breaks, and treatment of well-known IMIDs.Psoriasis is considered as a common chronic immune-mediated skin disorder characterized by abnormal keratinocyte proliferation. selleck Luteolin, an anti-inflammatory natural flavonoid with well-accepted inhibition effect against keratinocyte proliferation, was hypothesized to have a potential therapeutic effect for psoriasis. In this paper, we investigated the relieving effect of luteolin against imiquimod-induced psoriasis-like lesions on BALB/c mice and its possible anti-inflammatory mechanisms in lipopolysaccharide-stimulated macrophages (RAW264.7 cells). We found that luteolin ameliorated psoriasis-like skin lesions, suppressed the cutaneous infiltration of macrophages, T cells and neutrophils, and downregulated the expression of cytokines like IL-6, IL-1β, TNF-α, IL-17A and IL-23 in both skin lesions and eyeball blood of model mice. In vitro, we observed luteolin significantly suppressed the levels of psoriasis-related pro-inflammatory cytokines, such as IL-17A, IL-6, TNF-α and IL-23, and inflammatory mediators like nitric oxide NO, inducible NOS, COX-2 in RAW264.7 cells. The anti-inflammatory activity was accomplished by inhibiting NF-κB expression and activation. This study demonstrates luteolin is effective in alleviating psoriasis-like skin lesions and downregulating inflammatory response via NF-κB pathway, suggesting luteolin as a potential molecule for further therapeutic research of inflammation-related skin diseases like psoriasis.The unique properties of polymer-hybrid nanosystems enable them to play an important role in different fields such as biomedical applications. Hybrid materials, which are formed by polymer and inorganic- or organic-base systems, have been the focus of many recently published studies whose results have shown outstanding improvements in drug targeting. The development of hybrid polymer materials can avoid the synthesis of new molecules, which is an overall expensive process that can take several years to get to the proper elaboration and approval. Thus, the combination of properties in a single hybrid system can have several advantages over non-hybrid platforms, such as improvements in circulation time, structural disintegration, high stability, premature release, low encapsulation rate and unspecific release kinetics. Thus, the aim of the present review is to outline a rapid and well-oriented scenario concerning the knowledge about polymer-hybrid nanoparticles use in biomedical platforms. Furthermore, the ultimate methodologies adopted in synthesis processes, as well as in applications in vitro/in vivo, are the focus of this review.As a process entailing a high turnover of the host cell molecules, viral replication is required for a successful viral infection and requests virus capacity to acquire the macromolecules required for its propagation. To this end, viruses have adopted several strategies to harness cellular metabolism in accordance with their specific demands. Most viruses upregulate specific cellular anabolic pathways and are largely dependent on such alterations. RNA viruses, for example, upregulate both glycolysisand glycogenolysis providing TCA cycle intermediates essential for anabolic lipogenesis. Also, these infections usually induce the PPP, leading to increased nucleotide levels supporting viral replication. SARS-CoV-2 (the cause of COVID-19)that has so far spread from China throughout the world is also an RNA virus. Owing to the more metabolic plasticity of uninfected cells, a promising approach for specific antiviral therapy, which has drawn a lot of attention in the recent years, would be the targeting of metabolic changes induced by viruses. In the current review, we first summarize some of virus-induced metabolic adaptations and then based on these information as well as SARS-CoV-2 pathogenesis, propose a potential therapeutic modality for this calamitous world-spreading virus with the hope of employing this strategy for near-future clinical application.Hypopharyngeal cancer is squamous cell carcinoma (SCC) with the worst prognosis among the head and neck cancers. Overall, the 5-year survival rate remains poor although diagnostic imaging, radiation, chemotherapy, and surgical techniques have been improved. The mortality of patients with hypopharyngeal cancer is partly due to an increased likelihood of developing a second primary malignancy and metastasis. In this study, we found that MLCK expression, compared to healthy tissue, was up-regulated in hypopharyngeal tumor tissue. Of particular interest, a low 5-year survival rate was positively correlated with MLCK expression. We hypothesized that MLCK might be a target for hypopharyngeal cancer prognosis and treatment. In order to explore the function of MLCK in the development of cancer, we knockdown MLCK in hypopharyngeal cancer FaDu cells. The results showed that MLCK knockdown reduced the migration and invasion of FaDu cells. 4-amino-2-trifluoromethyl-phenyl retinate (ATPR) is the derivative of all-trans retinoic acid (ATRA), which was able to reduce both MLCK expression and activity in FaDu cells. ATPR induced FaDu cells apoptosis in a dose-dependent manner and also inhibited cell growth both in vivo and in vitro. Further experiments showed that overexpression of MLCK reduced ATPR induced-migration inhibition while increase of ATPR induced apoptosis, which suggested that MLCK was involved in ATPR's anti-cancer function. In conclusion, MLCK is a novel prognostic marker and therapeutic target for hypopharyngeal cancer. By targeting MLCK, ATPR exhibits its potential application in the treatment of this type of cancer. Long non-coding RNA (lncRNA) has been proposed to regulate tumorigenesis, however, the role of small nucleolar RNA host gene 8 (SNHG8) in nasopharyngeal carcinoma (NPC) remains unclear. Levels of SNHG8 in NPC tissues and cells were analyzed with real-time quantitative PCR method. Cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were performed to detect cell viability, migration, and invasion. Luciferase activity assay and RIP assay were performed to explore relationships among SNHG8, microRNA-656-3p (miR-656-3p), and special AT-rich sequence-binding protein 1 (SATB1). We found SNHG8 level was increased expression in NPC tissues and cells.In vitro assays revealed that SNHG8 stimulates NPC cell proliferation, colony formation, cell migration, and cell invasion. In vivo assay confirmed knockdown of SNHG8 could hamper tumor growth. Furthermore, we showed SNHG8 serves as a sponge for miR-656-3p to regulate SATB1 expression, and participated in NPC progression.