ABSTRACT
Objective:To explore the psychometric characteristics of the Chinese version of the health-related social capital scale.Methods:From March to May 2020, after the original scale was translated into Chinese following the Brislin improved translation model, 251 community-dwelling senior citizens aged 65 and above were selected by convenient sampling method. Data analysis was conducted using SPSS 22.0 and AMOS 22.0, including tests of significance, correlation analysis, exploratory factor analysis, and confirmatory factor analysis.Results:Exploratory factor analysis extracted three factors: social participation, social cohesion, and reciprocity, which accounted for a cumulative contribution rate of 61.72%. Confirmatory factor analysis showed that the three-factor model fitted well(χ 2/ df=1.22, RMSEA=0.04, CFI=0.98, GFI=0.93, IFI=0.98, TLI=0.97). Social capital was significantly correlated with perceived social support positively ( r=0.36, P<0.01), and with loneliness negatively ( r=-0.30, P<0.01). The three factors were significantly correlated with the total scale ( r=0.85, 0.50 and 0.52, respectively, all P<0.01). And correlations between the items of each factor were 0.24-0.55, 0.30-0.59, 0.44-0.70, respectively(all P<0.01). The Cronbach's α coefficients of the total scale and three factors were 0.74, 0.72, 0.65 and 0.62, respectively(all P<0.01), and their retest reliability were 0. 92, 0. 87, 0. 82 and 0. 96, respectively(all P<0.01). Conclusion:The Chinese version of health-related social capital scale conforms to the three-factor model with good reliability and validity, which can be used to assess the social capital status of community-dwelling older adults in China.
ABSTRACT
Objective:To observe the expression of sirtuin 3 (Sirt3) and mitochondrial damage-associated proteins in lipopolysaccharide (LPS)-induced acute kidney injury mouse model and renal tubular epithelial cells, and to explore the role of Sirt3 in LPS-induced abnormal mitochondrial dynamics in renal tubular epithelial cells.Methods:Eighteen specific pathogen free (SPF) male C57BL/6 mice were randomly assigned to control group, LPS 24 h group and LPS 48 h group. The control group was intraperitoneally injected with physiological saline (0.1 ml/10 g), and LPS 24 h group and LPS 48 h group were intraperitoneally injected with LPS (10 mg/kg) solution. Renal functional indexes of mice were analyzed by automatic biochemical analyzer. The pathological change of the kidney was observed by HE staining, and the expressions of dynamin-related protein-1 (Drp1), optic atrophy type 1 (Opa1) and Sirt3 were evaluated by Western blotting. Expression and distribution of Sirt3 in kidney was assessed by immunohistochemistry. Human renal tubular epithelial cells (HK-2) were exposed to 10 μg/ml LPS for 24 h, and the expression of Drp1, Opa1 and Sirt3 were detected by Western blotting. Cell apoptosis was assessed by Hoechst-33342 staining. After transfection to HK-2 cells with pcDNA3.1-Sirt3 recombinant plasmid, the expressions of Sirt3, Drp1, Opa1 and cell apoptosis were detected by the same methods as above.Results:(1) The levels of blood urea nitrogen and serum creatinine in LPS group were significantly higher than those in control group (both P<0.05), and the pathological changes of kidney were obvious. (2) Compared with the control group, the expression of mitochondrial fission-associated protein Drp1 in renal tissue of LPS group was significantly higher ( P<0.05), and the expression of mitochondrial fusion associated protein Opa1 was significantly lower ( P<0.05). (3) Compared with the control group, the expression of Sirt3 in LPS group was significantly lower ( P<0.05), and immunohistochemistry results showed that Sirt3 was mainly expressed in glomerular vascular endothelial cells and renal tubular epithelial cells. (4) In vitro, LPS stimulation induced increased Drp1 expression in HK-2 cells ( P<0.05), decreased Opa1 and Sirt3 expression (both P<0.05), and increased apoptosis ( P<0.05). (5) LPS-induced mitochondrial dynamics disturbance and apoptosis were alleviated by pcDNA3.1-Sirt3 recombinant plasmid transfection. Conclusions:LPS can induce down-regulation of Sirt3 expression and disturbance of mitochondrial dynamics, and Sirt3 may play a protective role in LPS-induced acute kidney injury by regulating mitochondrial dynamics.