In this paper we analysed the influence of water—abstracts of Huangqi on the anti — tumour effects of polyresistin oral use. Results showed Huangqi could strengthen the anti—tumour effects of polyresistin. As in the group treated with Huangqi— polyresistin the reaction of spleen T cells to Con—A stimulation increased, but the viability of tumour cells decreased. Huangqi—Polyresistin prolonged the survival term of tumourborne mice and lowered their mortaity. Based on the facts that polyresistin is peptidoglycan,Polyresistin can activate monocyte—macrophage system and Huangqi induce the production of IFN?. We think the positive regulation of IFNr on the synthesis and cytotoxic—effect of TNF? may be one of the most important mechanisms of Huangqi to strengthen the anti— tumour effects of polyresistin.

Otjective To study whether there is the apoptosis of neural cells and the expressionof Bcl-2 protein in intracerebral hemorrhage (ICH) in model of rats, for the further understanding the mechanism of the delayed damage of the neural cells around the hematoma after ICH. Methods Fifty SD rats were randomly divided into 5 groups, ten in each. With the Group A as the control, the rest 40 were used to set up intracerebral hemorrhage model. The brains were taken out at 12th, 24th, 48th and 72th hours, respectively. Apoptosis cells were detected with terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL), and the expression of Bcl-2 protein was detected with immunochemical stainging methed (SP). Results In the control group, no apoptosis cells and Bcl-2protein were detected. In rest groups, the apoptosis cells and Bcl-2 protein were expressed in different degree.Apoptosis rates verified and corresponded with the time after ICH, with the peak at 48th -72th hour after hemorrhage.The peak rate of apoptosis cells was (24. 50± 2.69)% and Bcl-2 protein expression was (20. 76 ± 1.97)% . There was significant difference between the experimental groups and control (P＜0.05), and no linear relationship between the apoptosis rate and the expression of Bcl-2 protein. Conclusion Apoptosis may be an important factor in the secondary trauma of ICH. There is a time leg after hemorrhage. All this is instructive to clinical treatment in time. Bcl-2 protein keeps increasing in a certain time after hemorrhage, but not synchronize with the cell apoptosis. This indicates that bcl-2 has the effect to reduce the apoptosis of neural cells.

OBJECTIVETo investigate the regulatory mechanism of bone marrow mesenchymal stem cells(BMSC) on the biological profiles of KATO-III( cell lines of gastric cancer.

METHODSTranswell cubicle was applied to build the co-cultured model in non-contact style. The differences of cell proliferation and the resistance of anti-tumour drug (5-fluoropyrimidinedione, 5-FU and Cisplatin, CDDP) between co-cultured group and single cultured group were evaluated by Cell Counting Kit 8-assay(CCK-8). The invasion ability was detected by Transwell assay. The expressions of stem cell makers, apoptosis-related factors and epithelium-mesenchymal transition (EMT)-related factors were detected by RT-PCR.

RESULTSThe proliferation ability of KATO-III( cells in co-cultured group was significantly stronger than that in single cultured group. The growth rate of KATO-III( cells in co-cultured group was significantly higher than that in single cultured group after treatment of 5-FU and CDDP(P<0.05). The mRNA expression level of Bcl-2 was significantly higher in co-cultured group KATO-III( cells(P<0.05), while the mRNA expression level of Bax was significantly lower in co-cultured group KATO-III( cells(P<0.05) in comparison with those in single cultured group. As compared to KATO-III( cells in single cultured group, the number of infiltrating-membrane cells was significantly higher (37.33±5.22 vs 14.56±2.54, P<0.01) in co-cultured group, and the mRNA expression levels of Snail and N-cadherin were significantly higher in co-cultured group KATO-III( cells (P<0.05), while the mRNA expression level of E-cadherin was significantly lower in co-cultured group KATO-III( cells (P<0.05). The expressions of CD133, Nanog and Sox-2 mRNA in co-cultured group KATO-III( cells were significantly higher than those in single cultured group(P<0.05).

CONCLUSIONSIn co-cultured model sharing non-contact style, BMSC can enhance such properties of KATO-III( gastric cancer cells as the proliferation, the invasion and the chemoresistance. Furthermore, the regulatory mechanisms may be related to the increase of the expressions of some stem cell markers in gastric cancer cells.

Antineoplastic Agents ; Apoptosis ; Bone Marrow Cells ; Cadherins ; Cell Line, Tumor ; Cell Proliferation ; Cisplatin ; Coculture Techniques ; Epithelial-Mesenchymal Transition ; Fluorouracil ; Humans ; RNA, Messenger ; Stem Cells ; Stomach Neoplasms