Applied Biochemistry and Biotechnology最新文献

Inflammatory Bowel Disease (IBD) refers to the inflammatory disorders of the colon and small intestine. The effect of the essential oil from Tamarix aphylla (TAEO) on inflammation and apoptosis has been investigated using a rat TNBS-induced colitis model. The study utilized macroscopic and histopathological evaluations, cytokine profiling by ELISA, and protein expression assays to assess the effects of TAEO on ulceration, cytokine levels, apoptotic proteins, and anti-apoptotic proteins. Sound experimental groups received several dosages of TAEO (10, 30, and hundred mg/kg) and dexamethasone serving as a comparative control. TAEO significantly reduced mucosal damage in a dose-dependent manner, with dosages of 30 and 100 mg/kg effectively decreasing the ulcer index compared to controls (p < 0.001). It also modulated cytokine profiles, notably reducing TNF-α (p < 0.05 for 30 mg/kg; p < 0.001 for 100 mg/kg), IL-1β, and TGF-β (p < 0.05 for 30 mg/kg; p < 0.001 for 100 mg/kg), while increasing IL-10 at higher doses (p < 0.01 for 30 mg/kg; p < 0.001 for 100 mg/kg). Furthermore, TAEO reduced the expression of pro-apoptotic proteins Bax and caspase-3 (p < 0.001 for both at 100 mg/kg), and enhanced the anti-apoptotic protein Bcl-2. Reductions in NF-κB and p38 MAPK activation were also significant (p < 0.01 and p < 0.001, respectively, for 100 mg/kg). Notably, high-dose TAEO (100 mg/kg) significantly activated the Nrf2 pathway more than dexamethasone (p < 0.001), promoting antioxidant defenses. Histopathological assessments confirmed these findings, showing substantial improvements in tissue architecture and reductions in inflammatory markers. TAEO possesses strong anti-inflammatory, anti-apoptotic, and antioxidant actions in TNBS-induced colitis with high therapeutic potential against IBD. The effects are specific towards higher doses, suggesting a dose-dependent mechanism of action, and justifying further testing.

The protein encoded by the Disco-interacting protein 2 homolog B (DIP2B) gene contains DNA methyltransferase and adenosine monophosphate (AMP) binding sites. Although DIP2B has been implicated in tumorigenesis, its diagnostic and prognostic significance across various cancers remains unclear. A comprehensive data analysis was performed using multiple bioinformatics platforms and tools, including the TCGA and GTEx databases, the R programming language, STRING, Cytoscape, TISIDB, cBioPortal, GSCALite, HPA, NetworkAnalyst, and CancerSEA. DIP2B expression was elevated in multiple cancer types, with variations observed across different immune and molecular subtypes. DIP2B was implicated in numerous cancer-related signaling pathways and showed enhanced diagnostic and prognostic significance across malignancies. Transcription factor analysis identified specificity protein 1 (SP1), specificity protein 3 (SP3), and histone deacetylase 1 (HDAC1) as potential regulators of DIP2B expression.In addition, a positive correlation was found between DIP2B and central memory CD8 T cells in cancers, suggesting a potential role in immune modulation. DIP2B shows promise as a prognostic biomarker and may represent anovel target for immunotherapy.

Multicopper oxidases such as laccases have emerged as valuable biocatalysts in environmental and industrial processes due to their ability to oxidize a variety of phenolic and aromatic compounds using molecular oxygen as the sole electron acceptor. In the present study, laccase from different Achromobacter species, having close 16 S rRNA identity related to Achromobacter sp. strain 206,011 (accession no. MK949376.1), was screened. Maximum microbial growth and enzyme production were both observed at 24 h under optimized conditions. Optimum enzyme activity was observed at 40 °C and pH 5.0. The laccase maintained over 85% activity with metal ions up to 10 mM concentration, demonstrating strong metal tolerance and suitability for biotechnological applications in metal-rich environments. Partial purification of the crude enzyme revealed two prominent bands on SDS-PAGE, approximately at 50 kDa and 200 kDa, suggesting the possible presence of laccase isozymes. Native-PAGE further confirmed enzymatic activity through guaiacol oxidation. The laccase was subsequently evaluated for its bioremediation potential through dye decolorization assays, demonstrating promising activity across different dye types. These findings support the potential of this laccase as a robust biocatalyst for environmental applications, particularly in the treatment of dye-laden effluents.

In recent years, the incidence of cardiovascular disease (CVD) has risen annually, among which acute myocardial infarction is a common, critical, and severe disease in clinical practice. Advances in tissue engineering and 3D printing have enabled biological scaffolds to emerge as a novel therapeutic approach for cardiac repair in AMI treatment. This study fabricated 3D-printed scaffolds using a porcine cardiac decellularized extracellular matrix (dECM)/caffeic acid-grafted chitosan (CSCA)/sodium alginate (SA)/nanoclay (NC) bioink, characterized by its physicochemical properties and cytocompatibility. Four bioink formulations with varying dECM concentrations were tested, with optimal printable parameters determined as 10% NC, 1% CSCA, and 1.5% SA. The 3D-printed sheet scaffolds exhibited abundant porous internal structures. For scaffolds 0D10N1.5SA, 0.5D10N1.5SA, 1D10N1.5SA, and 1.5D10N1.5SA, swelling rates were 220.99 ± 7.49%, 216.33 ± 8.02%, 207.43 ± 8.71%, and 202.30 ± 13.5%, respectively, while elastic moduli were 38.62 ± 2.25 kPa, 32.98 ± 2.67 kPa, 29.46 ± 1.70 kPa, and 19.68 ± 2.07 kPa. All scaffolds demonstrated good hydrophilicity and mechanical properties. In the biocompatibility test, it was observed that the number of cells on the scaffolds increased gradually with the increase in culture time. In particular, when the content of dECM increased, the number of cells also increased accordingly. More importantly, the cells could migrate into the scaffolds to form scaffold materials with biological functions. These results not only verify the excellent biocompatibility of the scaffold but also demonstrate its clear potential for applications in the development of cardiac tissue engineering scaffolds and implantable therapeutic devices following myocardial infarction.

Superoxide dismutase (SOD) is an antioxidant enzyme containing different metal ion, which can reduce oxidative stress and treat ulcerative colitis (UC). In addition, SOD's therapeutic effect can be enhanced when combined with other antioxidant enzymes, such as catalase (CAT). In this study, the probiotic Escherichia coli Nissle 1917 (EcN) was used as a chassis strain to develop two engineered variants, EcNc-RtSOD and EcNc-MLH. By using two cryptic plasmids, these strains were modified to constitutively express RtSOD and RtSOD-CAT (MLH), respectively. Furthermore, the engineered EcN strains were found to significantly reduce DSS-induced intestinal inflammation and promote intestinal mucosal healing in UC mice.Biochemical analyses revealed that the levels of superoxide dismutase (SOD) and catalase (CAT) in intestinal tissues were significantly elevated, while malondialdehyde (MDA) content was markedly reduced. Compared with the DSS group, the expression level of interleukin-6 (IL-6) in colon tissues of mice treated with RtSOD and MLH decreased by 24.04% and 37.68%, respectively. Similarly, the expression level of interleukin-1β (IL-1β) was reduced by 14.22% and 28.73%, respectively, in the RtSOD and MLH treatment groups compared to the DSS group. This study proposes a novel strategy for UC treatment that utilizes therapeutically engineered bacterial strains.

The aim of the present study was to investigate the effects of cyanidin-3,5-O-glucoside (C35G) on intestinal inflammation, mucosal barrier integrity, and fibrogenesis in a dextran sodium sulfate (DSS, 2.5%)-induced mouse model of ulcerative colitis (UC), as well as to elucidate the mechanisms underlying its effects. After a 28-day C35G intervention, UC mice showed significant improvements in clinical symptoms, including weight loss and an increased disease activity index (DAI). Additionally, there was an elevation in serum levels of inflammatory factors such as IL-1β, IL-6, IL-17 A, IL-18, and TNF-α. C35G increased the colonic mRNA levels of Zo1, Claudin1, and Occludin, and reduced intestinal epithelial permeability, ultimately promoting the restoration of mucosal barrier integrity in UC mice. In addition, C35G influenced the colonic Nrf2/Keap1 pathway by upregulating the mRNA levels of Cat, Sod1, Sod2, and Mgst1. This modulation was accompanied by an increase in the serum levels of SOD and catalase, as well as a reduction in the levels of the oxidative stress marker MDA. The C35G-induced inhibition of NLRP3 inflammasome activation reduced the expression of intestinal fibrotic factors (α-SMA and Collagen I), ultimately attenuating intestinal fibrosis. Moreover, C35G stimulated autophagy in the intestinal epithelial tissues of UC mice by increasing the protein expression of LC3-II, Beclin 1, p-AMPK, and ULK1 while decreasing the levels of p62, p-Akt, and p-mTOR. These results suggested that C35G reduces oxidative stress and inflammation by acting as an antioxidant and modulating the Nrf2/Keap1 pathway. Additionally, C35G regulates autophagy through the AMPK/Akt/mTOR/ULK1 pathway, thereby improving intestinal inflammation, restoring the compromised intestinal barrier, and preventing intestinal fibrosis in mice with UC.

The intersection of the global obesity epidemic with viral infection pandemics poses a significant public health problem. Obesity increases virus severity by inducing dyslipidemia-characterized by defective low-density lipoprotein (LDL) and high-density lipoprotein (HDL) particles-and establishes a condition of chronic, low-grade inflammation that undermines both innate and adaptive immunity. Moreover, cholesterol-enriched lipid rafts (LRs) in the plasma membrane, which are crucial for viral entry and replication, provide a molecular connection between dysregulated lipid metabolism and viral life cycles. Although exercise is acknowledged for its benefits to metabolic and immunological health, a thorough synthesis of its precise function in influencing the relationship between obesity and viral infection is lacking. This review examines the impact of exercise on lipid metabolism and adipose tissue function, as well as its subsequent effect on antiviral immunity. We discuss how exercise training may mitigate obesity-induced dyslipidemia, promote the health of white adipose tissue, reduce inflammation, and enhance both humoral and cellular immune responses. We also compile research about the direct impacts of exercise on different viral illnesses. In summary, obesity intensifies viral infections via dyslipidemia and compromised immunity. This study has identified a significant gap by demonstrating that regular exercise is a crucial non-pharmacological strategy for mitigating these hazards. We have outlined the comprehensive mechanism by which exercise enhances lipid metabolism and adipose tissue function, consequently strengthening antiviral immunity and disrupting the cycle of obesity-related susceptibility to severe viral diseases. Consequently, physical exercise should be regarded as a fundamental preventive measure.

Lignin is a heteropolymer component of ligno-cellulosic biomass made up of monomers connected together by various linkages, the most common of which is the β-O-4 bond. As previously demonstrated, lytic polysaccharide monooxygenase (LPMO) can catalyse the oxidative cleavage of β-O-4 linkage of lignin model compound guaiacyl glycerol-β guaiacyl ether (GGE). But the enhancement of enzymatic activity and stability remains a critical challenge for biocatalytic lignin valorization. In this study, an LPMO-cobalt phosphate organic-inorganic hybrid nanoflower (Co@LPMO-HNF) was developed as a robust biocatalyst for the cleavage of β-O-4 bond. The Co@LPMO-HNF was biochemically and morphologically characterized. Co@LPMO-HNF displayed an optimum temperature of 100 °C and pH 8, exhibiting 1.65-fold higher activity than free LPMO. The Michaelis-Menten kinetic parameters indicated that the Co@LPMO-HNF had 20 fold higher V_max and 13 fold higher turnover number (k_cat) as compared to free LPMO for GGE. The catalytic efficiency (k_cat/K_m) of Co@LPMO-HNF was found to be 700 M^- 1s^- 1which was significantly comparable to free LPMO (650 M^- 1s^- 1). Notably, Co@LPMO-HNF achieved 97% GGE conversion within 24 h versus 40% for the free enzyme and retained 52% of its activity after four catalytic cycles. This is first study to report the synthesis of LPMO based cobalt phosphate nanoflowers (Co@LPMO-HNF) with enhanced activity and stability for the oxidative cleavage of lignin derived compounds. Thus, LPMO loaded hybrid nanoflowers could be of great potential for the sustainable oxidation of lignin and its model compounds.