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The theory of "liver opens at the eyes" was first seen in Yellow Emperor's Internal Canon of Medicine， which is the ancient people's summary of the connection between the liver and the eyes. The theory of "liver opens at the eyes" suggests the characteristic of "co-damage and co-recover of liver and eyes". It has been found in clinical practice that liver diseases and eye diseases often occur together， and "liver and eyes co-recover" is an ideal choice. The key to achieving "liver and eyes co-recover" is to analyze its pharmacological material basis and mechanism. With the development of modern medicine， more and more evidence indicates that the liver and eyes have complex and close relationships in physiological and pathological aspects. In a pathological state， there is a phenomenon of "liver and eyes co-damage"， and after the intervention of traditional Chinese medicine， "liver and eyes co-recover" occurs. "Liver and eyes co-damage and co-recover" can be explained through the "co-material basis and co-action mechanism". On this basis， the research group tentatively proposed that the liver and eyes had "four common characteristics" （4CCs）， namely "co-damage， co-recover， co-material basis， and co-action mechanism" from the theoretical connotation of traditional Chinese medicine， clinical practice， and molecular biology. Additionally， the group also took the intervention of Prunella vulgaris， traditional Chinese medicine， for removing liver fire and improving eyesight on immune liver injury （ILI） and allergic conjunctivitis （AC） as examples to analyze 4CCs. This project aims to deeply analyze the scientific connotation of the theory of "liver opens at the eyes"， reveal the common characteristics and biological essence of liver and eyes， explore a new research paradigm of "liver and eyes co-recover"， and provide a reference for the study of common problems of multi-organ associated diseases.
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Objective:To determine the equilibrium solubility and the apparent oil/water partition coefficients of nicotinate-curcu-min ester,so as to provide basis for the new formula design. Methods:Nicotinate-curcumin ester was dissolved in buffer solution with pH of 1.2-7.8. HPLC was used to detect the equilibrium solubility of nicotinate-curcumin ester in various solutions. The apparent oil/water partition coefficients in octanol-water and octanol-buffer solution system were measured by a shaking-flask method. Results:The solubility of nicotinate-curcumin ester in pH 6.8 was the highest. The apparent oil-water partition coefficients of nicotinate-curcumin ester in pH 1.2,5.8,6.5 and 7.8 were lgPapvalues within the range(lgPap=1.69-1.98) beneficial to the absorption in vivo. But in pH 2,5 and 6.8,the lgPapvalues were greater than 2 with strong lipophilicity. Conclusion:The equilibrium solubility as well as ap-parent oil/water partition coefficients of nicotinate-curcumin ester is greatly influenced by the pH value of media. In the pH value with relatively high solubility,lipophilicity is stronger,suggesting it is difficult to be absorbed by the body and needs to be further studied on dosage forms.
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Objective:To explore the effects of the process parameters of film dispersion-ultrasonic method on particle diameters and encapsulation efficiency of solid lipid nanoparticles of nicotinate-curcumin in order to obtain the process parameters resulting in smaller particle diameters and higher encapsulation efficiency .Methods: The content of nicotinate-curcumin was determined by HPLC.With the particle diameters and encapsulation efficiency of solid lipid nanoparticles of nicotinate -curcumin as the evaluation in-dicators , the process parameters of film dispersion-ultrasonic method were optimized by orthogonal experimental design and 95％confi-dence interval overlap method as the statistical analysis .Results:The optimum technological parameters of the solid lipid nanoparticles were as follows:the water bath temperature was 40℃and the rotation speed of eggplant bottle was 80 r· min-1 .The average particle size of solid lipid nanoparticles was 107.8 nm, polymer dispersity index ( PDI) was 0.583, and the encapsulation efficiency was 68.91％.Conclusion:The rotation speed of eggplant shaped bottle has notable influence on the particle diameters of solid lipid nanop -articles of nicotinate-curcumin prepared by film dispersion-ultrasonic method , while the water-bath temperature shows great influence on the encapsulation efficiency .Under the optimum conditions , it is possible to obtain the solid lipid nanoparticles with relatively smaller average particle diameters and higher encapsulation efficiency .
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Objective: To provide basis for the preparation process study by establishing an HPLC determination method for nicotinate-curcumin ester.Methods: A C18 column(250 mm×4.6 mm,5 μm) was used at 30℃ with the mobile phase of acetonitrile-0.5% acetic acid glacial(65∶35) at a flow rate of 1.0 ml·min-1.The UV detection wavelength was 280 nm.Results: The good linear relationship of nicotinate-curcumin ester was shown within the range of 5.200-104.000 μg · ml-1(r=0.9999 4), The average recovery of nicotinate-curcumin ester and its nanoparticles was 100.1% and 100.9%with RSD of 1.260% and 0.995 0%(n=6), respectively.Conclusion: The method is convenient, accurate and reproducible, and suitable for the determination of nicotinate-curcumin ester nanoparticles and the studies on the preparation technology.
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Aim To explore the anti-proliferation effects of curcumin trinicotinate ( CurTn ) on vascular smooth muscle cell ( VSMC ) and its mechanism. Methods The cells were cultured in DMEM supple-mented with 10% fetal bovine serum. MTT assay was used to examine cell proliferation. FCM was used to observe cell cycle. The expressions of PCNA, Cy-clinD1 and p-ERK1/2 were analyzed using Western blot. Results CurTn could inhibit the proliferation of VSMC and showed a certain amount-time relationship. What’ s more, CurTn could increase the G1 phase pro-portion of cell, decrease the S phase proportion and the expression level of PCNA protein. It was also found that CurTn significantly inhibit the protein expression of p-ERK1/2 and Cyclin D1 . Conclusion CurTn may inhibit the proliferation of VSMC via downregulating the expression of CyclinD1 and p-ERK1/2 .
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Objective To explore the effects of the Chinese medicine, modified Erchen decoction, on the serum lipid spectrum of ApoE-/-mice, and to explore its possible anti-atherosclerotic mechanism.Methods Forty-four male 7-8-week old ApoE-/-mice were used in this experiment.ApoE-/-mouse models of atherosclerosis were generated by high-cholesterol diet for 4 weeks.And then, they were given simvastatin or modified Erchen decoction by gavage.The body weight of mice was recorded every week, The mice were sacrificed after treated with the drugs for 8 weeks continuously, and the plasma lipid was determined by enzymatic method.The aortic valves and arches were stained with oil red O to depict atherosclerotic plaques and liver structural changes of the mice were examined by pathology.Results Modified Erchen decoction lowered plasma lipid ( including TCHOL and LDL-C ) significantly ( P<0.01 ) .The body weight was increased in the mice of all groups, but it was more pronounced in the mice of model group than in the blank and modified Erchen decoction groups.The serum CHOL and LDL-C levels were significantly lowered in the modified Erchen decoction group (P<0.01).The area of atherosclerotic plaques in the aortic wall was significantly reduced in the mice of modified Erchen decoction group as shown by oil red O staining.The pathological changes of hepatocytes were less severe and the structure of hepatic lobules was better preserved in the mice of modified Erchen decoction group.Conclusions The Chinese medicin modified Erchen decoction can effectively reduce serum lipids, regulate lipid metabolism, and ameliorate the process of atherosclerosis in ApoE-/-mice.
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Objective To establish a stable and efficient method of culturing imDCs in vitro,and to explore the effect of GW5074, which blocks ERK1/2 signal pathway in the process of imnature dentritic cells (imDCs) on inducing differentiation of the na(i)ve allogeneic CD4+ T cells into Treg cells in vitro. Methods The imDCs and mature DCs (mDCs) were isolated and cultured from the peripheral blood mononuclear cells (PBMC) derived from a healthy adult male volunteer, and they were identified by cell morphology, cell surface marker and cell functions respectively. Na(i)ve CD4+ T cells were isolated from newborn umbilical vein blood and were divided into 5 groups to be cultured: (1) Blank control group: Na(i)ve CD4+ T cells were cultured alone;(2) Positive control group: The irrDCs were Middle-concentration GW5074 group;(5) High-concentration GW5074 group. In the last three groups, imDCs and na(i)ve CD4+ T cells were co-cultured, the same as the positive control group, but these groups were added by GW5074 dilution at the concentrations of 8, 24, and 40μmol/Lrespectively. After co-culture for 5 days, the transformation ratio from naive CD4+T cells to Treg T cells was detected by flow cytometry. Results On the surface of imDCs, there was stronger pression of CD1a, but weaker expression of CD80 and CD83. On the contrary, on the surface of mDCs, there was weaker expression of CD1a, but stronger expression of CD80 and CD83. The stimulation index in imDCs group and mDCs group was 1.12±0.03 and 2.85±0. 07 respectively. The transformation ratio of Treg T cells in blank control group, positive control group, low-concentration GW5074 group, middle-concentration GW5074 group and high-concentration GW5074 group was (5. 81±1.36)%, (35.73±2.07)%, (22.53±2.11)%, (11.55±1.73)%, and (4.97±1.83)%respectively. One-way ANOVA analysis revealed that there was no significant difference between high-concentration GW5074 group and blank control group, P＞0. 05, but significant difference between the remaining groups, P＜0.01. Conclusion High purity of imDCs can be obtained from PBMC by induction with rhGM-CSF and rhIL-4. ERK1/2 signal pathway plays a role in inducing the immune tolerance. GW5074 can inhibit differentiation of na(i)ve CD4+ T cells into Treg T cells.
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Aim To investigate the effect of intestinal cholesterol absorption inhibitor Ezetimibe on lipid accumulation in RAW264.7 cells and identify the underlying mechanism.Method RAW264.7 cells were pretreated with the indicated concentrations of Ezetimibe (0,0.003,0.01 and 0.03 mol·L~(-1))for 24 hours or pretreated with the optimal concentration(0.03 mol·L~(-1))of Ezetimibe for different periods (0,6,12 and 24 h),followed by incubation with 50 mg·L~(-1) oxLDL for 24 hours,then the number of intracellular lipid droplets and lipid content were measured by using oil red O staining and HPLC; the expression of NPC1L1 was measured by Western blot.Results Pretreatment with indicated concentrations of Ezetimibe caused a concentration-dependent inhibition of intracellular lipid accumulation;pretreatment with 0.03 mol·L~(-1) Ezetimibe caused a time-dependent inhibition of intracellular lipid accumulation.It was noted that pretreatment with 0.03 mol·L~(-1) Ezetimibe for 24 hours inhibited CE by about 47%+0.1% compared with control group(oxLDL alone).Immunoblotting results showed that NPC1L1 was expressed in RAW264.7 cells and it was down-regulated after Ezetimibe treatment.Conclusions Ezetimibe causes concentration-dependent and time-dependent inhibition of lipid accumulation in RAW264.7 cells;it also reduces NPC1L1 expression in RAW264.7 cells.
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In order to study the effects and the possible mechanisms of Daxx overexpressed in HepG2 to hydrogen peroxide treatment, and to search new targets for cancer chemotherapy, HepG2cells were transfected using lipofectamine 2000, and selected by treatment with G418. Stable cell lines were confirmed by reverse transeriptase polymerase chain reaction (RT-PCR) targeting vector gene. Experiments include the following groups: (1) control group (non-transfected cells); (2) transfected with empty vector (HepG2/GFP cells); and (3) transfected with pEGFP-C1-Daxx (HepG2/GFP-Daxx cells). After incubation with hydrogen peroxide (H2O2) for 24 h, cellular viability was analyzed by MTT, and cellular apoptosis was measured by flow cytometric analysis. Gene expression at protein level was detected by Western blot. The RT-PCR results showed that Daxx RNA in cells transfected with pEGFP-C1-Daxx was increased significantly compared with that in the HepG2/GFP cells. Fluorescence microscopy revealed that Daxx protein was localized in the nuclei. Hydrogen peroxide was used to induce apoptosis of HepG2 cells and observed that the hydrogen peroxide decreased the viability of HepG2 cells in concentration-dependent pattern. The IC50 values in three groups (Normal cells, HepG2/GFP cells and HepG2/GFP-Daxx cells) were 0.72, 0.76, and 0.49 mmol/L respectively. The apoptotic ratio was significantly higher in HepG2/GFP-Daxx cells as compared to the other two groups. HepG2/GFP-Daxx cell incubated with hydrogen peroxide, showed a significant increase in the activation of caspase-3 and JNK as compare with the other groups. Over-expression of Daxx facilitated HepG2 cells apoptosis induced by hydrogen peroxide. Furthermore, there may be a synergetic relation with apoptosis and increase of JNK activity.
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AIM: To elucidate the effects of losartan on the expression ofmatrix metalloproteinases-2, JNK1/2 and proliferation in cardiac fibroblast. METHODS: Neonatal rat cardiac fibroblasts were cultured. The cells proliferation was determined by MTT. To determine effects of AngⅡ on JNK1/2 activity, cells were incubated (for 0, 2, 5, 10, 30, 60, 120 min) in serum-freemedia with AngⅡ, and the other group fibroblasts were exposed to serum-free media with or without AngⅡ and losartan (AngⅡ 100 nmol/L, AngⅡ 100 nmol/L+losartan 100 nmol/L, losartan100 nmol/L, losartan for 45 min before). Cells protein was collected with MBST buffer. The relative abundance of MMP-2, JNK1/2 and p-JNK1/2 in cells was determined by immunoblotting. The secretion of MMP-2 in media of cell culture was determined by ELISA. RESULTS: AngⅡ increased the proliferation of CFB in a dose-dependent manner, whereas losartan decreased the proliferation of CFB stimulated by AngⅡ in a dose-dependant manner, too (P＜0.05). The relative abundance of JNK1/2 was highest in AngⅡ of the 2-min-stimulated group. AngⅡincreased expression of JNK1/2 and MMP-2 protein (P＜0.05), on the contrary, losartan inhibited JNK1/2 and MMP-2 protein expression.CONCLUSION: AngⅡ induce the increase of proliferation of CFB, expression of JNK1/2 and MMP-2 in CFB, and losartan inhibits these effects of AngⅡ.
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Objective To investigate the effect of angiotensin Ⅱ-1 receptor antagonist losartan on expression of tumor necrosis factor-alpha (TNF-?) in the ventricular myocardium in the renovascular hypertension rats. Methods Renovascular hypertension model was obtained by clip left renal artery in Sprague-Dawley(SD) rats. After operation the rats were divided into 3 groups: sham group, two-kidney one clip (2K1C) group, and losartan treatment group(2K1C and losartan 20 mg/kg?d by drinking). Tail blood pressure was determined every week. Animals were euthanized after treatment with losartan for four weeks. Cardiac index(CI)was calculated by HW/BW, and TNF-? protein of ventricle myocardium was determined by ELISA and immunohistochemistry. Results Losartan significantly decreased blood pressure(P
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To produce monoclonal antibody (mAb) specifically against human thrombomodulin (hTM), an immune-tolerizing procedure was employed to generate monoclonal antibodies specific to hTM. Female BALB/c mice were first immunized with CHO cells following at 10 min, 24 h, 48 h by intraperitoneal injection of different doses of cyclophosphamide (CP) 2 times at an interval of 2 weeks, thereby tolerizing the mice to common epitopes shared between CHO and CHO-TM5 cells. Subsequently the selected mice with the lowest titer of serum polyclonal antibody by cellular enzyme-linked immunoabsorbent assay (CELISA) were immunized with CHO-TM5 cells, which have stable high level expression of hTM, to produce antibodies specific to hTM 3 times at an interval of 2 weeks. On the third day after the third immunization, mouse with the highest titer of serum polyclonal antibody was sacrificed and spleen cells were harvested to prepare hybridoma cells with SP2/0 cells at the ratio of 10 to 1. Hybridoma cells were then cultured at 96 well plates for screening with CELISA. To improve probability to obtain specific mAb, CELISA was applied twice. The first CELISA was done with polyethylene ELISA plate with a monolayer of CHO-TM5 cells. The positive clones from the first screen were then selected by reacting with similar screening ELISA plate but having CHO cells monolayer instead. Only clones that were positive for the first screening and negative for the second screening were kept, and called as CHO-TM5 +CHO- hybridoma cells. BALB/c mice were intraperitoneally injected with the selected hybridoma cells. Ascites were collected and monoclonal antibodies were purified using FPLC, and its Ig class, subclass, and titer were then determined respectively. The specificity of the yielded mAb was identified with CELISA, flow cytometry, ABC immunohistochemistry and immunoblotting. Detection of CELISA showed that 100 mg/kg dose of CP could tolerize the mouse to common epitopes shared between CHO and CHO-TM5 cells. And CELISA also discovered that all hybridomas positive for CHO-TM5 cells were negative for CHO cells. Five lines of positive hybridoma cells had been obtained altogether and 2F7 was selected randomly for next investigation. The Ig subclass of the mAb 2F7 was IgG1 and the titer of ascitic mAb was 1?10-6. Furthermore, the content of ascitic mAb was 19.56 g/L and chromosome numbers is 98. Flow cytometry, CELISA and Western blotting assays demonstrated that mAb 2F7 could specifically recognize hTM expressed on CHO-TM5 and human umbilical vascular endothelial cells (HUVEC). Meanwhile, the tissue specificity of mAb 2F7 was also identified by immunohistochemical ABC staining. On the other hand, Western blotting assays indicated that mAb 2F7 could recognize the antigen protein with 105 ku molecular mass under reduction condition. Moreover, the dissociation constant of mAb 2F7, 1.22? 10-9 mol/L, indicated the affinity higher than some others. The results suggest that the immunotolerizing protocol provides a convenient general method for producing antibodies specific to desired protein isoforms. mAb 2F7 can specifically recognize the natural hTM expressed mainly on vascular endothelial cells, which will potentially useful for investigating the functions and clinic values of hTM.
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Aim To study the effects of probucol on THP-1 macrophage apoptosis and CD36、Caveolin-1 expression induced by ox-LDL.Methods Apoptosis of THP-1 macrophages was determined by flow cytometry analysis.RT-PCR and immunofluorescence were used to detect CD36,Caveolin-1 mRNA level and protein expression respectively.Results Probucol had no effect on mRNA level of CD36,Caveolin-1 in THP-1 macrophages,but it attenuated Caveolin-1 protein expression.Conclusions Probucol can inhibit apoptosis induced by ox-LDL in THP-1 macrophages by down-regulating Caveolin-1 protein expression.
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Aim To study the effect of Macrophage colony-stimulating factor(M-CSF) on MMP-9 in RAW 264.7 cell and explore the relationship between atherosclerosis caused by M-CSF and the activity of MMP-9. Methods Gelatin zymography analysis was used to investigate the effect of M-CSF and PD98059 on the activity of MMP-9 in cultured RAW 264.7 cell.Western blot was used to study the effect of M-CSF and PD98059 on the express of p-ERK1/2 in cultured RAW 264.7 cell. Results The enzyme activity of MMP-9 was significantly increased after 24-hour M-CSF treatment.Meanwhile, M-CSF upregulated the expression of p-ERK1/2. Pre-treatment with PD98059 blocked partly the increased expression of p-ERK1/2 and the activity of MMP-9 induced by M-CSF. Conclusion M-CSF can induce the secretion of MMP9 in RAW 264.7 cell, which may be mediated by the phosphorylation of ERK1/2.
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Aim To study the interference role of Bcl-2 siRNA on HL-60 cells. Methods Bcl-2 siRNA was synthesized in vitro transcription with silencer siRNA construction kit. The synthesized siRNA was transfected into HL-60 cells with lipid siPORT transfection. Forty-eight hours after the transfection, we used MTT and immunofluorescence to detect cell proliferation and apoptosis,and used RT-PCR and immunofluorescence to detect the level of Bcl-2 mRNA and Bcl-2 protein expression. Result Bcl-2 siRNA reduced the level of Bcl-2 mRNA and Bcl-2 protein expression in HL-60 cells and induced cell apoptosis. There was no difference on the effect of other groups compared with the control. Effective Bcl-2 siRNA specifically degraded Bcl-2 expression in the levels of mRNA and protein and induced HL-60 cells apoptosis.Conclusion These results indicate that siRNA is a highly specific tool for targeted gene knockdown. siRNA-mediated gene silencing is a reliable approach for large-scale screening of gene function and drug target validation.
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To deepen the teaching reform on comprehensive medical function experiment in our school,the mode of opening system of experiment teaching of medical function is proposed.The definition and characteristics of the opening system is discussed in this paper,and its theoretical foundation,guideline,goal location,effect and pending problems are also explored preliminarily.
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<p><b>OBJECTIVE</b>To study the features of vascular smooth muscle cell (VSMC) proliferation induced by endothelin-1 (ET-1).</p><p><b>METHODS</b>VSMCs of spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats were cultured and treated with ET-1. Basic fibroblast growth factor (bFGF) gene expression was measured using both Northern blot and an enzyme-linked immunoassay.</p><p><b>RESULTS</b>ET-1 resulted in an increase in bFGF transcripts at 8 - 24 h; bFGF levels were significantly higher in VSMCs treated with ET-1 than in those not treated. However, VSMCs growth responses in SHR and WKY were different. Smooth muscle cells of SHR were hyper-responsive to ET-1. Maximal bFGF mRNA levels were elevated 3.5-fold at 4 h of stimulation in WKY and 8-fold at 8h in SHR4. Moreover, the proliferation of VSMCs induced by ET-1 was inhibited by antisense phosphorothioate oligodeoxynucleotides (10 micromol/L AS-bFGF) but not sense bFGF oligomers at the same concentrations, being reduced by 80% in SHR and 40% in WKY vs control, respectively. Furthermore, the effect of AS-bFGF oligomers on SHR SMC proliferation is significantly greater than on WKY SMC proliferation.</p><p><b>CONCLUSION</b>ET-1 may be required for exaggerated vascular growth responses in SHR and bFGF may be involved.</p>
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Animales , Ratas , División Celular , Células Cultivadas , ADN sin Sentido , Farmacología , Relación Dosis-Respuesta a Droga , Endotelina-1 , Farmacología , Factor 2 de Crecimiento de Fibroblastos , Genética , Regulación de la Expresión Génica , Músculo Liso Vascular , Biología Celular , Metabolismo , Oligonucleótidos , Farmacología , ARN Mensajero , Genética , Metabolismo , Ratas Endogámicas SHR , Ratas Endogámicas WKY , Factores de TiempoRESUMEN
Objective To study the effect of caveolin-1 gene expression on the proliferation of human gastric adenocarcinoma cells,and to explore the possibility for its future usage in gene therapy.Methods The full-length caveolin-1 gene was stably transfected into the MGC803 cell line by lipofectin.The Pcl neo vector was transfected at the same time as mock control.The expression of caveolin-1 was detected by Western blot in both the caveolin-1 gene transfected MGC803 cells and the controls.The cell cycle was analyzed by flow cytometry.Results After transfected with caveolin-1,MGC803 cells significantly up-regulated the expression of caveolin 1 and extended their doubling time.The cell proliferation was inhibited and the cell cycle was arrested in the G_0/G_1 phase.Conclusion Caveolin-1 can inhibit the proliferation of MGC803 cells and induce cell cycle arrest in G_0/G_1 phase.
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AIM: To investigate the relationship between the prevention of probucol on restenosis and vascular remodeling after percutaneous transluminal angioplasty(PTA) in rabbits. METHODS: New Zealand rabbit thoracic aorta atherosclerosis was induced by 3.5F ballon catheter injury following a 4-weeks feeding of high cholesterol diet, and PTA was performed by using 3.5F balloon catheter. Probucol(1g/d) or vitamin E (400 mg/d) was administrated one week before PTA. Two weeks after PTA, the bore and outside diameter (OD) of arteries, the area circumscribing by intimal elastic lamina (IEL), the area circumscribing by extral elastic lamina (EEL), medial area (MA), neointima area/medial area (NEA/MA) were analyzed by computerized digitizer system. Lipids of serum were measured by means of biochemical assay.RESULTS: After two weeks of PTA, the intima proliferation and lumen restenosis were observed obviously. However, with probucol treatment for 3 weeks, the restenosis of aorta was inhibited significantly by increasing bore, outside diameter, and lumen area of rabbits aortas and decreasing NEA, NEA/MA. Furthermore, probucol regulated vascular remodeling by increasing the area circumscribing by IEL [(3.50?0.20)mm 2 vs (1.59?0.23) mm 2, P
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Object To investigate the effects of tetramethylpyrazine (TMP) and Danshen (DS) on the growth and metastasis of Lewis lung carcinoma and tumor angiogenesis. Methods C 57BL mice with Lewis lung carcinoma were used in this study, which were injected respectively with TMP injection 50, 100, and 200 mg/(kg?d) and DS injection 5, 10, and 20 g/(kg?d), ip, for 21 days. Then the volume, weight, and numbers of the metastatic foci on lungs, tumor microvessel density (MVD) were determined, the expression of vascular endothelial growth factor (VEGF) of Lewis lung carcinoma was observed. Results TMP could remarkably reduce the volume, weight, and numbers of the metastatic foci, MVD, and the expression of VEGF of Lewis lung carcinoma. But DS did not show remarkably effect on Lewis lung carcinoma. Conclusion TMP can remarkably inhibit the growth and metastasis of Lewis lung carcinoma on mice, and its mechanism might be relative to inhibiting the expression of VEGF and angiogenesis. DS injection has no remarkably effect on Lewis lung carcinoma.