Assessment of causal association between thyroid function and lipid metabolism: a Mendelian randomization study / 中华医学杂志(英文版)

BACKGROUND@#Thyroid dysfunction is associated with cardiovascular diseases. However, the role of thyroid function in lipid metabolism remains partly unknown. The present study aimed to investigate the causal association between thyroid function and serum lipid metabolism via a genetic analysis termed Mendelian randomization (MR).@*METHODS@#The MR approach uses a genetic variant as the instrumental variable in epidemiological studies to mimic a randomized controlled trial. A two-sample MR was performed to assess the causal association, using summary statistics from the Atrial Fibrillation Genetics Consortium (n = 537,409) and the Global Lipids Genetics Consortium (n = 188,577). The clinical measures of thyroid function include thyrotropin (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) levels, FT3:FT4 ratio and concentration of thyroid peroxidase antibodies (TPOAb). The serum lipid metabolism traits include total cholesterol (TC) and triglycerides, high-density lipoprotein, and low-density lipoprotein (LDL) levels. The MR estimate and MR inverse variance-weighted method were used to assess the association between thyroid function and serum lipid metabolism.@*RESULTS@#The results demonstrated that increased TSH levels were significantly associated with higher TC (β = 0.052, P = 0.002) and LDL (β = 0.041, P = 0.018) levels. In addition, the FT3:FT4 ratio was significantly associated with TC (β = 0.240, P = 0.033) and LDL (β = 0.025, P = 0.027) levels. However, no significant differences were observed between genetically predicted FT4 and TPOAb and serum lipids.@*CONCLUSION@#Taken together, the results of the present study suggest an association between thyroid function and serum lipid metabolism, highlighting the importance of the pituitary-thyroid-cardiac axis in dyslipidemia susceptibility.

Effect of sitostero-3-O-glucoside on proliferation, apoptosis and collagen synthesis of keloid fibroblasts / 中国比较医学杂志

Objective To explore the effect of sitostero-3-O-glucoside on proliferation, apoptosis and collagen synthesis of keloid fibroblasts ( KF) . Methods Cell viability was measured by MTT assay after cells were cultured with 0 (control), 3. 125, 6. 25, 12. 5, 25, 50, 100 μg/mL sitostero-3-O-glucoside. Cell proliferation was measured by EdU staining. Cell apoptotic rate and cell cycle were measured by flow cytometry. The level of COL I and COL III was detected by enzyme linked immunosorbent assay (ELISA). Results 3. 125, 6. 25, 12. 5, 25, 50, 100 μg/mL sitostero-3-O-glucoside reduced cell viability ( P< 0. 01 ) , increased inhibitory rate of cell proliferation ( P< 0. 01 ) , IC50 =27. 54 ± 2. 18 μg/mL. Compared with the control group, 12. 5, 25, 50μg/mL sitostero-3-O-glucoside reduced the cell proliferation rate (P< 0. 01), increased the cell early and late apoptotic rates (P< 0. 01), the cell cycle was arrested at G1 phase (P< 0. 01), and the levels of COL I and COL III were down-regulated (P< 0. 01). Conclusions The results show that sitostero-3-O-glucoside can significantly inhibit the proliferation, induce cell apoptosis and inhibit the synthesis of collagen of keloid fibroblasts.