Nowadays, coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), whose infectivity is awfully strong, has been a major global threat to the public health. Since lung is the major target of SARS-CoV-2, the infection can lead to respiratory distress syndrome (RDS), multiple organ failure (MOF), and even death. The studies on viral structure and infection mechanism have found that angiotensin-converting enzyme 2 (ACE2), a pivotal enzyme affecting the organ-targeting in the RAS system, is the receptor of the SARS-CoV-2 virus. Currently, the detection of SARSCoV-2 is mainly achieved using open plate real-time reverse-transcription polymerase chain reaction (RT-PCR). While open plate method has some limitations, such as a high false-negative rate, cumbersome manual operation, aerosol pollution and leakage risks. Therefore, a convenient method to rapidly detect SARS-CoV-2 virus is urgently and extremely required for timely epidemic control with the limited resources. In this review, the current real-time methods and principles for novel coronavirus detection are summarized, with the aim to provide a reference for real-time screening of coronavirus in areas with insufficient detection capacity and inadequate medical resources. The development and establishment of a rapid, simple, sensitive and specific system to detect SARS-CoV-2 is of vital importance for distinct diagnosis and effective treatment of the virus, especially in the flu season.

Background. Shu Gan Jie Yu (SGJY) capsule has a good effect on relieving depressive symptoms in China. However, the mechanism of action is still unclear. Therefore, systemic pharmacology and molecular docking approaches were used to clarify its corresponding antidepressant mechanisms. Methods. Traditional Chinese Medicine Database and Analysis Platform (TCMSP), the Encyclopedia of Traditional Chinese Medicine (ETCM), and Swiss Target Prediction servers were used to screen and predict the bioactive components of the SGJY capsule and their antidepressive targets. Mild to moderate depression (MMD) related genes were obtained from GeneCards and DisGeNET databases. A network of bioactive components-therapeutic targets of the SGJY capsule was established by STRING 11.5 and Cytoscape 3.9.0 software. Gene function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed by utilizing Database for Annotation, Visualization, and Integrated Discovery (DAVID) platform. Active components were taken to dock with the hypothetical proteins by iGEMDOCK and SwissDock, and the docking details were visually displayed by UCSF Chimera software. Then, the related research literature of the SGJY capsule was reviewed, summarized, sorted, and analyzed, including experimental evidence and clinical experience. Results. Seven active components and 45 intersection targets were included in the study. PPI network had genuinely uncovered the potential therapeutic targets, such as AKT1, HSP90AA1, ESR1, EGFR, and PTGS2. KEGG pathway analysis showed that the mechanism of the SGJY capsule on MMD was mainly involved in the PI3K-Akt signaling pathway. Conclusions. In this study, we have successfully predicted the biochemically active constituents, potential therapeutic targets, and comprehensively predicted the related drug-gene interaction of the SGJY capsule for treating MMD and provided a basis for subsequent experiments.

Objective: To identify potential druggable targets for Alzheimer's disease (AD) by analyzing circulating inflammatory proteins using Mendelian randomization (MR).Methods: Two‐sample MR analysis was employed to investigate the causal relationships between 91 circulating inflammatory proteins and AD. The primary MR method utilized was the inverse variance weighted (IVW) model, while the weighted median (WM) and MR‐Egger models were applied for sensitivity analysis. To assess the heterogeneity of instrumental variables (IVs), Cochran's Q‐test and I² statistics were utilized. Additionally, ChEMBL and DGIdb databases with Bayesian colocalization analysis were consulted to identify potential druggable proteins.Results: MR analysis identified eight inflammatory proteins significantly associated with AD risk. Among these proteins, TNFB [odds ratio (OR): 1.06, 95% Confidence Interval (CI): 1.02–1.11, p = 8.77×10⁻³], TSLP (OR: 1.10, 95% CI: 1.01–1.19, p = 0.028), S100A12 (OR: 1.09, 95% CI: 1.01–1.18, p = 0.03), CD244 (OR: 1.07, 95% CI: 1.00–1.13, p = 0.036), and IL33 (OR: 1.08, 95% CI: 1.00 –1.17, p = 0.048) were identified as proteins associated with elevated AD risk. Conversely, three inflammatory proteins exhibited a protective effect against AD, including NRTN (OR: 0.91, 95% CI: 0.85–0.99; p = 0.019), CCL4 (OR: 0.95, 95% CI: 0.91–1.00, p = 0.029), and MMP1 (OR: 0.93, 95% CI: 0.87–1.00, p = 0.049). Notably, according to the gene‐drug analysis, TSLP, S100A12, CD244, CCL4, and MMP1 were identified as druggable. Additionally, MMP1 (PP4 = 0.92) and CCL4 (PP4 = 0.87) in the prefrontal cortex had the strongest colocalization evidence (PP4 > 0.85), suggesting they could potentially serve as novel therapeutic targets for AD.Conclusions: Integrative genetic analyses indicate that genetically determined circulating levels of TSLP, S100A12, CD244, CCL4, and MMP1 exert causal effects on AD risk. These findings nominate all five proteins as potential therapeutic targets, with MMP1 and CCL4 representing priority candidates warranting further mechanistic investigation and clinical validation.

Epigallocatechin‐3‐gallate (EGCG), the most abundant and biologically active catechin in green tea, has been widely reported to exhibit anti‐cancer properties in various tumor types. However, its therapeutic potential and underlying mechanisms on glioma remain ambiguous. This study aimed to investigate the in vitro and in vivo effects of EGCG on glioma, with a specific focus on elucidating its molecular mechanisms, particularly the modulation of integrin‐mediated signaling pathways and matrix metalloproteinases' (MMPs) expressions. The anti‐proliferative effects of EGCG were evaluated in human glioma cell lines (U87, U251, and LN229) using CCK‐8, EdU, and colony formation assays. Cell migration and invasion were assessed by wound healing and transwell assays, while apoptosis was analyzed via flow cytometry. The potential molecular mechanisms underlying the inhibitory effects of EGCG on integrin αvβ3/FAK/ERK signaling pathway and MMP‐2/MMP‐9 were explored by western blotting analyses. In vivo antitumor efficacy of EGCG was evaluated using an intracranial xenograft model in nude mice, with or without co‐administration of temozolomide (TMZ). Toxicity was monitored through body weight changes and histopathological examination. EGCG inhibited cell proliferation with IC ₅₀ values of 127.8 μM (U87), 172.9 μM (U251), and 104.7 μM (LN229) in glioma cells, while inducing apoptosis. Meanwhile, EGCG suppressed migration and invasion of glioma cells in a dose‐dependent manner. Mechanistically, EGCG downregulated the integrin αvβ3/FAK/ERK signaling pathway and inhibited the expression of MMP‐2/MMP‐9. In vivo, EGCG monotherapy exerted notable tumor growth inhibition, and its combination with TMZ led to enhanced therapeutic efficacy without observable systemic toxicity. EGCG exerts potent anti‐glioma effects in inhibiting cell proliferation, migration, and invasion, while promoting apoptosis, mechanically through regulating the integrin αvβ3/FAK/ERK signaling axis and suppressing MMP‐2/MMP‐9 expressions. These findings highlight EGCG as a safe and promising phytochemical adjuvant for glioma therapy, particularly in combination with conventional chemotherapy.