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ObjectiveTo investigate the relationship between plasma surfactant protein⁃A （SP⁃A） expression level and silicosis progression， and to provide early evidence for exploring whether SP⁃A can be used as a biomarker for clinical monitoring of silicosis disease progression. MethodsWe recruited 187 silicosis patients in Guangdong Province hospital for occupational disease prevention and treatment between November， 2019 and November，2020. Their peripheral venous blood samples were collected for the plasma isolation. The level of pulmonary SP⁃A was detected by enzyme-linked immunosorbent assay. ResultsThere was a statistically significant difference in the level of SP⁃A among the silicosis groups （P<0.05）， and the plasma SP-A level of the silicosis patients in stage Ⅲ was higher than that in stage Ⅰ and stage Ⅱ （P<0.05）. Smoking had effect on plasma SP⁃A levels， Age， working years and drinking had no effect on plasma SP⁃A levels. ConclusionThe expression level of SP⁃A in the plasma of silicosis patients is increased， which has a certain correlation with the disease stage， and plays a certain early warning role in the occurrence and development of silicosis， and may be a potential biomarker for the diagnosis and prognosis of silicosis.
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Objective: To investigate the role of surfactant associated protein-A (SP-A) in the development and progression of silicosis, and its mechanism. Methods: Homozygous and heterozygous mice of SP-A knockout of specific pathogen free (SPF) grade were selected for mating, and mice with SP-A-/- genotype were selected for subsequent experiments. SP-A wild-type (SP-A+/+) and SP-A-/- mice were divided into SP-A+/+ control group, SP-A-/- control group, SP-A+/+ silicosis group and SP-A-/- silicosis group with six mice in each group by random number table method. Mice in both silicosis groups were given 20.0 μL 250 g/L silica suspension by tracheal exposure, and mice in both control groups were injected with 0.9% sodium chloride solution at the same volume. On the 28th day after modeling, mice were sacrificed. Lung tissues were used for lung histopathology examination. The apoptosis of alveolar type Ⅱ epithelial cells of mice was detected by TUNEL method. The mRNA expression of B-lymphoblastoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), cysteinyl aspartate specific proteinase (Caspase)-3 and Caspase-9 in lung tissues of mice was detected by quantitative real-time polymerase chain reaction. Results: The histopathological result of mice showed that thickened alveolar septum, scattered silicon nodule and collagen fiber formation were observed in the mice lungs of SP-A+/+ silicosis group, and a large number of inflammatory cells were observed in silicosis nodule, after exposure to silica dust. SP-A-/- silicosis group resulted in a more severe pulmonary inflammation and interstitial fibrosis compared to SP-A+/+ silicosis group. The apoptosis of alveolar type Ⅱ epithelial cells and the mRNA relative expression levels of Bax, Caspase-3 and Caspase-9 in lung tissues of mice in each silicosis groups were increased compared with their control groups (all P<0.05). The above four indexes of mice in SP-A-/- silicosis group were higher than those in SP-A+/+ silicosis group (all P<0.05). There was no significant difference in the expression of Bcl-2 mRNA in lung tissues of these four groups (P>0.05). Conclusion: Knockout of SP-A can aggravate inflammation and pulmonary fibrosis in silicosis model mice, and promote apoptosis of alveolar type Ⅱ epithelial cells. The mechanism may be related to the Bcl-2/Bax/Caspase-3 signaling pathway which affects the apoptosis of mitochondrial pathway.
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Objective:To analyze the serum lipid levels, and its influencing factors, of male residents around an uranium mine in order to provide a scientific basis for health risk assessment for such residents.Methods:With such a mine as the center, the surveyed subjects were divided into four groups as within 5, 10, 15 and 20 km of this mine, respectively. These male residents living around the mine were randomly selected as subjects. A health questionnaire survey was conducted among the subjects. The indicator such as height, weight and blood pressure were measured by means of the standard method. Peripheral venous blood was extracted from the subjects, and their venous blood glucose and serum lipid were detected. The levels of serum lipid and detectable rates of abnormal serum lipid were analyzed by using univariate analysis, and multivariate logistic regression analysis was used to analyze the influencing factors of dyslipidemia.Results:A total of 867 males at age 40 to 69 was included in the vicinity of the mine. The mean levels ( ± s) of TC, TG, LDL-C, and HDL-C were (5.46±1.11), (1.92±1.64), (3.19±1.02), and (1.39±0.43) mmol/L, respectively. 384 subjects with dyslipidemia were totally detected in the residents, and the detection rate was 44.29% (384/867). Of the residents with dyslipidemia, the majority was abnormal in two lipid related indexes (45.57%, 175/384). Univariate analysis result showed that there was statistically significant difference in TG level in different distance groups ( F=3.34, P<0.05). There were statistically significant differences in the abnormal detection rates of TG and HDL-C in subjects in different distance groups ( χ2=9.52, 10.18, P<0.05). The detection rates of dyslipidemia were significantly different in the groups of BMI, blood pressure and blood glucose ( χ2=45.91, 32.31, 11.42, P<0.05). Multivariate logistic regression analysis showed that excluding marital status and degree of education, the BMI, blood pressure and blood glucose all had an impact on dyslipidemia. The residents with overweight ( OR=2.08, 95% CI: 1.52-2.86) and obeseness ( OR=2.88, 95% CI: 1.58-5.24) had a higher risk for dyslipidemia than those with normal weight. The risks for dyslipidemia in the residents with hypertension ( OR=1.94, 95% CI: 1.45-2.60) and hyperglycemia ( OR= 2.17, 95% CI: 1.27-3.69) were higher than those with normal blood pressure and blood glucose, respectively. Conclusions:The detection rate of dyslipidemia is higher in male residents around the mine. The BMI, alcohol consumption, blood pressure, blood glucose and distance from the mine are influencing dyslipidemia and other relevant indexes. Overweight is an independent risk factor for dyslipidemia and its components. The distances from uranium mine has no significant effect on the dyslipidemia of male residents.
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OBJECTIVE: To explore the molecular mechanism underlying 1,2-dichloroethane(1,2-DCE) induced apoptosis by screening differentially expressed proteins in human astrocytes( HAs). METHODS: HAs were cultured in complete medium with 1,2-DCE at various concentrations of 0-80 or 0-40 mmol/L. After 24 hours,apoptosis of HAs was evaluated using flow cytometry and staining with annexin Ⅴ-fluoresce in isothiocyanate and propidium iodide. An AAH-APO-1-2 protein chip was used to screen differentially expressed proteins and quantitative real-time polymease chain reaction(qRT-PCR) was used to verify related differentially expressed genes(DEGs). RESULTS: At 1,2-DCE concentrations of0-80 mmol/L,the total apoptosis rate of HAs increased with 1,2-DCE concentrations in a dose-dependent manner( P <0. 01). Seven different kinds of proteins were screened out by apoptotic protein chip. Among them,the expression of insulin-like growth factor-binding protein( IGFBP)-1,IGFBP-4 and cytochrome C( Cyto C) were up-regulated,while the expression of P27,cysteine aspartic acid specific protease-3( Caspase-3),B-cell lymphoma-2 interacting mediator of cell death( BIM) and BH3 interacting domain death agonist( BID) were down-regulated compared with the control group. The result of DEGs verified by qRT-PCR showed that the expression of mRNA of IGFBP-1,IGFBP-4 and Cyto C at 1,2-DCE concentrations of 40 mmol/L was up-regulated. This result was in consistent with the trend of target expression in the protein chip. The mRNA expression of Caspase-3,BIM and BID was also up-regulated. CONCLUSION: 1,2-DCE induces apoptosis of HAs through mitochondrial pathway.