Notes

Power over APOBEC3B induction as well as cccDNA corrosion through NF-κB and miR-138-5p.
Inflammation is a natural process that occurs in the organism in response to harmful external agents. Despite being considered beneficial, exaggerated cases can cause severe problems for the body. The main inflammatory manifestations are pain, increased temperature, edema, decreased mobility, and quality of life for affected individuals. Diseases such as arthritis, cancer, allergies, infections, arteriosclerosis, neurodegenerative diseases, and metabolic problems are mainly characterized by an exaggerated inflammatory response. Inflammation is related to two categories of substances pro- and anti-inflammatory mediators. Among the pro-inflammatory mediators is tumor necrosis factor-α (TNF-α). It is associated with immune diseases, cancer, and psychiatric disorders that increase its excretion. Thus, it becomes a target widely used in discovering new anti-inflammatory drugs. In this context, secondary metabolites biosynthesized by plants have been used for thousands of years and continue to be one of the primary sources of new drug scaffolds against inflammatory diseases. To minimize costs related to the drug discovery process, computer-aided drug design (CADD) techniques are broadly explored to increase the chances of success. In this review, the main natural compounds that are derived from alkaloids, flavonoids, terpene, and polyphenols as promising TNF-α inhibitors will be discussed. Finally, we applied a molecular modeling protocol involving all compounds described here, suggesting that their interactions with Tyr59, Tyr119, Tyr151, Leu57, and Gly121 residues are essential for the activity. Such findings may prove useful for research groups worldwide to design new anti-inflammatory TNF-α inhibitors.
Berberine (BBR) is an isoquinoline alkaloid extracted from Chinese medicine, exerting various pharmacological effects. BBR is partially metabolized by cytochrome 3A4 (CYP3A4) in vivo. Some reports indicated that BBR could inhibit the activity of CYP3A4. However, the underlying mechanisms are not entirely understood. CYP3A4 is transcriptionally regulated by two nuclear receptors nuclear transcription X receptor (PXR) and constitutive androstane receptor (CAR). It degraded via the ubiquitin-proteasome system. Hence, we tried to explore the mechanisms of CYP3A4 inhibition on both transcriptive and protein levels.

Western Blot, RT-PCR, and Co-immunoprecipitation were used to perform the experiments.

Our results showed that BBR inhibited the transcription of CYP3A4 gene by downregulating PXR. In addition, BBR accelerated the degradation of CYP3A4 protein via the polyubiquitination pathway.

These findings may lead to the determination of novel drug-drug interactions with BBR and contribute to the future clinical application of BBR.
These findings may lead to the determination of novel drug-drug interactions with BBR and contribute to the future clinical application of BBR.Nanoparticles (NPs) are projected to play a significant role in fighting against coronavirus disease (COVID-19). The various properties of NPs like magnetic and optical can be exploited to build diagnostic test kits. The unembellished morphological and physiochemical resemblances of SARS-CoV-2 with synthetic NPs make them a potent tool for mediation. Nanoparticles can be analytically functionalized with different proteins, polymers, and functional groups to perform specific inhibitory functions while also serving as delivery vehicles . Moreover, NPs can also be employed to prepare broad-spectrum respiratory drugs and vaccines that can guard seasonal flu and prepare the human race for the pandemic in the future. The present review outlines the role of NPs in detection, diagnostic and therapeutic against members of the coronavirus family. We emphasize nanomaterial-based approaches to address coronaviruses in general and SARS-CoV-2 in particular. We discuss NPs based detection systems like graphene (G-FET), biosensors, and plasmonic photothermal associated sensors. Inorganic, organic virus-like & self-assembly protein (VLP), and photodynamic inactivation of SARS-CoV-2 are also presented as therapeutic approaches exploiting NPs.Wound healing is a varied and complex process designed to promptly restore standard skin structure, function, and appearance. To achieve this goal, different immune and biological systems participate in coordination through four separate steps, including homeostasis, inflammation, proliferation, and regeneration. Each step involves the function of other cells, cytokines, and growth factors. However, chronic ulcers, which are classified into three types of ulcers, namely vascular ulcers, diabetic ulcers, and pressure ulcers, cannot heal through the mentioned natural stages. It causes mental and physical problems for these people and, as a result, imposes high economic and social costs on society. In this regard, using a system that can accelerate the healing process of such chronic wounds, as an urgent need in the community, should be considered. Therefore, in this study, the innovations of drug delivery systems for the healing of chronic wounds using hydrogels, nanomaterial, and membranes are discussed and reviewed.
Currently, it has been recognized that High-Density Lipoproteins (HDL) functionality plays a much more essential role in protection from atherosclerosis than circulating HDL-cholesterol (HDL-C) levels per se. Cholesterol efflux from macrophages to HDL, cholesterol efflux capacity (CEC) has been shown to be a key metric of HDL functionality. Thus, quantitative assessment of CEC may be an important tool for the evaluation of HDL functionality, as improvement of HDL function may lead to a reduction of the risk for Cardiovascular disease (CVD).

Although the cardioprotective action of HDLs is exerted mainly through their involvement in the reverse cholesterol transport (RCT) pathway, HDLs also have important anti-inflammatory, antioxidant, antiaggregatory and anticoagulant properties that contribute to their favorable cardiovascular effects. BV-6 Certain genetic, pathophysiologic, disease states and environmental conditions may influence the cardioprotective effects of HDL either by inducing modifications in lipidome and/or protein composition or in the enzymes responsible for HDL metabolism.
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