OBJECTIVETo study the effect of acupuncture on tumor and its mechanism.

METHODSLiver cancer, gastric cancer and hypodermic tumor rat models were made by implantation of replicated Walker-256 cell strain. The 3 model rats were respectively divided into two groups at random, a model control group and an electroacupuncture group. The electroacupuncture groups were treated with electroacupuncture (EA) at "Zusanli" (ST 36), "Hegu" (LI 4) and "San-yinjiao" (SP 6), once each day, 15 min one session, for 15 days. The gross tumor volume and the tumor inhibitory rate, and the levels of humoral immunity index, including serum 1gG, IgM, IgA and C3, C4, and the levels of cellular immunity index, including CD4+, CD8+ and CD4+/CD8+ in the peripheral blood in each group were detected.

RESULTSThe gross tumor volumes in the EA groups were significantly smaller than those in the model control group (P<0.01). The contents of IgG, IgM and C3 in the EA groups increased significantly compared with those in the model control group (P<0.05 or P<0.01). The contents of IgA and C4 in the EA groups did not significantly change (P>0.05). The content of CD4+ and CD4+/CD8+ in the EA groups are significantly higher than those in the model control group (P<0.05 or P<0.01).

CONCLUSIONAcupuncture at "Zusanli" (ST 36), "Hegu" (LI 4) and "Sanyinjiao" (SP 6) can increase immune function and inhibit tumor growth in Walker-256 liver cancer, gastric cancer and hypodermic tumor rats.

Animals ; Carcinoma 256, Walker ; immunology ; pathology ; therapy ; Electroacupuncture ; Male ; Rats ; Rats, Wistar

OBJECTIVETo establish an animal model of tumor-associated depression and observe their biological behaviors and biochemical indices.

METHODSFour groups of SD rats kept in separate cages were subjected to tumor cell inoculation with or without chronic unpredictable moderate stress administered before or after the inoculation. The depressive behaviors of the rats were examined by open-field test, and the concentration of 5-HT in the hippocampus was measured by spectrophotofluorometry. The body weight of the rats and volume of the implanted tumor were monitored and sugar water test was performed.

RESULTSThe rats subjected to chronic stress displayed significant depression, manifested by reduction in movement in the central area and total movement distance with prolonged resting time and shortened time of activity. These rats maintained high levels of depression even 12 days after withdrawal of chronic stress. Compared with the control group, the depressive rats showed obviously reduced sugar water consumption and hippocampal 5-HT level. Tumors of different sizes were observed in all rats in the 4 groups.

CONCLUSIONA rat model of tumor-associated depression is established, and the tumor-bearing rats exhibit obvious depressive behaviors and reduced level of neural substance (5-HT), which provides a good basis for studying the association of depression with tumorigenesis,progression and prognosis of tumor.

Animals ; Carcinoma 256, Walker ; complications ; psychology ; Depressive Disorder ; etiology ; Disease Models, Animal ; Female ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Stress, Psychological ; complications

OBJECTIVETo study the histopathological effect of hepatic arterial infusion of lipiodol on transplanted hepatoma in rats.

METHODSFourty-one rats bearing Walker-256 transplanted hepatoma were randomly divided into embolization group (n = 35, divided in 5 subgroups, with 7 rats in each) and control group (n = 6). Lipiodol (0.5 ml/kg)emulsified with 0.2 - 0.3 ml of 76% urografin (v:v = 1:1) was infused via gastroduodenal artery into hepatic artery in embolization group. Rats in the control group were given via the same route urografin only. Histopathological changes of the treated tumors were examined by light and transmission electron microscopy.

RESULTSIn the control rats treated with urografin alone, the average tumor size increased 2.8 fold on day 3, while that in the lipiodol treated rats increased 1.7 fold (P < 0.01). Compared with the control group, on day 3, 5, 10 after embolization treatment, tumor necrosis was more extensive (P < 0.01). In one of the treated rats, the tumor was completely necrotic on day 10. Inflammatory reaction was marked in the early post-embolic period, but it was replaced by fibrous tissue encapsulation. From day 1 on, in 17 of the 18 treated rats, apoptotic cells, identified by typical morphology under light and electronic microscopes, were observed, mainly in the tumor periphery.

CONCLUSIONIn addition to cellular necrosis, apoptosis may be another important mechanism leading to cell death in hepatoma treated with transarterial embolization.

Animals ; Apoptosis ; Carcinoma 256, Walker ; pathology ; therapy ; Chemoembolization, Therapeutic ; Iodized Oil ; therapeutic use ; Liver Neoplasms, Experimental ; pathology ; therapy ; Male ; Necrosis ; Neoplasm Transplantation ; Random Allocation ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the main mechanisms of Aitongxiao Recipe (ATXR) for anti-tumor at the molecular level, and to clarify different efficient drugs' roles in anti-tumor, thus in-depth explaining the objectivity and substance of "cancer toxic" theory.

METHODSWalker-256 tumor strain was used for Wistar rat transplanted liver cancer modeling. After successful modeling rats were randomly divided into 5 groups, i. e., the ATXP group, the qi regulating and blood circulating group (as the assembled I group), the heat clearing and detoxification group (as the assembled II group), the body resistance strengthening and cultivating group (as the assembled III group), and the model group, 10 in each group. Corresponding medication was given to rats in each group for 14 successive days. Finally rats were sacrificed and the tumor mass was taken out. The apoptosis rate and the cell cycle of tumor cells were detected by flow cytometry Annexin V/PI. The protein and mRNA expressions of Bcl-2 and survivin were detected using immunohistochemistry and real-time fluorescent quantitative PCR.

RESULTS(1) The apoptosis of hepatoma carcinoma cells could be obviously promoted in the ATXP group. The cell cycle could also be affected, making major cells arrest at G0/G1 phase. The proliferation of hepatoma carcinoma cells was effectively prevented. The efficacy in the assembled II group was in line with that in the ATXP group with no statistical difference (P>0.05). It was also effective in the assembled III group, but its efficacy was not as good as that in the former two groups, showing statistical difference (P<0.01). (2) ATXP could obviously down-regulate the protein and mRNA expressions of Bcl-2 and survivin in hepatoma carcinoma cells. Drugs for heat clearing and detoxification showed significant effects on down-regulating the protein and mRNA expressions of Bcl-2 and survivin in hepatoma carcinoma cells. Their effects were similar to that of ATXP (P>0.05). The effects of drugs for body resistance strengthening and cultivating were not as good as the former two, showing statistical difference (P<0.01). Drugs for blood circulating and stasis removing could up-regulate the protein and mRNA expressions of Bcl-2 and survivin to some extent.

CONCLUSIONS(1) ATXP could increase the apoptosis ratio of hepatoma carcinoma cells obviously through down-regulating the protein and mRNA expressions of Bcl-2 and survivin, thus inhibiting their proliferation. (2) Drugs for heat clearing and detoxification played the most important roles in ATXP. The evil heat and dampness (damp-heat insidious pathogen) is the most fundamental carcinogenic factors. The insufficiency of vital qi is also one of the pathogenic factors. The mechanisms of phlegm, stasis, and other pathological products are not clear and await further studies.

Animals ; Apoptosis ; Carcinoma 256, Walker ; metabolism ; Carcinoma, Hepatocellular ; metabolism ; pathology ; Cell Cycle ; Cell Line, Tumor ; Drugs, Chinese Herbal ; pharmacology ; Liver Neoplasms ; metabolism ; pathology ; Male ; Microtubule-Associated Proteins ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Rats ; Rats, Wistar

This experimental study was designed to investigate the effects and the expressions of microvessel density (MVD), vascular endothelial growth factor (VEGF) on the transplanted tumor in the rat model with Walker-256 after energy controllable steep pulse(ECSP). The experiment revealed that the steep pulse electrical field has better effect on tumor, compared with the control. The positive cell staining intensity of VEGF in the control group was significantly higher than that in ECSP group (P < 0.05). The number of MVD in the tumor tissues of ECSP group was significantly lower than that of tumor control group (P < 0.05). These results showed that ECSP could inhibit the growth and angiogenesis of tumor and its pathway is to down-regulate the expression of VEGF possibly.
Animals ; Carcinoma 256, Walker ; blood supply ; therapy ; Electric Conductivity ; Electric Stimulation Therapy ; methods ; Electromagnetic Fields ; Electroporation ; methods ; Female ; Male ; Neovascularization, Pathologic ; Rats ; Rats, Wistar ; Vascular Endothelial Growth Factor A ; metabolism

This study sought to evaluate the effect of steep pulsed electric fields (SPEFs) on the immune response of Wistar mice inoculated with Walker256 sarcoma. Thirty mice were randomly divided into three groups: control group (group A, inoculated with Walker256 sarcoma, not treated), treatment group (group B, inoculated with Walker256 sarcoma, treated by SPEFs), and normal control group (group C, inoculated with normal saline, not treated). Tumor size was measured before and every 3 days after treatment by vernier caliper. MTT methods were used to assess the lymphocytes proliferation and the natural killer (NK) cells activity. TNF-a activity was measured by ELISA. Statistical analysis was performed utilizing the SPSS10.0 software package. The experiment results revealed that tumor growth was significantly inhibited in group B as compared with group A (P < 0.01), and that lymphocytes proliferation, NK cells activity and TNF-a activity in group B were not significantly different from those in group C (P = 0.953, P = 0.130, P = 0.080, respectively) but markedly higher than those in group A (P < 0.05). The results also showed that SPEFs could not only kill tumor cells but also induce antitumor immune response and improve the immune function of the host efficiently.
Animals ; Carcinoma 256, Walker ; immunology ; pathology ; therapy ; Electromagnetic Fields ; Female ; Killer Cells, Natural ; immunology ; Leukocytes ; immunology ; Lymphocyte Activation ; Male ; Mice ; Neoplasm Transplantation ; Pulse ; Random Allocation ; Spleen ; cytology ; Tumor Necrosis Factor-alpha ; biosynthesis

OBJECTIVETo investigate the anticancer effects of Erbie San on the rats bearing Walker-256 liver cancer and the potential mechanism of its angiogenesis effects.

METHODWistar rats bearing Walker-256 liver cancer were used in this study. The experimental groups were treated with Erbie San 1.25, 2.5, 5 g x kg(-1) x d(-1), and 5-Fluorouracil injection 75 mg x kg(-1), respectively. The tumor's weight, the expression of VEGF, Endostatin and the ratio of VEGF/endostatin in serum of each groups were observed.

RESULTCompared to the model group, Erbie San 2.5, 5 g x kg(-1) x d (-1) and 5-Fluorouracil injection groups can reduce the tumor's weight significantly (P<0.05 or P<0.01). The expression of VEGF was reduced, while endostatin was increased, and the ratio of VEGF/endostatin was reduced (P<0.05 or P<0.01).

CONCLUSIONErbie San can effectively inhibit the growth of Walker-256 liver cancer of rats and can inhibit the expression of VEGF but increase the expression of endostatin, which suggest that Erbie San has the inhibition of angiogenesis which is responsible for its anticancer effects.

Animals ; Carcinoma 256, Walker ; blood ; pathology ; Drugs, Chinese Herbal ; pharmacology ; Endostatins ; blood ; Gene Expression Regulation, Neoplastic ; drug effects ; Liver Neoplasms ; blood ; pathology ; Male ; Neovascularization, Pathologic ; blood ; pathology ; Rats ; Rats, Wistar ; Tumor Burden ; drug effects ; Vascular Endothelial Growth Factor A ; blood