Objective: To understand the current status of BMI of the elderly and related factors in longevity areas in China, and provide scientific evidence for the control of BMI level in elderly population. Methods: Data used in this study were obtained from Healthy Aging and Biomarkers Cohort Study, a sub-cohort of the Chinese Longitudinal Healthy Longevity Survey. A total of 2 825 elderly in 8 longevity areas in China were surveyed and measured in 2017. The BMI levels of 2 217 elderly aged 65 years and older were calculated and in follow up. The ordered classification logistic regression model was used to analyze the influencd factors for the BMI in the elderly. Results: The BMI of the elderly in 8 longevity areas in China was (22.36±3.87) kg/m², and it was (22.76±3.58) kg/m² for males and (21.75±3.98) kg/m² for females. The BMI levels were normal in 1 165 elderly persons. The prevalence of underweight, overweight and obesity were 15.8%, 24.0% and 7.7%, respectively. Multivariate analysis showed that the main factors affecting the BMI of people under 100- years old were age (65-: OR=2.78, 95%CI: 1.87-4.15; 80-: OR=1.47, 95%CI: 1.00-2.17), smoking status (OR=0.46, 95%CI: 0.32-0.66), annual household income (<30 000 Yuan: OR=1.26, 95%CI: 1.07-1.47; 30 000-70 000 Yuan: OR=1.52, 95%CI: 1.12-1.86), and frequency of tea intake(OR=1.36, 95%CI: 1.01-1.71), while the factor in people aged ≥100 years was gender (OR=3.68, 95%CI: 1.32-10.36). Conclusions The prevalence of underweight, overweight and obesity were high in the elderly from longevity areas in China. It is necessary to pay attention to the trend of overweight and obesity due to smoking, higher annual household income and regular tea drinking in the elderly men.

ObjectiveTo investigate the induction of ferroptosis by polyphyllin Ⅱ （PPⅡ） in hepatocellular carcinoma HepG2 cells and its underlying mechanism. MethodThe effect of PPⅡ （0， 1.5， 3.0， 4.5， 6.0， 9.0， 18.0 mg·L^-1） on the in vitro proliferation of HepG2 cells was assessed using the methyl thiazolyl tetrazolium （MTT） assay. Colony formation ability of HepG2 cells was evaluated through a colony formation assay. Cell migration ability was assessed via a scratch assay. Lactate dehydrogenase （LDH） content in HepG2 cells was measured using a kit. Reactive oxygen species （ROS） levels in HepG2 cells were observed using a fluorescence inverted microscope. Malondialdehyde （MDA）， glutathione （GSH）， and free Fe²⁺ content in HepG2 cells were detected using respective kits. The mitochondrial ultrastructure in HepG2 cells was observed by transmission electron microscopy. The expression of ferroptosis-related proteins p53， solute carrier family 7 member 11 （SLC7A11）， glutathione peroxidase 4 （GPX4）， long-chain acyl-CoA synthetase 4 （ACSL4）， and transferrin receptor 1 （TFR1） in HepG2 cells was detected using Western blot. ResultCompared with the control group， the PPⅡ treatment groups showed significantly decreased survival rate of HepG2 cells in a dose-dependent manner （P<0.01）， significantly reduced number of cell colonies （P<0.01）， significantly shortened scratch healing distance， inverse correlation of the migration distance with drug concentration （P<0.01）， significantly increased LDH leakage in cells （P<0.01）， significantly enhanced relative fluorescence intensity of intracellular ROS， and significantly increased accumulation of lipid peroxide MDA （P<0.01）， decreased intracellular GSH content with increasing drug concentration （P<0.01）， and significantly enhanced fluorescence intensity of FeRhoNox-1 in cells （P<0.01）. Moreover， cells exhibited vacuolation， and mitochondria showed significant shrinkage with reduced or even disappeared cristae. Compared with the results in the control group， the expression of p53， ACSL4， and TFR1 proteins significantly increased， while the expression of SLC7A11 and GPX4 proteins significantly decreased in the PPⅡ treatment groups （P<0.05）. ConclusionIn summary， PPⅡ induces ferroptosis in HepG2 cells by regulating the p53/SLC7A11/GPX4 signaling axis， promoting ACSL4 expression and Fe³⁺ uptake， leading to an imbalance in the antioxidant system.