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Article in English | WPRIM | ID: wpr-878305


Objective@#Several COVID-19 patients have overlapping comorbidities. The independent role of each component contributing to the risk of COVID-19 is unknown, and how some non-cardiometabolic comorbidities affect the risk of COVID-19 remains unclear.@*Methods@#A retrospective follow-up design was adopted. A total of 1,160 laboratory-confirmed patients were enrolled from nine provinces in China. Data on comorbidities were obtained from the patients' medical records. Multivariable logistic regression models were used to estimate the odds ratio ( @*Results@#Overall, 158 (13.6%) patients were diagnosed with severe illness and 32 (2.7%) had unfavorable outcomes. Hypertension (2.87, 1.30-6.32), type 2 diabetes (T2DM) (3.57, 2.32-5.49), cardiovascular disease (CVD) (3.78, 1.81-7.89), fatty liver disease (7.53, 1.96-28.96), hyperlipidemia (2.15, 1.26-3.67), other lung diseases (6.00, 3.01-11.96), and electrolyte imbalance (10.40, 3.00-26.10) were independently linked to increased odds of being severely ill. T2DM (6.07, 2.89-12.75), CVD (8.47, 6.03-11.89), and electrolyte imbalance (19.44, 11.47-32.96) were also strong predictors of unfavorable outcomes. Women with comorbidities were more likely to have severe disease on admission (5.46, 3.25-9.19), while men with comorbidities were more likely to have unfavorable treatment outcomes (6.58, 1.46-29.64) within two weeks.@*Conclusion@#Besides hypertension, diabetes, and CVD, fatty liver disease, hyperlipidemia, other lung diseases, and electrolyte imbalance were independent risk factors for COVID-19 severity and poor treatment outcome. Women with comorbidities were more likely to have severe disease, while men with comorbidities were more likely to have unfavorable treatment outcomes.

Adult , Aged , COVID-19/virology , China/epidemiology , Comorbidity , Female , Humans , Male , Middle Aged , Retrospective Studies , Severity of Illness Index , Treatment Outcome
Article in Chinese | WPRIM | ID: wpr-802261


Objective:To investigate the regulatory effect of Sinisan(SNS) on the polarization of RAW264.7 macrophages induced by lipopolysaccharide (LPS). Method:RAW264.7 cells stimulated by LPS were used as the in vitro model. The cells were intervened with the different concentrations of SNS in advance. The effects of different concentrations of SNS on the proliferation of RAW264.7 cells were detected by methyl thiazolyl tetrazolium (MTT) colorimetry. The degree of cell differentiation was detected by enzyme-linked immuno sorbent assay(ELISA) method. The contents of M1 polarization factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1β (IL-1β) and M2 polarization factors interleukin-10 (IL-10) in cell culture supernatant were detected by ELISA method, mRNA levels of M1 polarization factors TNF-α, IL-6 and M2 polarization factors IL-10, arginase-1 (Arg-1) were detected by Real-time fluorescence quantitative polymerase chain reaction(Real-time PCR) method. Result:SNS had no effect on the cell viability of RAW264.7 cells, inhibited LPS-induced cell proliferation, decreased LPS-stimulated cell differentiation, down-regulated M1 polarizing factors TNF-α, IL-6, IL-1β release and TNF-α, IL-6 mRNA levels, and increased the release of IL-10 and mRNA levels of IL-10 and Arg-1. Conclusion:SNS inhibits the inflammation of RAW264.7 cells induced by LPS, and its mechanism may be related to the regulation of polarization balance of M1/M2 macrophages.

Article in Chinese | WPRIM | ID: wpr-701203


AIM:To investigate the effects of kaempferol-3-O-rutinoside(KR)on the proliferation,migration of vascular smooth muscle cells(VSMC)and the activation of transforming growth factor βreceptor 1(TGFBR1)signaling pathway in the cells.METHODS: The viability of VSMC was detected by MTT assay.The proliferation of VSMC was measured by EdU staining.The migration ability of VSMC was examined by Transwell assay.The protein levels of the mi-gration-associated proteins matrix metalloproteinase 2(MMP2)and matrix metalloproteinase 9(MMP9)were detected by Western blot.Molecular docking study was conducted to explore the interaction between KR and TGFBR 1.The protein le-vels of the phosphorylated TGFBR1,Smad2 and Smad3 were determined by Western blot.RESULTS: KR inhibited the viability of VSMC in a dose-and time-dependent manner.KR reduced the ratio of EdU-positive cells in a dose-dependent manner.KR dose-dependently suppressed the migration ability of VSMC and decreased the protein levels of MMP 2 and MMP9(P<0.05).KR docked into TGFBR1 with the binding energy of -9.804 kcal/mol by forming hydrogen bonds with SER-280,ARG-215,ASP-290 and LYS-335 of TGBFR1.KR dose-dependently suppressed the activation of TGFBR 1 and its downstream proteins Smad2 and Smad3(P<0.05).CONCLUSION: KR inhibits the proliferation and migration of VSMC,possibly via blocking the TGFBR1 signaling pathway.