Protein-based plant immune inducers are special compounds that can induce plant defense responses. They are mainly derived from pathogenic microorganisms, biocontrol microorganisms, host plants, and host-pathogen interaction processes. Protein elicitors improve plant resistance by triggering plant pathogen-associated molecular patterns to trigger immunity and effectors to trigger immune responses that frequently involve reactive oxygen species, Ca²⁺, salicylic acid, jasmonic acid, gibberellin, and ethylene cascade signaling pathways. They can bolster plant resistance against bacterial, fungal, and viral diseases, as well as environmental stress. Here we summarize the sources, mechanisms of action, and current applications of protein-based elicitors, identify existing problems, and outline future development trends. We propose that future research should focus on improving the persistence and stability of these elicitors, exploring the combined use of multiple elicitors or their combination with other agents, and their application in plant breeding., aiming for developing green biopesticides using protein-based elicitors.

Cardiovascular diseases (CVD) are the leading cause of death among residents in China and significantly impact patients’ quality of life. The pathogenesis of CVD is complex, with chronic low-grade inflammation as a predominant feature. The nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is a key regulator of inflammatory responses and plays a crucial role in innate immune responses. Its abnormal activation leads to excessive inflammation and pyroptosis, which is closely associated with the development of atherosclerosis, myocardial infarction, diabetic cardiomyopathy, and other CVDs. Recent studies suggest that exercise, as a safe and effective non-pharmacological intervention, can mitigate cardiovascular inflammation and pyroptosis by inhibiting NLRP3 inflammasome activation, thereby playing a positive role in CVD prevention and treatment. However, the theories and mechanisms of exercise-mediated NLRP3 inflammasome intervention in CVD remain underexplored. Therefore, this review summarizes the relationship between the NLRP3 inflammasome and CVD, explores the effects of different types, intensities, and durations of exercise on NLRP3 inflammasome activation, and provides a comprehensive analysis of the signaling pathways involved in exercise interventions targeting the NLRP3 inflammasome for the prevention and treatment of CVD. The aim is to provide new insights and references for exercise-based prevention and management of CVD.

Metabolic syndrome (MS) is a multifaceted metabolic disorder marked by obesity, hyperlipidemia, liver steatosis, and insulin resistance, posing a significant risk to human well-being. Research on the gut microbiome, metabolites produced by gut microbiota, and their ecological niche has revealed the pivotal role of gut microbiota in the pathogenesis of MS. The advancement of MS is intricately linked to the composition and function of gut microbiota. The gut microbiota and its metabolites have been identified as potential biomarkers for MS, providing early indications of disease progression and offering opportunities for prevention and treatment. Studies have demonstrated that aerobic exercise is a viable and safe intervention for modulating gut microbiota composition. Aerobic exercise has been shown to enhance gut microbiota diversity, regulate metabolites produced by gut bacteria, and strengthen the integrity of the intestinal mucosal barrier. The implementation of aerobic exercise as an intervention to modulate gut microbiota has been shown to be efficacious in the prevention of MS by mitigating inflammation, enhancing insulin sensitivity, optimizing lipid metabolism, and fortifying the integrity of the intestinal mucosal barrier. This study aims to systematically review the characteristics of gut microbiota in patients with MS, particularly those who are obese, diabetic, or have non-alcoholic fatty liver disease. The research will also investigate the correlation between MS and gut microbiota, examine the molecular crosstalk, and assess the impact and mechanisms of aerobic exercise intervention in regulating gut microbiota to prevent MS. The ultimate goal is to offer a novel perspective and potential strategy for using aerobic exercise to modulate gut microbiota and prevent the onset of MS.

Hepatocellular carcinoma (HCC) is one of the most prevalent and deadly malignancies worldwide, with many patients failing to benefit sustainably from emerging immunotherapies and targeted therapies due to drug resistance. Current commonly used biomarkers, such as alpha-fetoprotein (AFP), tumor mutation burden (TMB), and programmed cell death protein 1 (PD-1), lack efficacy in indicating the outcomes of HCC immunotherapy and targeted therapy. Therefore, identifying effective biomarkers to accurately predict therapeutic efficacy is crucial for optimizing clinical decision-making. Recent studies have shown that N6-methyladenosine (m⁶A) modification, one of the most common and important RNA modifications in eukaryotes, plays a significant role in the HCC resistance to immunotherapy and targeted therapy. We summarize the research progress regarding to the roles and mechanisms of m⁶A modification and its functional proteins in the resistance to immunotherapy and targeted therapy in HCC, and also discuss the potential application of m⁶A modification as biomarkers for predicting the efficacy of these treatments.

Macrophages are an important class of immune cells that are mainly derived from myeloid progenitor cells in the bone marrow. They function in phagocytosis and antigen presentation, and participate in innate immune and inflammatory responses. Lysophosphatidic acid (LPA) is an active phospholipid signaling molecule that induces macrophage differentiation and polarization, regulates macrophage migration and infiltration, and modulates the inflammatory response in which macrophages participate. In this paper, we review the molecular mechanisms underlying the role of LPA in macrophages in recent years by taking the role of LPA in macrophages as an entry point: LPA plays an important role in macrophage differentiation and polarization by inducing related regulatory factors and cytokines; LPA receptors mediate related signaling pathways to regulate macrophage migration and infiltration; and the ATX/LPA signaling axis and related cytokines are involved in macrophage inflammatory regulation. In addition, the regulatory role and potential clinical value of LPA in tumor-associated macrophages and macrophage inflammatory response diseases are reviewed. At present, the molecular mechanism of action of LPA in macrophages has not been fully elucidated. And an in-depth study of the receptor expression, biological roles, and regulatory mechanisms of LPA in macrophages will provide new strategies for the treatment of macrophage-associated diseases and cancers.

Polyamines are a class of polycations that are ubiquitous in living organisms and play a vital role in physiological activities. In tumors, polyamine homeostasis is often dysregulated, and high levels of polyamine are required for tumor cell growth and tumor progression, rendering the polyamine metabolism pathway a reasonable target for tumors therapy. However, even though researchers have discovered druggable regulators of the polyamine metabolic pathway, due to the compensatory response, low bioavailability, rapid metabolism, and high toxicity, targeting a single regulator has some limitations. Therefore, drug synergism can achieve better therapeutic effects at lower doses and lower toxicity, which is more advantageous than monotherapy. Here we review the advance of this drug combination therapy based on polyamine metabolism in tumors treatment in recent years.

Aptamers are a type of single-chain oligonucleotide that can combine with a specific target. Due to their simple preparation, easy modification, stable structure and reusability, aptamers have been widely applied as biochemical sensors for medicine, food safety and environmental monitoring. However, there is little research on aptamer-target binding mechanisms, which limits their application and development. Computational simulation has gained much attention for revealing aptamer-target binding mechanisms at the atomic level. This work summarizes the main simulation methods used in the mechanistic analysis of aptamer-target complexes, the characteristics of binding between aptamers and different targets (metal ions, small organic molecules, biomacromolecules, cells, bacteria and viruses), the types of aptamer-target interactions and the factors influencing their strength. It provides a reference for further use of simulations in understanding aptamer-target binding mechanisms.

Serine/arginine-rich splicing factor 6 (SRSF6) is a member of the serine and arginine-rich (SR) protein family, and it plays a crucial regulatory role in RNA splicing. Dysregulation of SRSF6 expression or function can lead to aberrant alternative splicing of certain genes, and contribute to the development and progression of inflammatory diseases, including tumors, diabetes, and pleural fibrosis. However, the role of SRSF6 in inflammation remains unclear. In this study, we found that the expression of inflammatory factors, including tumor necrosis factor-α (TNF-α) and cyclooxygenase-2 (COX-2), was induced by lipopolysaccharides (LPS). Concurrently, both the levels of SRSF6 mRNA and protein expression significantly increased with prolonged LPS stimulation (P<0.05). Furthermore, we investigated the change of SRSF6 expression on the expression of inflammatory factors. The results showed that upregulation of SRSF6 enhanced the expression of LPS-induced inflammatory factors (P<0.05), while downregulation of SRSF6 inhibited their expression (P<0.05). Additionally, the activation of the nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways was suppressed by SRSF6 knockdown (P<0.05), indicating that SRSF6 is involved in regulating inflammatory responses in macrophages. Myeloid differentiation factor 88 (MyD88) is a key adaptor protein in the TLR4 signaling pathway, with its splicing isoforms MyD88-L and MyD88-S exerting pro-inflammatory and anti-inflammatory effects, respectively. Analysis of RNA-binding protein database and RNA immunoprecipitation showed that SRSF6 binds to MyD88 mRNA. Splicing analysis indicated that downregulation of SRSF6 promoted the expression of the anti-inflammatory MyD88-S mRNA isoform (P<0.01). Moreover, knockdown of MyD88-S could rescue the expression of inflammatory factors suppressed by SRSF6 downregulation. These findings suggest that SRSF6 regulates MyD88 alternative splicing in macrophages, thereby affecting the activation of inflammatory signaling pathways and the expression of inflammatory factors. This study provides a foundation for further elucidating the role of SRSF6 in inflammatory diseases.

Quercetin (Que) is a flavonoid compound widely distributed in nature with various biological activities. Its anti-inflammatory effect plays a crucial role in many diseases, closely related to its regulation of histone post-translational modifications. However, there have been no detailed reports on the anti-inflammatory effects of quercetin regulating histone post-translational modifications. In this study, we first investigated the effect of quercetin on the M1 macrophages polarization. The results showed that quercetin can significantly down-regulate the levels of interleukin-1β (IL-1β) and interleukin-6 (IL-6) in M1 macrophages. Next, we used the super stable isotope labeling by amino acids in cell culture (super-SILAC) method derived from SILAC technology based on mass spectrometry to systematically analyze the post-translational modification levels of histone in macrophages treated with quercetin. A total of 30 histone modification sites were quantified, of which 12 histone lysine acetylation marks were significantly downregulated and 4 lysine methylation sites were upregulated (fold change >1.2, P<0.05), and some sites were verified by Western blot (WB), which was consistent with the mass spectrometry results. In conclusion, a comprehensive analysis of quercetin on regulating macrophage histone modifications in this study provides reliable data references and new insights for studying its anti-inflammatory mechanism.

Limosilactobacillus reuteri is a microbe intricately linked to humans and animal health. A thorough assessment of its safety and potential benefits is imperative prior to its application in human and animals. In this investigation, we performed a comprehensive analysis encompassing genome sequencing, genomic analysis, and phenotypic characterization of L. reuteri Q35, an exceptionally proficient producer of reuterin. The whole genome sequencing results showed that the complete genome sequence spans 2 145 158 bp with a GC content of 38.9% and encompasses 2 121 genes. Initial identification of antibiotic-resistant genes, virulence factors, and toxin-coding genes in the genome substantiated the strain’s low-risk status. Subsequent tests for antibiotic resistance, acute oral toxicology, and hemolysis further confirmed its elevated safety level. The genome of L. reuteri Q35 was found to contain genes associated with adhesion and stress tolerance. Following exposure to artificial gastric juice and bile salt, the strain exhibited a higher survival rate and demonstrated a strong scavenging ability for hydroxyl free radicals in antioxidant capacity tests. These findings suggested that L. reuteri Q35 possesses unique probiotic properties. Additionally, the genome of strain Q35 harbors three truncated oxaloyl-CoA decarboxylase genes (oxc1, oxc2 and oxc3), overexpression of which resulted in a significant increase in ammonium oxalate degradation from 29.5% to 48.8%. These findings highlight that L. reuteri Q35 exhibits both favorable safety characteristics alongside beneficial properties, making it a promising candidate for treating metabolic disorders such as hyperoxaluria.

The medicinal value of vanilla planifolia is of great interest. We analyzed the common principal components of VOCs in different parts of vanilla planifolia, and the human serum albumin (HSA), β-lactoglobulin (β-La) and α-lactalbumin (α-La) were used as template proteins to establish a chain analysis approach with the ‘solid phase microextraction gas chromatography-mass spectrometry-multispectroscopy-physical modelling-pharmacokinetics’ (S-M-P-P). The mechanisms of the transport and pharmacodynamics for the common principal components of vanilla planifolia were analyzed. The results showed that the common primary VOCs in different parts of vanilla planifolia was vanillin (Van), which attenuated the endogenous fluorescence of HSA/β-La/α-La by static bursting, and formed hydrogen bonds and Van der Waals forces with HSA, and noncovalent complexes with β-La/α-La through hydrophobic forces. Their interaction facilitates the transport of Van in vivo to intestinal and hepatic tissues and its metabolism by CYP1A2 and CYP2C9 enzymes to exert its pharmacological effects. This study provides a comprehensive and in-depth investigation of the transport mechanisms and pharmacological effects of VOCs from vanilla planifolia, which provides an important reference for understanding the medicinal potential of plant derived VOCs.

Neuregulin 4 (NRG4) is a newly discovered adipokine, which plays crucial roles in many physiological processes such as energy balance, and glucose and lipid metabolism. The transcriptional regulation of NRG4 gene remains largely unknown. Our previous 5′RACE analysis showed that the transcription start sites (TSS) of chicken NRG4 gene were dispersed over a region of 200 bp, suggesting that chicken NRG4 gene possesses a dispersed promoter. In the present study, the promoter activity of the proximal exon and intron of chicken NRG4 gene was analyzed. Dual-luciferase reporter assay demonstrated that the genomic fragment (-122/+452) containing exon 1, intron 1, and exon 2 of chicken NRG4 gene had strong bidirectional promoter activity. Bioinformatics analysis showed that there was a putative binding site of the transcription factor CCAAT enhancer-binding protein α (C/EBPα) in exon 2 of chicken NRG4 gene. Reporter gene assay showed that both deletion and site-directed mutagenesis of theC/EBPα binding site abrogated the regulatory effect of C/EBPα on the promoter activity of the -122/+452 fragment of chicken NRG4 gene. Gene expression correlation analysis showed thatC/EBPα and NRG4 gene expression were positively correlated in chicken adipose tissues. ChIP-PCR revealed thatC/EBPα directly binds to the exon 2 of NRG4 gene in chicken adipose. In conclusion, the proximal exon and intron of chicken NRG4 gene has bidirectional promoter activity, and C/EBPα directly regulates NRG4 gene expression in chicken adipose via binding to its exon 2.

In mass spectrometry-based proteomics experiments, achieving high-throughput and efficient proteolytic digestion is crucial to ensure optimal protein cleavage and enhance the depth of protein identification (including the number of identified proteins and the coverage of protein amino acid sequences). Trypsin is the most widely used protease in mass spectrometry-based proteomics due to its ability to specifically cleave the carboxyl terminus of arginine and lysine. However, it was found that Trypsin has some missed enzymatic efficiency for the cleavage of lysine residues. Therefore, in actual proteomics sample preparation, a combination of Trypsin and LysC will be used to ensure adequate cleavage of lysine residues. Our study revealed that the commonly employed LysC-Trypsin tandem cleavage method exerts an impact on the enzymatic cleavage of protein samples by Trypsin due to the subsequent cleavage of Trypsin by initially added LysC. Consequently, we adjusted the order of LysC and Trypsin tandem digestion, with Trypsin cleavage being performed first followed by the addition of LysC to target any missed lysine residues. We comprehensively compared and analyzed three distinct sequential digestion methods, namely Trypsin-Trypsin (T-T), LysC-Trypsin (L-T), and Trypsin-LysC (T-L), in terms of their effects on protein sample preparation quality. The results demonstrated that the Trypsin-LysC sequential digestion approach not only minimizes missed protein lysine/arginine cleavage sites without increasing experimental costs, at the same time yielding peptides with a moderate amino acid sequence length. The use of Trypsin-LysC digestion enhances the adsorption and separation of peptide samples in RP-HPLC, as well as improves the depth of protein detection and amino acid sequence coverage during tandem mass spectrometry analysis. This research work offers a novel technical solution and serves as a valuable reference for proteome sample preparation.

Metastasis is the main risk factor for poor prognosis of laryngeal squamous cell carcinoma (LSCC). Chemokines are closely related to metastasis in the tumor microenvironment. CXCL8 is a cytokine-like secreted protein that plays key roles in the malignant development of a variety of tumors, but has not been elucidated in LSCC. In this paper, we elucidated the role of CXCL8 in LSCC cells and found miRNAs that targeted CXCL8, which may become new targets for the diagnosis and treatment of LSCC. Firstly, the GEPIA showed that CXCL8 was highly expressed in head and neck cancer (P <0.05). The real-time fluorescence quantification (qRT-PCR) found that CXCL8 was highly expressed in LSCC cells. The enzyme-linked immunoassay also found that CXCL8 was highly secreted in the supernatant of LSCC cells (P <0.001). Then, the CCK8 assay confirmed that knockdown of CXCL8 significantly inhibited the proliferation of FD-LSC-1 and AMC-HN8 cells (the average inhibition rate was 34.0% and 19.5%, respectively); The EdU assay also confirmed that knockdown of CXCL8 significantly inhibited the proliferation of LSCC cells (P <0.05). The transwell assay confirmed that knockdown of CXCL8 also significantly inhibited the migration and invasion of FD-LSC-1 cell (average inhibition rate was 40.0%, 38.5%, respectively); Knockdown of CXCL8 also significantly inhibited the migration and invasion of AMC-HN8 cell (average inhibition rate was 37.5%, 53.5%, respectively). The analysis of bioinformatics predicted that CXCL8 may be a target of miR-513b-5p. The dual luciferase reporter assay confirmed that miR-513b-5p could bind to the CXCL8-3′UTR. QRT-PCR assay also confirmed that overexpression of miR-513b-5p could decrease the 60% of the CXCL8 expression (P <0.01). Cell function rescue assays found that overexpressed of CXCL8 could effectively reversed proliferation, migration and invasion of LSCC cells weakened by miR-513b-5p (P <0.05). In summary, miR-513b-5p inhibited the proliferation, migration and invasion of LSCC cells by targeting CXCL8.

It is the focus of higher education reform in the new era to comprehensively promote the construction of ideology and political education based on the characteristics of professional courses and enhancing the effectiveness of ideology and political education. As an important basic course for medical students in colleges, molecular biology is closely related to basic medical disciplines and clinical medicine, and is a rapidly developing cutting-edge discipline, which has the natural advantage of serving as a carrier of ideology and political education. In this study, the innovative integration of project-based group study (PBGS) with the outcome-oriented behavior (OBE) of moral education is applied to the teaching of the ideology and politics of the medical molecular biology course, and the integration of the two has made a useful exploration to enhance the effectiveness of the ideology and politics teaching of the course. Taking students as the center, we have constructed an ideology and politics teaching system for medical molecular biology courses by combining on-line and off-line teaching activities through improving the teaching objectives, innovating the teaching design, digging into the case of ideology and politics, introducing a variety of teaching methods, strengthening the management of teaching practice, and optimizing the evaluation mode. After two years of teaching practice, this model has effectively improved the teaching effect of the medical molecular biology course. The academic performance of the students in the practice group has improved significantly, and the teachers and students have been given excellent evaluation. The results of the questionnaires before and after class showed that more than 80% of the students believed that their horizons had been broadened and their knowledge had been increased through learning. More than 50% of the students believed that their learning ability and innovation consciousness had been improved; their scientific research quality had been improved; and their confidence in studying medicine had been strengthened. By strengthening the cultivation of students’ scientific research and innovation capabilities, we guided students to participate in subject competitions and won many national awards. Throughout the teaching process, we aim to expand the breadth and depth of ideology and political education, cultivate scientific spirits, innovation ability, moral cultivation, and humanistic qualities. In sum, our work provides experiences for the cultivation of high-quality medical talents.