ABSTRACT
Objective: To explore the inhibitory effect of Shiquandabu decoction on the spontaneous len tumor of the SV40 T antigen transgenic (TG) mice, and to clarify its molecular mechanism. Methods: The SV40 T antigen TG mice were randomly divided into control group (n=39) and drug treatment group (n=25). The mice in control group were fed normally, while the mice in drug treatment group were fed with Shiquandabu decoction at the 3rd week after birth, the survival time of mice was recorded. Three mice in control group and drug treatment group were randomly chosen to collect the blood from the tail vein and the amino acid levels were measured respectively 8 and 15 weeks after Shiquandabu decoction administration. Then the mice were sacrificed and the liver tissue was collected. Gene chip hybridization was used to detect the differences in the expressions of ribosomal function related genes in liver tissue of the mice in two groups and the related signal pathway was explored. Results: The survival analysis demonstrated that the survival rate of TG mice in drug treatment was higher than that in control group (P0. 05). The canonical analysis showed that thirteen genes involved in ribosomal function from 9 083 genes in liver tissue in drug treatment group had the changes compared with control group (P<0.05). Conclusion: Shiquandabu decoction can effectively prolong the lifetime of the TG mice by improving the levels of serum amino acids and promoting the liver ribosomal protein synthesis.
ABSTRACT
Objective:To explore the inhibitory effect of Shiquandabu decoction on the spontaneous len tumor of the SV40 T antigen transgenic (TG) mice,and to clarify its molecular mechanism.Methods:The SV40 T antigen TG mice were randomly divided into control group (n=39) and drug treatment group (n=25).The mice in control group were fed normally,while the mice in drug treatment group were fed with Shiquandabu decoction at the 3rd week after birth,the survival time of mice was recorded.Three mice in control group and drug treatment group were randomly chosen to collect the blood from the tail vein and the amino acid levels were measured respectively 8 and 15 weeks after Shiquandabu decoction administration.Then the mice were sacrificed and the liver tissue wascollected.Gene chip hybridization was used to detect the differences in the expressions of ribosomal function related genes in liver tissue of the mice in two groups and the related signal pathway was explored.Results:The survival analysis demonstrated that the survival rate of TG mice in drug treatment was higher than that in control group (P＜0.05).Compared with control group,the serum levels of alanine,valine,leucine,isoleucine,threonine,methionine,proline,tyrosine,lysine,sarcosine,citrulline,ornithine and hydroxylysine of the mice in drug treatment group 8 weeks after administration of Shiquandabu decoction were increased (P＜0.05);and the serum levels of cystathionine,taurine,methylhistidine,anserine and ethanolamine were decreased (P＜0.05).Fifteen weeks after administration,compare with control group,the serum levels of threonine and citrulline of the mice in drug teeatment group were increased (P＜0.05),but the serum levels of other amino acids had no significant difference (P＞ 0.05).The canonical analysis showed that thirteen genes involved in ribosomal function from 9 083 genes in liver tissue in drug treatment group had the changes compared with control group (P＜ 0.05).Conclusion:Shiquandabu decoction can effectively prolong the lifetime of the TG mice by improving the levels of serum amino acids and promoting the liver ribosomal protein synthesis.
ABSTRACT
BACKGROUND AND OBJECTIVES: As a part of efforts to evaluate effectiveness of aorta cell lineages derived from the transgenic mice in which expression of the temperature-sensitive SV40 large T antigen has been targeted to vascular smooth muscle, localization of the T antigen gene in chromosome of the established cell lineages was characterized. Expression pattern of p53 in an aorta cell line or those of r-actin and the T antigen in the various tissues of the transgenic mice, respectively, were also examined. MATERIALS AND METHODS: Chromosomal DNA obtained from the aorta cell lines, which were derived from the transgenic mice, was analyzed by genomic Southern blot method to identify the transgene in genome. mRNA was prepared from the various tissues of the transgenic mouse and was examined by Northern blot analysis to detect expression of r-actin gene. Reverse transcription polymerase chain reaction (RT-PCR) was also performed to examine transcription pattern of p53 gene in an aorta cell line. Immunohistology for detecting the T antigen expression in the tissues of the transgenic mouse was also carried out. RESULTS: Correct integration of the SV40 T antigen transgene in chromosome was observed in two aorta cell lines, although their copy numbers inserted were different from each other. Alternative splicing of the primary p53 RNA was identified in the aorta cells when cultured at the restrictive temperature, but not in the cells at permissive temperature. Several tissues of the transgenic mouse showed expression of the viral oncoprotein T antigen. CONCLUSION: An established aorta cell line may be useful model to study the mechanism regulating the proliferation of vascular smooth cells in mice. Mutant form (s) of the p53 tumor suppressor protein generated by the translation of the alternatively spliced mRNA might be involved in the blockade of apoptosis in some aorta cells when cultured at the restrictive temperature. However, expression of the viral gene in the tissues of the transgenic mice seemed not to be precisely regulated by temperature-dependent manner.