCR, ELISA and immunocytochemistry, and its neuroprotection for lactacystin-damaged PC12 cells was evaluated by MTT assay. Results Virus stock of GDNF was harvested with the titer of 5.6×10^5 TU/mL. After tmnsduction, GDNF-BMSCs successfully secreted GDNF to supematant with nigher concentration （800 pg/mL） than BMSCs did （less than 100 pg/mL）. The supematant of GDNF-BMSCs could significantly alleviate the damage of PC12 cells induced by lactacystin （10 μmol/L）. Conclusion Overexpression of lentivirus-mediated GDNF in the BMSCs cells can effectively protect PC12 cells from the injury by the proteasome inhibitor.

Novel insight into mechanisms of cholestatic liver injury

Cholestasis results in a buildup of bile acids in serum and in hepatocytes.Early studies into the mechanisms of cholestatic liver injury strongly implicated bile acidinduced apoptosis as the major cause of hepatocellular injury.Recent work has focused both on the role of bile acids in cell signaling as well as the role of sterile inflammation in the pathophysiology.Advances in modern analytical methodology have allowed for more accurate measuring of bile acid concentrations in serum,liver,and bile to very low levels of detection.Interestingly,toxic bile acid levels are seemingly far lower than previously hypothesized.The initial hypothesis has been based largely upon the exposure of μmol/L concentrations of toxic bile acids and bile salts to primary hepatocytes in cell culture,the possibility that in vivo bile acid concentrations may be far lower than the observed in vitro toxicity has far reaching implications in the mechanism of injury.This review will focus on both how different bile acids and different bile acid concentrations can affect hepatocytes during cholestasis,and additionally provide insight into how these data support recent hypotheses that cholestatic liver injury may not occur through direct bile acid-induced apoptosis,but may involve largely inflammatory cell-mediated liver cell necrosis.

Bile-acid-induced cell injury and protection

Several studies have characterized the cellular and molecular mechanisms of hepatocyte injury caused by the retention of hydrophobic bile acids （BAs） in cholestatic diseases. BAs may disrupt cell membranes through their detergent action on lipid components and can promote the generation of reactive oxygen species that, in turn, oxidatively modify lipids, proteins, and nucleic acids, and eventually cause hepatocyte necrosis and apoptosis. Several pathways are involved in triggering hepatocyte apoptosis. Toxic BAs can activate hepatocyte death receptors directly and induce oxidative damage, thereby causing mitochondrial dysfunction, and induce endoplasmic reticulum stress. When these compounds are taken up and accumulate inside biliary cells, they can also cause apoptosis. Regarding extrahepatic tissues, the accumulation of BAs in the systemic circulation may contribute to endothelial injury in the kidney and lungs. In gastrointestinal cells, BAs may behave as cancer promoters through an indirect mechanism involving oxidative stress and DNA damage, as well as acting as selection agents for apoptosis-resistant cells. The accumulation of BAs may have also deleterious effects on placental and fetal cells. However, other BAs, such as ursodeoxycholic acid, have been shown to modulate BA-induced injury in hepatocytes. The major beneficial effects of treatment with ursodeoxycholic acid are protection against cytotoxicity due to more toxic BAs; the stimulation of hepatobiliary secretion; antioxidant activity, due in part to an enhancement in glutathione levels; and the inhibition of liver cell apoptosis. Other natural BAs or their derivatives, such as cholyI-N- methylglycine or pharmacological properties. cholylsarcosine, interest owing have also aroused to their protective

Detection of apoptosis induced by new type gosling viral enteritis virus in vitro through fluorescein annexin V-FITC/PI double labeling

AIM: To achieve a better understanding of the pathogenesis of new type gosling viral enteritis virus (NGVEV) and the relationship between NGVEV and host cells. METHODS: The apoptosis of duck embryo fibroblasts (DEF) induced by NGVEV was investigated by fluorescence-activated cell sorter (FACS) and fluorescence microscope after the cells were stained with Annexin V-FITC and propidium iodide (PI). RESULTS: By staining cells with a combination of fluorescein annexin V-FITC and PI, it is possible to distinguish and quantitatively analyze non-apoptotic cells (Annexin V-FITC negative/PI negative), early apoptotic cells (Annexin V-FITC positive/PI negative), late apoptotic/necrotic cells (Annexin V-FITC positive/ PI positive) and dead cells (Annexin V-FITC negative/PI positive) through flow cytometry and fluorescence microscope. The percentage of apoptotic cells increased with the incubation time and reached a maximum at 120 h after infection, while the percentage of non- apoptotic cells decreased.

Antiproliferation and apoptosis induction of paeonol in HepG_2 cells

AIM： To investigate the antiproliferative effect of paeonol （Pae） used alone or in combination with chemotherapeutic agents [cisplatin （CDDP）, doxorubicin （DOX） and 5-fluorouracil （5-FU）] on human hepatoma cell line HepG2 and the possible mechanisms. METHODS： The cytotoxic effect of drugs on HepG2 cells was measured by 3-（4, 5-dimethylthiazol-2- yl）-2, 5-diphenyltetra-zolium bromide （MTT） assay. Morphologic changes were observed by acridine orange （AO） fuorescence staining. Cell cycle and apoptosis rate were detected by flow cytometry （FCM）. Drug-drug interactions were analyzed by the coefficient of drug RESULTS： Pae （7.81-250 mg/L） had an inhibitory effect on the proliferation of HepG2 cells in a dose-dependent manner, with the IC50 value of （104.77±7.28） mg/L. AO fluorescence staining and FCM assays showed that Pae induced apoptosis and arrested cell cycle at S phase in HepG2 cells. Further, different extent synergisms were observed when Pae （15.63, 31.25, 62.5 rag/L） was combined with CDDP （0.31-2.5 mg/L）, DOX （0.16-1.25 mg/L）, or 5-FU （12.5-100 mg/L） at appropriate concentrations. The IC50 value of the three drugs decreased dramatically when combined with Pae （P 〈 0.01）. Of the three different combinations, the sensitivity of cells to drugs was considerably different.CONCLUSION： Pae had a significant growth-inhibitory effect on the human hepatoma cell line HepG2, which may be related to apoptosis induction and cell cycle arrest. It also can enhance the cytotoxicity of chemotherapeutic agents on HepG2 cells, and the S phase arrest induced by Pae may be one of the mechanisms of these interactions.