Antiviral treatments of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
have been extensively pursued to conquer the pandemic. To inhibit the viral entry to the
host cell, we designed and obtained three peptide sequences via quartz crystal
microbalance measurement screening, which showed high affinity at nanomole to the S1
subunit of the spike protein and wild-type SARS-CoV-2 pseudovirus. Circular dichroism
spectroscopy measurements revealed significant conformation changes of the S1 protein
upon encounter with the three peptides. The peptides were able to effectively block the
infection of a pseudovirus to 50% by inhibiting the host cell lines binding with the S1
protein, evidenced by the results from Western blotting and pseudovirus luciferase
assay. Moreover, the combination of the three peptides could increase the inhibitory
rate to 75%. In conclusion, the three chemically synthetic neutralizing peptides and
their combinations hold promising potential as effective therapeutics in the prevention
and treatment of COVID-19.
The schematic diagram for the plating/stripping process of Zn. (a) Corrosion, by-products, and Zn dendrites are observed on a bare Zn electrode. (b) The Zn–THBA protective layer endows a dense and dendrite-free plating/stripping morphology.
Metformin is still being investigated due to its potential use as a therapeutic agent for managing overweight or obesity. However, the underlying mechanisms are not fully understood. Inhibiting the adipogenesis of adipocyte precursors may be a new therapeutic opportunity for obesity treatments. It is still not fully elucidated whether adipogenesis is also involved in the weight loss mechanisms by metformin. We therefore used adipose-derived stem cells (ADSCs) from inguinal and epididymal fat pads to investigate the effects and mechanisms of metformin on adipogenesis in vitro. Our results demonstrate the similar effect of metformin inhibition on lipid accumulation, lipid droplets fusion, and growth in adipose-derived stem cells from epididymal fat pads (Epi-ADSCs) and adipose-derived stem cells from inguinal fat pads (Ing-ADSCs) cultures. We identified that cell death-inducing DFFA-like effector c (Cidec), Perilipin1, and ras-related protein 8a (Rab8a) expression increased ADSCs differentiation. In addition, we found that metformin inhibits lipid droplets fusion and growth by decreasing the expression of Cidec, Perilipin1, and Rab8a. Activation of AMPK pathway signaling in part involves metformin inhibition on Cidec, Perilipin1, and Rab8a expression. Collectively, our study reveals that metformin inhibits lipid storage, fusion, and growth of lipid droplets via reduction in Cidec and its regulatory factors in ADSCs cultures. Our study supports the development of clinical trials on metformin-based therapy for patients with overweight and obesity.
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