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AIM:To investigate the effect of lutein on the viability of breast cancer cells and its possible mech -anism.METHODS:The human breast cancer T47D cells were divided into control group and lutein(6.25,12.5,25,50 mg/L)treatment groups.The effect of lutein on the viability of T47D cells was measured by MTT assay.The mRNA ex-pression of nuclear factor erythroid 2-related factor 2(Nrf2),glutathione peroxidase 1(GPx1)and superoxide dismutase 2 (SOD2)was detected by RT-qPCR.Fluorescent probes DCFH-DA was used to determine the production of reactive oxygen species(ROS).The protein expression of Nrf2 and p65 was determined by Western blot.RESULTS: The MTT results showed that lutein inhibited T47D breast cancer cell viability in a dose-and time-dependent manner.The RT-qPCR results showed that the mRNA levels of Nrf2, GPx1 and SOD2 were higher in lutein treatment groups than those in the control group(P<0.05),and with the increased concentrations and extension of intervention time of lutein, the relative mRNA levels were all increased.The ROS levels were significantly decreased in the lutein-treated groups(P<0.05).The results of Western blot demonstrated that the protein expression of Nrf 2 was significantly increased(P<0.05), and p65 protein was decreased(P<0.05)in a dose-dependent manner with lutein treatment for 48 h.CONCLUSION: Lutein signifi-cantly inhibits the viability of breast cancer cells,and the inhibition roles may be related to up-regulation of the expression of Nrf2,antioxidant enzymes GPx1 and SOD2 mRNA expression and down-regulation of oxidative stress,thus blocking the NF-κB signaling pathway.
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<p><b>OBJECTIVE</b>To observe the effect of Tetramethyl pyrazine (TMP) on the cytokines and inflammatory mediators in the serum and the synovial fluid of collagen-induced arthritis (CIA)rats, and further to investigate its possible mechanisms for treating rheumatoid arthritis (RA).</p><p><b>METHODS</b>Type II CIA rat model was established. Rats in the TMP group were administered with TMP at 50 mg/kg and 100 mg/kg, once daily. Dexamethasone at 2.0 mg/kg was intramuscularly injected to those in the Dexamethasone treated group, once daily. Normal saline at 2 mL/kg was given to those in the normal control group and the model group, once daily. All medication was started from the 7th day, lasting to the 35th day. CIA rats' foot swelling degree was observed. Contents of serum IL-1, IL-6, IL-2, NO and PGE2in the synovial fluid were detected by radioimmunoassay and nitrate reduction method.</p><p><b>RESULTS</b>Compared with the normal group, the foot swelling obviously increased, contents of NO and PGE2 in the synovial fluid were obviously elevated in the model group (P < 0.01). Compared with the model group, the foot swelling could be obviously inhibited by 100 mg/kg TMP and Dexamethasone; serum levels of IL-1 and IL-6 obviously decreased, serum IL-2 level obviously increased, contents of NO and PGE, decreased (P < 0.01). TMP 50 mg/kg could obviously inhibit the foot swelling of CIA rats (P < 0.01). There was no statistical difference in other indices (P > 0.05).</p><p><b>CONCLUSIONS</b>TMP at 100 mg/kg showed obvious inhibition on CIA rats. Its inhibitory effect might be correlated to inhibiting activities of endogenous cytokines and the generation of inflammatory mediators in inflammation local regions, improving contents of anti-inflammation cytokines, and inducing the balance of the inflammatory cytokine network.</p>