Data_Sheet_1_COVID-19 symptoms and compliance: The mediating role of fundamental social motives.ZIP

BackgroundUnderstanding the compliance of infected individuals and the psychological process underlying compliance during pandemics is important for preventing and controlling the spread of pathogens. Our study investigated whether fundamental social motives mediate the relationship between having infectious disease and compliance.MethodsAn online survey was conducted in March 2020, during the severe phase of the COVID-19 outbreak in China to collect data from 15,758 participants. The survey comprised self-report questionnaires with items pertaining to current symptoms (COVID-19 symptoms, other symptoms or no symptoms), the Fundamental Social Motive Inventory, and measures of compliance. Correlation analysis, linear regression analysis, and structural equation model were used for data analysis.ResultsThe participants with COVID-19 symptoms had lower levels of compliance than those without symptoms, and their lower compliance was caused by a decrease in disease avoidance (indirect effect = −0.058, 95% CI = [−0.061, −0.056]) and familial motives (indirect effect = −0.113, 95% CI = [−0.116, −0.062]). Whereas exclusion concern (indirect effect = 0.014, 95% CI = [0.011, 0.017]) suppressed the effects of COVID-19 symptoms on compliance, the effect disappeared in the multiple mediation model, while those of disease avoidance and familial motives remained.ConclusionOur findings emphasize the critical role of disease avoidance and familial motives in promoting compliance with public health norms during pandemics and suggest that enhancing these motives may serve as an effective intervention strategy to mitigate noncompliance among potentially infected individuals.</p

Characteristics of the experimental animals at the end of intervention study (n = 9).

<p>BBR, berberine; Diab+BBR, diabetic rats treated with berberine; Nor, normal lean rats; Nor+BBR, normal rats treated with berberine; FBG, fasting blood glucose; FINS, fasting serum insulin; TC, total cholesterol; TG, triglycerides; ALT, alanine aminotransferase; AST, aspartate transaminase. Data are presented as mean ± SE (n = 9).</p>a<p>: <i>P</i><0.05, compared with diabetic rats;</p>b<p>: <i>P</i><0.05, compared with normal rats(Nor).</p

FoxO1 expression in liver.

<p>(A) FoxO1 protein in liver. Nuclear and cytoplasmic proteins were extracted from liver and analyzed in a Western blot. TBP (TATA-binding protein) and GAPDH proteins are loading controls in the nuclear and cytoplasmic proteins. (B) Immunohistostaining of FoxO1 protein in liver. DAB dye (brown) was used to indicate the FoxO1 protein signal; (C) mRNA expression of FoxO1. mRNA was quantified in real time RT-PCR (n = 6). # <i>P</i><0.05, compared with Diab+Veh group; * <i>P</i><0.05, compared with normal group (Nor).</p

PEDF induction by Dex.

<p>The effect of Dex on the expression of PEDF was investigated in 3T3-L1 cells and C57BL/6J mice. <i>A</i>: The effects of Dex on PEDF mRNA expression in fully differentiated 3T3-L1 cells at 30 min, 1, 2, 3, 6 hours. <i>B</i>: PEDF expression in 3T3-L1 cells (fully differentiated) after Dex treatment at 2, 4, 6, and 8 days. <i>C</i>: The PEDF levels in the cell culture medium of 3T3-L1 cells after Dex treatment for 48 h. <i>D</i>: The effects of Dex on the PEDF promoter (hPEDFP1 and hPEDFP2) in 3T3-L1 cells. <i>E</i>: The effects of Dex on PEDF mRNA expression in the adipose tissue of C57BL/6J mice. <i>F</i>: The effects of Dex on serum PEDF in C57BL/6J mice. The data are shown as the mean ± SEM (n=4). “*” indicates P < 0.05 compared with control.</p

Lipogenesis in liver.

<p>(A) Lipogenic transcription factor proteins. Liver total protein was used in the Western blot. SREBP1, SREBP2 and ChREBP were detected in the fasted liver with specific antibodies. Beta-actin is a loading control. (B) FAS protein. The protein was detected in a Western blot in the fasted and fed liver, respectively. (C) FAS mRNA. mRNA was detected by qRT-PCR and normalized with beta-actin mRNA (n = 6). # <i>P</i><0.05, compared with Diab+Veh group; * <i>P</i><0.05, compared with normal group (Nor).</p

PEDF expression was inhibited by insulin in adipocytes.

<p><i>A</i>: Insulin treatment decreased PEDF mRNA expression in 3T3-L1 cells. <i>B</i>: Insulin reduced PEDF protein and blocked the PEDF increase in response to TNF-α in 3T3-L1 cells. <i>C</i>: Insulin treatment decreased PEDF protein and reversed the TNF-α-induced PEDF protein in 3T3-L1 cells. <i>D</i>: PEDF expression in 3T3-L1 cells after treatment with Dex, insulin, or Dex+insulin. <i>E</i>: The signaling pathway for insulin-induced inhibition of PEDF mRNA expression in 3T3-L1 cells. The 3T3-L1 cells were treated with insulin, MEK inhibitor PD98059, PI3K inhibitor LY294002, or mTOR inhibitor rapamycin, alone or in combination for 24 h. “*”, “§” indicates P<0.05 compared with the control group and TNF-α group, respectively. “#” indicates P<0.05 compared with insulin treatment. <i>F</i>: The effect of insulin treatment on NF-κB expression in the nuclear extracts of 3T3-L1 cells. Insulin blocks the effects of TNF on NF-κB expression. The data are presented as the mean ± SEM of three to four independent experiments.</p

Induction of PEDF by TNF-α.

<p><i>A</i>: PEDF mRNA expression in 3T3-L1 cells before and after TNF-α treatment at 30 min, 1, 2, 3, 6 hours in differentiated cells. <i>B</i>: PEDF levels in 3T3-L1 cell culture medium after TNF-α treatment for 48 hours. <i>C</i>: PEDF protein in differentiating 3T3-L1 cells with and without TNF-α treatment. Days of differentiation is indicated. <i>D</i>: The effects of TNF-α on PEDF mRNA expression in the adipocyte tissue of C57BL/6J mice. <i>E</i>: The effects of TNF-α on serum PEDF in C57BL/6J mice. The data are the mean ± SEM of four independent experiments. “*” indicates P<0.05 compared with the control group. </p

PEDF expression was inhibited by insulin in diabetic rats.

<p><i>A</i>: Insulin treatment decreased the serum PEDF in type 2 diabetic SD rats. <i>B</i>: Insulin treatment decreased PEDF protein in the adipose tissue of type 2 diabetic SD rats. <i>C</i>: Insulin treatment decreased PEDF mRNAs in the adipose tissue of type 2 diabetic SD rats. <i>D</i>: Insulin treatment decreased IL-6 and TNF-α mRNA expression in the adipose tissue of SD rats. White bars = TNF-α; black bars = IL-6. The data are presented as the mean ± SEM of four independent experiments. “*” indicates P<0.05 compared with the control group. “#” indicates P<0.05 compared with diabetic group. <i>NC</i>, normal control; <i>DM</i>, diabetic rats with no insulin therapy; <i>EI</i>, diabetic rats treated with insulin during early intervention study; EG, diabetic rats treated with gliclazide during early intervention study.</p

NF-κB induces PEDF expression.

<p><i>A</i>: The effects of TNF-α on PEDF expression in 3T3-L1 cells after NF-кB-p65 knockdown. The lentivirus vector CN45 that expresses siRNA for NF-κB p65 was transfected into 3T3-L1 cells with Fugene HD. The control lentivirus vector is PLVT7. <i>B</i>: NF-κB p65 expression in the nucleus of adipose tissue of STZ-induced type 2 diabetic rats. <i>C</i>: Serum PEDF levels in wild type and aP2-p65 overexpressing mice. <i>D</i>: PEDF expression in aP2-p65 overexpressing mice. PEDF was determined in the epididymal fat tissue of aP2-p65 transgenic mouse by Weston blot. <i>E</i>: Effects of NF-κB on the PEDF promoter activities. hPEDFP1 (promoter does not respond directly to NF-κB activation. The data are the mean ± SEM of three to four independent experiments. “*” indicates P<0.05 compared with the control group. “#” indicates P<0.05 compared with diabetic group.</p

PEDF Expression Is Inhibited by Insulin Treatment in Adipose Tissue via Suppressing 11β-HSD1

<div><p>Early intensive insulin therapy improves insulin sensitivity in type 2 diabetic patients; while the underlying mechanism remains largely unknown. Pigment epithelium-derived factor (PEDF), an anti-angiogenic factor, is believed to be involved in the pathogenesis of insulin resistance. Here, we hypothesize that PEDF might be down regulated by insulin and then lead to the improved insulin resistance in type 2 diabetic patients during insulin therapy. We addressed this issue by investigating insulin regulation of PEDF expression in diabetic conditions. The results showed that serum PEDF was reduced by 15% in newly diagnosed type 2 diabetic patients after insulin therapy. In adipose tissue of diabetic Sprague-Dawley rats, PEDF expression was associated with TNF-α elevation and it could be decreased both in serum and in adipose tissue by insulin treatment. In adipocytes, PEDF was induced by TNF-α through activation of NF-κB. The response was inhibited by knockdown and enhanced by over expression of NF-κB p65. However, PEDF expression was indirectly, not directly, induced by NF-κB which promoted 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) expression in adipocytes. 11β-HSD1 is likely to stimulate PEDF expression through production of active form of glucocorticoids as dexamethasone induced PEDF expression in adipose tissue. Insulin inhibited PEDF by down-regulating 11β-HSD1 expression. The results suggest that PEDF activity is induced by inflammation and decreased by insulin through targeting 11β-HSD1/glucocorticoid pathway in adipose tissue of diabetic patients. </p> </div