Captopril alleviates lung inflammation in SARS-CoV-2-infected hypertensive mice

Severe acute respiratory syndrome coronavirus 2(SARS-Co V-2)is the etiologic agent responsible for the global coronavirus disease 2019(COVID-19)pandemic.Numerous studies have demonstrated that cardiovascular disease may affect COVID-19 progression.In the present study,we investigated the effect of hypertension on viral replication and COVID-19 progression using a hypertensive mouse model infected with SARS-Co V-2.Results revealed that SARS-Co V-2 replication was delayed in hypertensive mouse lungs.In contrast,SARS-Co V-2 replication in hypertensive mice treated with the antihypertensive drug captopril demonstrated similar virus replication as SARS-Co V-2-infected normotensive mice.

Zika virus infection induces glycometabolic disorder in northern pig-tailed macaques

Dear Editor,The Zika virus(ZIKV)was first identified in Africa in 1947 but remained relatively obscure for nearly 70 years.However,from 2014 to 2016,ZIKV was introduced into Brazil from the Pacific Islands,leading to its rapid dissemination throughout the Americas(Fauci and Morens,2016).This mosquito-borne virus is distinguished by its capacity to cause congenital defects,as evidenced by the microcephaly epidemic in Brazil,and has been declared a Public Health Emergency of International Concern(Gulland,2016).Yuan et al.(2017)discovered that a specific mutation in the prM protein of American ZIKV strains increased infectivity in human and mouse neural progenitor cells.Despite reports of varying rates of microcephaly at different sites in Brazil,evidence from surveillance and observational studies indicates multifactorial etiologies beyond viral mutations(Barbeito-Andrés et al.,2018).

Scutellarin protects human cardiac microvascular endothelial cells with hypoxia-reoxygenation injury via JAK2/STAT3 signal pathway

Objective: To investigate the antagonistic cell injury effect and molecular mechanism of scutellarin(SCU)in hypoxia reoxygenation(HR) treated human cardiac microvascular endothelial cells(HCMECs).Methods: The method of 12 h hypoxia following by 12 h reoxygenation was used to culture HCMECs in vitro to built cell injury model. The groups were divided into control group, model(HR) group, and HR + SCU(0.1 μmol/L, 1 μmol/L, and 10 μmol/L) group. The cell viability was determined by MTT, and oxidative stress was detected by malondialdehyde(MDA) levels by biochemical assay kit. Protein expression of JAK2/p-JAK2 and STAT3/p-STAT3 were evaluated by Western blot.Results: The results of MTT and MDA showed that HR decreased the cell viability(P < 0.05) and increased MDA level significantly(P < 0.05), SCU played a contrary role in these processes. Western blot analysis indicates that, the expression of JAK2 and p-JAK2, STAT3, and p-STAT3 were increased in model group when compared with control group(P < 0.05); Compared with model group, their expression were reduced by SCU(P < 0.05).Conclusion: SCU took a protective effect on HR-treated HCMECs, and the molecular mechanism may be associated with the inhibition of JAK2/STAT3 signal transduction pathway.