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Wen-gong Yu

Publications and source records attributed to Wen-gong Yu.

5 recordsLinked to original sources

[Molecular mechanisms of antioxidant effects of propylene glycol mannate sulfate].

AIM: To investigate the antioxidant mechanisms of propylene glycol mannate sulfate (PGMS) in hyperlipidemic rats. METHODS: Male Wistar rats were given high lipid emulsion diet to establish hyperlipidemic model. PGMS was given every day at different doses (37.8 and 75.6 mg.kg-1, ig) to hyperlipidemic rats for three weeks. In addition, diethyldithiocarbamate (DDC) was given 200 mg.kg-1.3 d-1 (i.p.) to inhibit SOD activity. Then, the MDA content was examined using TBA method to show the oxidation level, and the activities of SOD, GSH-Px and CAT were examined following the kit protocols to indicate the capability of eliminating OFR. RT-PCR was applied to study the expression of Cu, Zn-SOD mRNA in rat liver. RESULTS: The MDA content of PGMS treatment groups decreased markedly compared with hyperlipidemic group, and the activities of SOD, GSH-Px and CAT increased distinctly. Cu, Zn-SOD mRNA expression was significantly increased by PGMS treatment. Furthermore, the application of DDC(the SOD inhibitor) reduced total SOD activity and Cu, Zn-SOD mRNA expression induced by PGMS, and the content of MDA increased correspondingly. CONCLUSION: PGMS can induce the activities of antioxidant enzymes and the mRNA expression of Cu, Zn-SOD, which contribute to the elimination of oxygen free radical. This may explain the molecular mechanism of antioxidant effects of PGMS.

Animals↗

[Inhibition of MCP-1 mRNA expression by propylene glycol mannate sulfate in hyperlipidemic rat aorta].

AIM: To study the effects of prophylene glycol mannate sulfate (PGMS) on monocyte chemoattractant protein-1 (MCP-1) mRNA expression in hyperlipidemic rat aorta and to clarify the molecular mechanism of PGMS for the prevention of atherosclerosis. METHODS: PGMS (37.8 and 75.6 mg.kg-1.d-1, ig) or PGMS (37.8 and 75.6 mg.kg-1.d-1, ig) combined with diethyldithiocarbamate (DDC, an inhibitor of SOD, 200 mg.kg-1 every three days, i.p.) were given to hyperlipidemic rats for three weeks. The MDA content and SOD activity were determined after 12 h of starvation, and MCP-1 mRNA expression in aorta was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: There was significant decrease (29.46% or 58.40)% of MCP-1 mRNA expression in aortic after the therapy. The SOD activity increased markedly and the MDA content decreased at the same time. After treatment with DDC, the SOD activity was inhibited and the MDA content increased, but with no significant effect on MCP-1 mRNA expression. CONCLUSION: PGMS inhibited MCP-1 mRNA expression with no relation to its effect on decreasing MDA content.

Animals↗

[Effect of propylene glycol mannate sulfate on blood lipids and lipoprotein lipase in hyperlipidemic rat].

AIM: To study the effect of propylene glycol mannate sulfate (PGMS) on blood lipids and lipoprotein lipase in hyperlipidemic rat, and its anti-hyperlipidemic mechanism. METHODS: PGMS was administered ig at different doses (37.8 mg.kg-1.d-1 and 75.6 mg.kg-1.d-1) to hyperlipidemic rats for three weeks and blood serum was obtained after starved 12 h. Total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol (LDL-C) and high density lipoprotein cholesterol (HDL-C) were examined. The mRNA expression of lipoprotein lipase (LPL) in liver, spleen and artery was detected by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: PGMS significantly decreased the levels of TC, TG and LDL-C and increased that of HDL-C in hyperlipidemic serum dose-dependently. PGMS was shown to increase the level of LPL mRNA expression, which is related directly to the controlling effects of PGMS on blood lipids. CONCLUSION: PGMS modulated blood lipids by promoting mRNA expression of LPL. This may be one important mechanism of PGMS to modulate blood lipids.

Animals↗

[Induction of CuZn-SOD mRNA expression and activity by PGMS in rat liver].

AIM: To study the effect of propylene glycol mannate sulfate (PGMS) on induction of CuZn-SOD. METHODS: Wistar rats were given PGMS p.o. at different doses (0, 18.9, 37.8 and 75.6 mg.kg-1.d) for ten days. Then the rats were sacrificed and the total RNA was extracted from the livers. The total RNA samples were loaded on a 1% agarose gel to detect the quality of total RNA. RT-PCR was applied to study the expression of CuZn-SOD mRNA in rat livers. The amplified products were detected by the 1.5% agarose gel electrophoresis. Simultaneously, the CuZn-SOD activities in rat liver were determined by nitrite method. RESULTS: The total RNA extracted from rat livers was integrated without being decomposed by RNase. The level of CuZn-SOD mRNA of the high-dosage group (75.6 mg.kg-1.d) was higher than that of the control group (0 mg.kg-1.d) (P < 0.01); the CuZn-SOD activities of the high-dosage group were significantly higher than those of the control group (P < 0.001) and the CuZn-SOD activities of the middle- (37.8 mg.kg-1.d) and low-dosage groups (18.9 mg.kg-1.d) were higher than those of the control group (P < 0.01). CONCLUSION: PGMS can increase the CuZn-SOD activities as well as CuZn-SOD on mRNA level. Therefore, it is possible for PGMS to counteract Atherosclerosis (AS) by inducing the expression of CuZn-SOD.

Animals↗

[Progress on gene targeting].

Gene targeting is a rising technology in molecular biology,which is defined as the introduction of exogeneous DNA to specific site in genome by homologous recombination,and consequently change the hereditary character of the cell. This technology provides a new and powerful means for research in developmental biology,molecular genetics,immunology and medicine. Progresses have been made in exploring gene structure and function,gene expression and regulation,transgene and gene therapy with the application of gene targeting. But there are some problems in gene targeting,especially for the low efficiency. This article just provided a review of the principle and program of gene targeting,and discussed the possible approaches to increase the efficiency of gene targeting.

English Abstract↗