RESUMEN
The coronavirus disease 2019 (COVID-19) that occurred in Wuhan, Hubei Province, China, has been declared a public health emergency of international concern and a pandemic by the World Health Organization. The Chinese government has temporarily taken strong response measures and effective procedures to stop the further expansion and development of the epidemic. It is important for clinicians to screen, diagnose, and monitor COVID-19.
RESUMEN
The present study aimed to evaluate the value of serum amyloid A (SAA) in coronavirus disease 2019 (COVID-19) and compared the efficacy of SAA and C-reactive protein (CRP) in predicting the severity and recovery of COVID-19. A retrospective study was conducted on COVID-19 patients hospitalized in Wuhan No. 1 Hospital (Hubei, China) from January 21, 2020 to March 4, 2020. A two-way ANOVA analysis was used to compare the serum CRP and SAA levels between mild group and severe group during hospitalization days. Linear regression was used to analyze the relationship between the serum CRP, SAA levels and treatment days in recovered patients. The Logistic regression analysis and the area under curve (AUC) were calculated to determine the probability for predicting the severity and recovery of COVID-19. The severe group displayed higher CRP and SAA levels compared with the mild group during hospitalization (P<0.001). Logistic regression indicated that SAA and CRP were independent risk factors for the severity of COVID-19. The corresponding AUC of CRP and SAA values for severity of COVID-19 were 0.804 and 0.818, respectively. Linear regression analysis revealed that CRP and SAA levels were negatively correlated with treatment days in recovered patients (r=-0.761, -0.795, respectively). Logistic regression demonstrated that SAA was an independent factor for predicting the recovery of COVID-19. However, CRP could not predict the recovery of COVID-19. The corresponding AUC of SAA for the recovery of COVID-19 was 0.923. The results of the present study indicated that SAA can be considered to be a biomarker for predicting the severity and recovery of COVID-19.
RESUMEN
Senescence of cardiomyocytes is considered a key factor for the occurrence of doxorubicin (Dox)associated cardiomyopathy. The NODlike receptor family pyrin domaincontaining 3 (NLRP3) inflammasome is reported to be involved in the process of cellular senescence. Furthermore, thioredoxininteractive protein (TXNIP) is required for NLRP3 inflammasome activation and is considered to be a key component in the regulation of the pathogenesis of senescence. Studies have demonstrated that pretreatment with honokiol (Hnk) can alleviate Doxinduced cardiotoxicity. However, the impact of Hnk on cardiomyocyte senescence elicited by Dox and the underlying mechanisms remain unclear. The present study demonstrated that Hnk was able to prevent Doxinduced senescence of H9c2 cardiomyocytes, indicated by decreased senescenceassociated ßgalactosidase (SAßgal) staining, as well as decreased expression of p16INK4A and p21. Hnk also inhibited TXNIP expression and NLRP3 inflammasome activation in Doxstimulated H9c2 cardiomyocytes. When TXNIP expression was enforced by adenovirusmediated gene overexpression, the NLRP3 inflammasome was activated, which led to inhibition of the antiinflammation and antisenescence effects of Hnk on H9c2 cardiomyocytes under Dox treatment. Furthermore, adenovirusmediated TXNIPsilencing inhibited the NLRP3 inflammasome. Consistently, TXNIP knockdown enhanced the antiinflammation and antisenescence effects of Hnk on H9c2 cardiomyocytes under Dox stimulation. In summary, Hnk was found to be effective in protecting cardiomyocytes against Doxstimulated senescence. This protective effect was mediated via the inhibition of TXNIP expression and the subsequent suppression of the NLRP3 inflammasome. These results demonstrated that Hnk may be of value as a cardioprotective drug by inhibiting cardiomyocyte senescence.