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Aim To evaluate the hypolipidemic effect of total phenylpropanoid glycoside extracted from Ligustrum robustum(Roxb.)Blume(CNTG)and its mecha-nisms.Methods The 60 hamsters were randomly divided into six groups,namely the control group,the model group,the positive control group(fenofibrate,150 mg·kg-1),the high(1 200 mg·kg-1),medium(600 mg·kg-1)and low(300 mg·kg-1)doses of CNTG groups.Only the control group was given control diet and other groups received high-fat diet.The changes of serum lipid were measured and analyzed in 1st week to ensure the successful establishment of the model.The drugs were administered daily for four weeks and the concentrations of lipids were determined in the 2nd week,3rd week and 4th week respectively.Quantitative real-time PCR and Western blot were used to assay the mRNA and protein expression of related signaling enzymes and proteins.Results Compared with the model group,the concentrations of serum TG,TC,LDL-C(P<0.05,P<0.01)and hepatic TG,TC(P<0.01)were effectively reduced in hamsters in CNTG-treated groups.Mechanism research found that CNTG increased the levels of phospho-AMPKα,LKB1 and phospho-LKB1 in liver(P<0.05).Conclusion CNTG prevents hyperlipidemia via activation of hepatic LKB1-AMPK pathway.
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Abrin is isolated from abrin seeds (Aburs precatoriusL.), which is a kind of cytotoxic protein. This article reviewed the anticancer effect and mechanisms of Abrin from five aspects in several years, which were the molecular structure and toxicity of Abrin, the characteristics of Abrin in anticancer effect, the role of Abrin in inhibiting cancer cell proliferation, the mechanisms of Abrin induced apoptosis of cancer cells, the anticancer mechanisms of Abrin in enhancing immune function. And the application prospect of Abrin immunotoxin targeted therapy and nano preparation will be expounded in this article. It will be helpful to further research about application on Abrin. It will provide the scientific basis for discovering new drug targets of cancer.
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Aim To establish hyperlipidemic model and study the molecular mechanism of triglyceride (TG)disorder in hamsters.Methods The male ham-sters were randomly divided to control group fed with standard diet and model group fed with high-fat diet, both of the groups had been fed with diet for 4 weeks. The levels of serum TG,TC,LDL-C,FFA were detec-ted at the end of 2nd and 4th week.The hepatic TG, TC,LPL activity were detected by enzymatic method at the end of 4th week.The molecular mechanism was tested by real-time PCR.Meanwhile the effect of posi-tive drug fenofibrate on the model of hyperlipidemia in hamsters was investigated.Results Compared with the control,the serum levels of TG,TC,LDL-C,FFA in the model group increased 2.57,1.93,2.49,1.25 times at the end of2nd week,and 3.93,1.90,2.27, 2.29 times at the end of 4th week,respectively.The positive drug significantly decreased the concentrations of serum TG and FFA. The mechanism research showed that the hepatic AMPK,PPARα,CPT-1 mRNA decreased in hamsters fed with high-fat diet,and the SREBP-1 c,ACC,SCD-1 ,AGPAT2,DGAT2 mRNA ex-pressions increased.The hepatic ApoB mRNA expres-sion was up-regulated while the MTTP and LPL mRNA expressions were down-regulated slightly.LPL activity significantly decreased in model hamsters compared with the control.The alternations of these enzymes and receptors were the critical factors for TG disorder. Conclusion The hamsters fed with high-fat diet for 4 weeks can form a good hyperlipemic model with HTG feature.AMPK,SREBP-1 c,ACC,SCD-1 ,DGAT2,AG-PAT2,PPARα,CPT-1 and LPL are not only the main mechanisms of TG disorder,but also the biomarkers of hypotriglyceridemic drugs.
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Aim To establish the hyperlipidemic model and ex-plore the mechanism of hypercholesterolemia in hamster. Meth-ods Hamsters were randomly divided into the control and model groups. The hamsters in the control group were fed with the standard chow and the model group were fed with the high fat di-et. Serum lipids and CYP7A1 activity were detected by enzymat-ic method. The molecular mechanism of cholesterol metabolism was investigated by real-time PCR. Results In comparison with the control group, the concentrations of serum TC, LDL-C, TG and hepatic TC, TG were significantly increased in the model group. The mechanism research showed that in hamsters fed with the high fat diet, the CYP7A1 activity and the mRNA expres-sions of hepatic LDL-R, SREBP-2, CYP7A1, LXRαwere down-regulated, the expression of hepatic FXR was up-regulated. Conclusion The hyperlipidemic model could be developed in hamsters fed with the high fat diet for 4 weeks. LDL-R, SREBP-2, CYP7A1, FXR and LXRαare the biomarkers of hypercholes-terolemia, and also the targets of hypolipidemic drugs.