Objective To investigate whether autophagy can be induced by 1,4-benzoquinone (1,4BQ) in HL60 cells,as well as the role of reactive oxygen species (ROS)in induced autophagy.Methods In order to determine a suitable 1,4-BQ treatment concentration for autophagy detection in HL60 cells,the cell vitality were examined by CCK8 assay.Logarithmic-growth-phased cells were divided into control group,1,4-BQgroup(10μmol/L 1,4-BQ,24 h),NAC group (antioxidant n-acetyl cysteine,5mmol/L,24 h) and the 1,4-BQ+NAC group (5 mmol/L NAC were preincubated for 1h prior to the treatment with 10 μmol/L 1,4-BQ for 24 h).The autophagic acidic vesicle were inspected by acridine orange staining,LC3 were detected by immunofluorescence staining,and expressions of LC3 and Beclin1 were quantitatively detected by Western blot.Results The results from cell viability test indicated that 1,4-BQ exhibited a dose-dependent toxicity to HL60cells.Compared with control group.the cell viability in 20.0、40.0μmol/L concentration were decreased obviously,and the differences had statistical significance (P＜0.05).Compare with contrd group acidic vesicle,LC3II,LC3II/LC3I and Beclin1 protein expressions were increased in 1,4-BQ group,after both respectively 12.4％ and 27％,the differences had statistital significance.While 1,4-BQ+NAC group was observed that acidic vesicle,LC3 and Beclin1 protein level were markedly lower than 1,4-BQ group,after both decreased 12.6％ and 22.6％ respectively,both the difference were statistically significant (P＜0.05).Conclusion 1,4-BQ can induce autophagy in HL60 cells,the induction of autophagy is at least partly resulted from ROS.Antioxidant can effectively suppress the occurrence of induced autophagy.

Objective To investigate whether autophagy can be induced by 1,4-benzoquinone (1,4BQ) in HL60 cells,as well as the role of reactive oxygen species (ROS)in induced autophagy.Methods In order to determine a suitable 1,4-BQ treatment concentration for autophagy detection in HL60 cells,the cell vitality were examined by CCK8 assay.Logarithmic-growth-phased cells were divided into control group,1,4-BQgroup(10μmol/L 1,4-BQ,24 h),NAC group (antioxidant n-acetyl cysteine,5mmol/L,24 h) and the 1,4-BQ+NAC group (5 mmol/L NAC were preincubated for 1h prior to the treatment with 10 μmol/L 1,4-BQ for 24 h).The autophagic acidic vesicle were inspected by acridine orange staining,LC3 were detected by immunofluorescence staining,and expressions of LC3 and Beclin1 were quantitatively detected by Western blot.Results The results from cell viability test indicated that 1,4-BQ exhibited a dose-dependent toxicity to HL60cells.Compared with control group.the cell viability in 20.0、40.0μmol/L concentration were decreased obviously,and the differences had statistical significance (P＜0.05).Compare with contrd group acidic vesicle,LC3II,LC3II/LC3I and Beclin1 protein expressions were increased in 1,4-BQ group,after both respectively 12.4％ and 27％,the differences had statistital significance.While 1,4-BQ+NAC group was observed that acidic vesicle,LC3 and Beclin1 protein level were markedly lower than 1,4-BQ group,after both decreased 12.6％ and 22.6％ respectively,both the difference were statistically significant (P＜0.05).Conclusion 1,4-BQ can induce autophagy in HL60 cells,the induction of autophagy is at least partly resulted from ROS.Antioxidant can effectively suppress the occurrence of induced autophagy.

Objective To explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population. Methods We conducted a retrospective observational study to investigate the relationship between lipid markers [including triglycerides, total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein (HDL) cholesterol, non-HDL-cholesterol, apolipoprotein A-I, apolipoprotein B, lipoprotein[a], and composite lipid profiles] and left ventricular hypertrophy. A total of 309,400 participants of two populations (one from Beijing and another from nationwide) who underwent physical examinations at different health management centers between 2009 and 2018 in China were included in the cross-sectional study. 7,475 participants who had multiple physical examinations and initially did not have left ventricular hypertrophy constituted a longitudinal cohort to analyze the association between lipid markers and the new-onset of left ventricular hypertrophy. Left ventricular hypertrophy was measured by echocardiography and defined as an end-diastolic thickness of the interventricular septum or left ventricle posterior wall > 11 mm. The Logistic regression model was used in the cross-sectional study. Cox model and Cox model with restricted cubic splines were used in the longitudinal cohort. Results In the cross-sectional study, for participants in the highest tertile of each lipid marker compared to the respective lowest, triglycerides [odds ratio (OR): 1.250, 95％CI: 1.060 to 1.474], HDL-cholesterol (OR: 0.780, 95％CI: 0.662 to 0.918), and lipoprotein(a) (OR: 1.311, 95％CI: 1.115 to 1.541) had an association with left ventricular hypertrophy. In the longitudinal cohort, for participants in the highest tertile of each lipid marker at the baseline compared to the respective lowest, triglycerides [hazard ratio (HR): 3.277, 95％CI: 1.720 to 6.244], HDL-cholesterol (HR: 0.516, 95％CI: 0.283 to 0.940), non-HDL-cholesterol (HR: 2.309, 95％CI: 1.296 to 4.112), apolipoprotein B (HR: 2.244, 95％CI: 1.251 to 4.032) showed an association with new-onset left ventricular hypertrophy. In the Cox model with forward stepwise selection, triglycerides were the only lipid markers entered into the final model. Conclusion Lipids levels, especially triglycerides, are associated with left ventricular hypertrophy. Controlling triglycerides level potentiate to be a strategy in harnessing cardiac remodeling but deserve to be further investigated.