RESUMEN
BACKGROUND: 2-Amino-2-[2-(4-octylphenyl)ethyl] propane-1,3-diol hydrochloride (FTY720) is a novel agent with protective effect on several markers of liver injury. It is a chemical substance derived by modifying myriocin from the ascomycete Isaria sinclairii. It has been reported that FTY720 is able to treat autoimmune encephalomyelitis, renal cancer, asthma, and multiple sclerosis. More potent clinical applications of FTY720 need to be investigated. OBJECTIVE: The aim of this study was to evaluate the protective effect of FTY720 on several markers of experimental liver injury and to investigate the possible mechanism of action. METHODS: Concanavalin A (Con A) at a dose of 15 mg/kg was intravenously. injected in mice, and 10 days before the Con A challenge, 1 mg/kg, 3 mg/kg, and 6 mg/kg of FTY720 were administered to mice. The liver injury was monitored biochemically by measuring serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and tumor necrosis factor-α (TNF-α) levels. TNF-α and nuclear factor-κB (NF-κB) in liver tissue were detected by Western blot analysis. RESULTS: FTY720, when administered intragastrically for 10 days in mice with Con A-induced liver injury, dose-dependently reduced serum ALT and AST and TNF-α levels. The differences were statistically significant (P ≤ 0.05). It was also found that FTY720 decreases TNF-α and NF-κB protein expression in liver tissue. CONCLUSIONS: FTY720 is able to improve several markers of Con A-induced liver injury in mice, including serum ALT, serum AST, TNF-α, and NF-κB, which might be at least in part related to its ability to reduce TNF-α/NF-κB cascade activity.
RESUMEN
BACKGROUND AND OBJECTIVE: It has been reported that there was a close relationship between lung cancer risk and environmental tobacco smoke at workplace. The aim of this study is to explore the relationship between workplace environmental tobacco smoke exposure and lung cancer risk among non-smoking subjects. METHODS: By searching Medline, CENTRAL (the Cochrane central register of controlled trials), EMBASE, CBM, CNKI and VIP et al, we collected both domestic and overseas published documents on workplace environmental tobacco smoke exposure and lung cancer risk. Random or fixed effect models were applied to conduct systematic review on the study results, the combined odds ratio (OR) and the 95% confidence interval (CI) were calculated as well. RESULTS: 22 reports were included into the combined analysis, which indicated that 25% lung cancer risk was increased by exposing to workplace environment tobacco smoke (OR=1.25, 95%CI: 1.13-1.39, P < 0.001). For female the increased risk was 22% (OR=1.22, 95%CI: 1.05-1.42, P=0.011). For male the increased risk was 54%, but it does not reach the statistical significance (OR=1.54, 95%CI: 0.74-3.18, P=0.247). CONCLUSIONS: Workplace environmental tobacco smoke exposure is an important risk factor of lung cancer risk among non-smoking subjects. Especially for non-smoking women who expose to workplace environment tobacco smoke have a close relationship with lung cancer.