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 m...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.展开更多
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 o...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.展开更多
基金supported by the National Key R&D Program of China(2020YFC0842000)National Natural Science Foundation of China(81960662)Science and Technology Department of Yunnan Province(202001AS070034)。
文摘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.
基金funded by the National Natural Science Foundation of China(Grant No.30960450,No.81560589,and No.81173110)Yunnan Province Science and Technology Department and Education Department(Grant No.2017FE467(-019),No.2018JS161,No.2014FA010,No.ZD2015009)Yunnan–USA joint research center of molecular medicines(No.2015ID001)
文摘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.
