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Flavonoids are widely distributed natural products with broad biological activities. Apigenin is a dietary flavonoid that has recently been demonstrated to interact with heterogeneous nuclear ribonucleoproteins (hnRNPs) and interferes with their RNA editing activity. We investigated whether apigenin possessed antiviral activity against enterovirus-71 (EV71) infection since EV71 infection requires of hnRNP proteins. We found that apigenin selectively blocks EV71 infection by disrupting viral RNA association with hnRNP A1 and A2 proteins. The estimated EC50 value for apigenin to block EV71 infection was determined at 10.3 µM, while the CC50 was estimated at 79.0 µM. The anti-EV71 activity was selective since no activity was detected against several DNA and RNA viruses. Although flavonoids in general share similar structural features, apigenin and kaempferol were among tested compounds with significant activity against EV71 infection. hnRNP proteins function as trans-acting factors regulating EV71 translation. We found that apigenin treatment did not affect EV71-induced nucleocytoplasmic redistribution of hnRNP A1 and A2 proteins. Instead, it prevented EV71 RNA association with hnRNP A1 and A2 proteins. Accordingly, suppression of hnRNP A1 and A2 expression markedly reduced EV71 infection. As a positive sense, single strand RNA virus, EV71 has a type I internal ribosome entry site (IRES) that cooperates with host factors and regulates EV71 translation. The effect of apigenin on EV71 infection was further demonstrated using a bicistronic vector that has the expression of a GFP protein under the control of EV71 5′-UTR. We found that apigenin treatment selectively suppressed the expression of GFP, but not a control gene. In addition to identification of apigenin as an antiviral agent against EV71 infection, this study also exemplifies the significance in antiviral agent discovery by targeting host factors essential for viral replication.

Purpose. The purpose of this study was to examine the effects of Baduanjin sequential therapy (BST) on the quality of life and cardiac function in patients with AMI after PCI. Subjects. 96 patients with AMI after PCI were randomly assigned as subjects to two groups: BST group who received 24 weeks of BST training and control group who received no training. Methods. The methods used in this study included the changes in SF-36 subscales, the measures of left ventricular ejection fraction (LVEF), N-terminal pro-B-type natriuretic peptide (NT-pro-BNP), the body mass index (BMI), and the abdominal circumference. Results. Of the 96 participants, 82 total patients completed the entire study. At 12 weeks, role physical and health transition of SF-36 were significantly different between the two groups, with a difference of 26.12 (95% CI, 11.59 to 40.64) in role physical and a difference of 15.94 (95% CI, 5.60 to 26.28) in health transition (p<0.05). However, there were statistically significant differences in all aspects of SF-36 between the two groups at 24 weeks (p<0.05). The BST also lowered abdominal circumference and BMI as compared with the control group. In the 24-week follow-up, a significant difference was found in the decline of the LVEF in the control group (p=0.020), while there was a nonsignificant difference in the BST group (p=0.552). Compared with the control group, the BST group reduced 50 pg/ml on the NT-pro-BNP at 24 weeks (p=0.013). The effects of BST exercise were maintained at 24 weeks after the intervention. No serious adverse events were observed. Conclusions. The BST appears to improve the quality of life in patients with AMI after PCI, with additional benefits of lowered abdominal circumference and BMI and improved level of cardiac function. This trial is registered with NCT02693795.

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