Background The pathogenesis of silicosis is complex and treatment methods are limited. SiO₂-induced increase of transforming growth factor-β1 (TGF-β1) can activate fibroblasts to promote collagen deposition, ultimately leading to fibrosis. Previous studies have confirmed that lipid metabolism plays an important role in the progression of silicosis. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC1α) mediates mitochondrial dysfunction and lipid metabolism pathways in diabetic models, but its role in silicosis has not been elucidated. Objective To investigate the effect of PGC1α on lipid metabolism disorder of macrophages induced by SiO₂ and its effect on the progression of silicosis fibrosis. Methods (1) Macrophages were divided into four groups by transfecting and silencing PGC1α and its control sequence in macrophages and followed by SiO₂ stimulation: negative control group (transfected with si-NC for 48 h), si-PGC1α group (transfected with si-PGC1α for 48 h), SiO₂ stimulation group (stimulated with 50 μg·mL⁻¹ SiO₂ for 36 h after transfection with si-NC for 48 h), and si-PGC1α+SiO₂ group (stimulated with 50 μg·mL⁻¹ SiO₂ for 36 h after transfection with si-PGC1α for 48 h). Western blot and cell immunofluorescence were used to test PGC1α expression, 4,4-difluoro-1,3,5,7,8-pentamethyl-4-bora-3a,4a-diaza-s-indacene (BODIPY 493/503) and total cholesterol (TC) and free cholesterol (FC) kits were used to test lipid accumulation, and the Oroboros2k-Oxygraph respiratory test system (O2K) was used to assess the effects of PGC1α on mitochondrial respiratory chain. ELISA kits were used to test TGF-β1 expressed in the macrophage supernatant. (2) Lung fibroblasts were divided into the same four groups as above, and stimulated with the supernatant of macrophages in the above groups. The expression of collagen Ι (COL Ι), E-cadherin (Eca), and fibronectin (FN) were detected by cell immunofluorescence and Western blot to further evaluate the effect of silencing PGC1α on fibrosis. Results The protein expression level of PGC1α stimulated by SiO₂ was decreased, and the relative expression level of PGC1α was 0.78 times that of the control group (P<0.05). After transfection with si-PGC1α, the expression of PGC1α was decreased, and the relative protein expression level of the si-PGC1α group was 0.86 times that of the control group (P<0.05). Compared with the SiO₂ stimulation group, the staining area of BODIPY 493/503 in the si-PGC1α+SiO₂ group was enhanced, and the cholesterol-related indexes [TC, FC and cholesterol ester (CE)] were increased to 1.38, 1.10, and 2.26 times those in the SiO₂ stimulation group (P<0.05). The activity of mitochondrial complex Ι was decreased, and the level of complex Ι in the si-PGC1α+SiO₂ group was 0.63 times that in the SiO₂ stimulation group (P<0.05). The secretion of TGF-β1 by macrophages increased, and the level of TGF-β1 in the si-PGC1α+SiO₂ group was 1.15 times that of the SiO₂ stimulation group (P<0.05). In addition, after stimulation of primary lung fibroblasts with macrophage supernatant, silencing PGC1α increased the expression levels of COL Ι and FN, while decreased the expression of Eca. The protein levels of COL Ι, FN, and Eca in the si-PGC1α+SiO₂ group were 1.39, 1.18, and 0.82 times those in the SiO₂ stimulation group, respectively (P<0.05). Conclusion Silencing PGC1α exacerbates SiO₂-induced lipid metabolism disorder, inhibits mitochondrial respiratory chain, and aggravates the fibrosis induced by SiO₂, suggesting that PGC1α may participate silicosis fibrosis by regulating mitochondrial respiratory chain and lipid metabolic disorder induced by SiO₂.

Objective: To evaluate the current status and related factors of influenza vaccination among health care workers (HCWs) in tertiary hospitals of Xining city after the implementation of the free influenza vaccination policy. Methods: In August 2018, the cluster sampling method was used to select four medical institutions in Xining that had previously conducted investigations and interventions. All HCWs(excluding logistic staff) in each medical institution were included in the study. A total of 3 260 valid respondents were included. Questionnaires were used to collect the demographic characteristics, influenza and influenza vaccination awareness, implementation of free policy in the influenza epidemic season from 2017 to 2018, influenza vaccination status, awareness of influenza vaccination schedule and free policy. The multivariate logistic regression model was used to analyze related factors of influenza vaccination. Results: The age of respondents was (31.41±5.00) years. The influenza vaccination rate was 6.80% (226/3 260) in 2017-2018 influenza epidemic season. After controlling for related factors, the awareness of the influenza vaccination schedule (OR=17.05, 95%CI: 5.86-49.59), vaccination frequency (OR=8.22, 95%CI: 2.98-22.61) and the free policy (OR=3.15, 95%CI: 1.49-6.67) had higher vaccination rate. Conclusion The influenza vaccination rate of HCWs in tertiary hospitals of Xining city was low. Increasing the awareness of the vaccination schedule, frequency and free policy may promote the influenza vaccination rate of HCWs.