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Objective:To study the effect of trigonelline on the change of indicators of serum transaminase, lipoprotein and liver lipid of model rats with non-alcoholic fatty liver diseases and on the expression level of Bcl-2 and Bax proteins.Methods:A total of 45 SD rats were randomly divided into Fthe control group, model group and trigonelline intervention group. Rats in the control group were fed with the common diet, while rats in the model group and intervention group were fed with the high fat diet. 8 weeks later, the intervention group received the intragastric administration of trigonellin e (with the dosage of 40 mg/kg/d) for 8 weeks; while control group and model group received the intragastric administration of saline with the equal dosage. Blood was taken from the abdominal aorta of rats 8 weeks later, detecting the level of a series of indicators of ALT, AST, TG, TC, HDL-C and LDL-C in the serum. After the rats were sacrificed, detect the indicators of TG, TC, SOD and MDA in the liver tissue of rats, as well as the expression of Bcl-2 and Bax in the liver tissue.Results: Results of histopathologic examination showed that the damage degree of liver for rats in the trigonellineintervention group was smaller than the one in the model group, with significantly reduced hepatic steatosis and the partially visible hepatic lobule. The levels of ALT, AST, TC and LDL-C in the serum of rats in the trigonelline group were significantly reduced, while the change in the levels of TG and HDL-C was not significantly different. The levels of TG, TC and MDA in the liver tissues were significantly decreased, while the level of SOD significantly increased; the expression of Bcl-2 protein in the liver tissues of rats in the trigonelline intervention group was significantly increased, while the expression of Bax protein significantly decreased.Conclusions: The trigonelline contributes to the therapeutic effect of non-alcoholic fatty liver diseases. It can also increase the expression of Bcl-2 protein and decrease the expression of Bax protein in the liver tissues, which can protect the liver.
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<p><b>BACKGROUND</b>To study the proliferation inhibition and anti-invasion of retinoic acid (RA) and 18β-glycyrrhetinic acid (GA) in highly metastasized lung cancer cell line (PGCL3), and to observe the combined effects of RA and GA.</p><p><b>METHODS</b>The proliferation inhibitive rate, the colony-formation rate in semi-solid agar, the invasive ability to reconstituted basement membrane, the chemotatic migration ability, the laminin adhesion ability, and the activity of cathepsin B (CB) were tested.</p><p><b>RESULTS</b>Treated with RA and GA, the proliferation of PGCL3 cells were inhibited obviously, and the inhibition degree was related to the dosage of the drugs. IC₅₀ of the proliferation inhibition were 12.58 μmol/L and 145.3 μmol/L respectively. Treated with 5.0 μmol/L RA, 25 μmol/L and 50 μmol/L GA, the invasive ability was decreased significantly (P < 0.01 and P < 0.001), and the inhibition was in a dose dependent manner. In combined treatment with 5.0 μmol/L RA and 25 μmol/L GA, the inhibition of invasion was greater than the sum of them used alone. Treated with GA of above concentrations and 10 μmol/L RA, the adhesion and migration ability and the secretion of CB of the PGCL3 cells were decreased significantly (P < 0.001). Treated with GA of above concentation, the colony formation rate in semi-solid agar was decreased significantly (P < 0.001)..</p><p><b>CONCLUSIONS</b>RA and GA can inhibit the proliferation and invasion of the PGCL3 human lung cancer cells and have the anti-invasion synergism. The mechanism of anti-invasion of RA and GA is to inhibit many points of invasive process.</p>
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<p><b>BACKGROUND</b>To study the anti-invasive effects and its mechanism and apoptosis induction of pentacyclic triterpenoid including glycyrrhizin (GL), 18β-glycyrrhetinic acid (GA), ursolic acid (UA) and oleanolic acid (OA) in highly potentially metastatic lung cancer cell line (PGCL3).</p><p><b>METHODS</b>The invasive ability, the adhesive ability, the migration ability and the activity of cathepsin B (CB) of PGCL3 cells treated with the four drugs were determined by the invasion test of reconstituted basement membrane, the laminin adhesion test, the chemotactic migration test and the enzymological method of CB. The apoptosis of the cells was detected with acridine orange-ethidium bromide fluorescent stain (AO/EB) and TUNEL.</p><p><b>RESULTS</b>The GL,GA, UA and OA could decrease the proliferative ability of PGCL3 cells, and their IC₅₀ values were 1.83 mmol/L, 145.3 μmol/L, 44.73 μmol/L and 40.71 μmol/L respectively. After treatment with 0.5 and 1.0 mmol/L GL, 25 and 50 μmol/L GA, 30 and 40 μmol/L UA, 35 and 45 μmol/L OA for 96 h, the invasive ability of the PGCL3 cells was significantly decreased compared with that of the control groups ( P < 0.01 or P < 0.001). The adhesive and migration ability, the secretion of CB and the colony-formation number in semi solid agar were significantly decreased after PGCL3 cells were treated with the above concentration of the four drugs for 96 h ( P < 0.05, P < 0.01 or P < 0.001), and the inhibition was in a dose-dependent fashion. The percentages of apoptosis of the cells were obviously increased after treatment with the above concentration of the four durgs for 48 h, compared with the control group ( P < 0.05 or P < 0.01).</p><p><b>CONCLUSIONS</b>All of the four drugs can inhibit the proliferative and invasive ability, and induce apoptosis of the PGCL3 human lung cancer cells. The mechanism of anti invasion may be to inhibit the adhesion, migration, and the CB secretion of the cells.</p>
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Background and purpose:18?-glycyrrhetinic acid(GA) is one of the important components of glycyrrhiza.Recent years,studies showed that GA has the effect of proliferation inhibition in human acute lymphoblastic leukemia cells,human liver carcinoma and lung cancer cells.We investigated the effects of GA on induction of apoptosis in human breast carcinoma(MCF7) cells.The previous studies have demonstrated that the dynamic change of intracellular free Ca~(2+) concentration([Ca~(2+)]i)plays important roles in many links of apoptosis-induced process.Therefore we also researched the relationship between GA-induced apoptosis and [Ca~(2+)]i in MCF-7 cells.Methods:After MCF-7 cells were treated with 50-250 ?mol/L GA for 24 h,cell viability for proliferation was assessed by MTT assay.MCF-7 cells treated with 100 ?mol/L and 150 ?mol/L GA for 24 h,the apoptotic rates in MCF7 cells were examined by terminal deoxynucleotide transferase mediated dUTP nick-end-labeling method,flow cytometry with Annexin V/ propidium iodide fluorescent stain and single cell gel electrophoresis assay(SCGE).For cells treated with 150 ?mol/L GA for 24 h,i was measured by Fure-2 fluorescein load method.For cells treated with 150 ?mol/L GA combined with 100 ?mol/L BAPTA-AM or 0.5 mmol/L EGTA for 24 h,cell apoptosis were examined by SCGE.Results:For cells treated with GA from 100 ?mol/L to 250 ?mol/L,the rate of proliferative inhibition was increased significantly(P
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AIM: To inhibit the expression of tyrosinase gene in murine B16 melanoma cells by antisense nucleotide. METHODS: The antisense recombinant pcDNA3.1(-)-tyr was constructed and was used to infect murine B16 melanoma cells for expression of tyr antisense nucleotide. The effect of antisense nucleotide of tyr on the expression of tyr gene was detected by determination of the activity of tyrosinase and of the production of melanin, Dopa staining and electronic microscope. RESULTS: The tyr antisense recombinant was successfully constructed and injected into murine B16 melanoma cell. The activity of tyrosinase in B16 cells infected with pcDNA3.1 (-)-tyr decreased to 0.0498?0.0036, compared to the tyrosinase activity of 0.0916?0.0132 in the control cells without treatment (P