3 Biotech最新文献

Cyanobacterial extracellular polymeric substances (EPSs) are considered eco-friendly and sustainable green alternatives for several applications in the food, biotechnological and commercial sectors. However, exploration of high-value EPSs from cyanobacteria is still very limited. In the present investigation, we have screened among paddy field and hot-spring isolates to identify strain with high yield of EPSs. We have used the isolated cyanobacterium Neowestiellopsis sp. strain VKB03 from a paddy field for the extraction and functional analysis of EPSs. Alcian blue and toluidine blue staining confirm the presence of an acidic EPSs layer around the wall surface of the cyanobacterium. SEM analysis proves the porous and web-like nature of EPSs. The biochemical composition of isolated EPSs indicated the presence of high sugars, proteins, phosphate, acetyl, and uronic acids without sulphate and pyruvic acid constituents. Additionally, GC-MS analyses of EPSs reveal the presence of alditol products of sugar, lipids, ester, hydrocarbons C₁₁- C_29, and nucleosides. Moreover, FT-IR spectrum analyses speculated the presence of functional groups like carboxylate groups, phosphate groups, α-pyranose groups, and glycosidic linkage. Thermal stability has been elucidated by thermogravimetric (TGA) and differential scanning calorimetry (DSC) analyses reveal high thermal firmness of EPSs with high water (8987.5%) and oil (1729.5%) holding capacities. The emulsifying activity of EPSs exhibits positive results against tested substrates. The findings highlight the considerable potential of paddy field cyanobacterial EPSs for applications in industrial and commercial sectors for human welfare.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-026-04717-y.

[This corrects the article DOI: 10.1007/s13205-025-04690-y.].

In the present study, Fusarium species, the incitant of collar rot associated yellowing in black pepper was identified and characterized adopting polyphasic approach. The disease was characterized by the symptoms including general decline in plant health, flaccidity, foliar yellowing followed by defoliation, necrosis of internal vasculature and collar region, collar rot and subsequent wilting of the vines and the severity was more pronounced during post-monsoon season. The isolates representing diverse black pepper cultivating tracts were initially identified as Fusarium species based on macro- and micro-morphological traits. Subsequent molecular analysis with internal transcribed spacer (ITS), partial elongation factor 1-alpha (ef1-α) and β-tubulin (β-tub) genes revealed the association of Fusarium solani and F. equiseti. Initial pathogenicity was proved by in vitro assay in which epinasty, collar rot and wilting occurred within 8-10 days. In the in planta assay, the symptoms observed were foliar yellowing followed by shriveling, drooping, vascular browning and wilting on injured and uninjured plants 20-25 and 55-65 days post-inoculation, respectively. The present study enunciated the association of F. solani and F. equiseti with collar rot associated yellowing of black pepper which warrant further investigations on its spatio-temporal distribution, pathogen diversity, weather-host-pathogen interaction and formulating prospective disease management strategies.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-026-04727-w.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is closely connected to obesity and ranks as one of the most common liver disorders worldwide. Bambusa vulgaris is a medicinal plant traditionally used as an alternative remedy in Southeast Asia. This study aimed to evaluate the therapeutic potential and underlying mechanisms of Bambusa vulgaris leaf extract in obesity-related MASLD using both in silico and in vivo approaches. Gas chromatography-mass spectrometry (GC-MS) analysis of the methanolic extract identified several key phytochemicals, including 2-[2,N-dimethyl-2-aminoethyl]benzofuran, β-sitosterol, 2-methoxy-4-vinylphenol, 2,3-dihydrobenzofuran, 2,4,4-trimethylpentan-1-ol, phenol, 2,6-dimethoxyphenol, terpinen-4-ol, and 4-hydroxy-3-methylacetophenone. In silico pharmacokinetic and molecular docking analyses showed that most of these compounds exhibit favourable drug-like properties, including high aqueous solubility, gastrointestinal absorption, blood-brain barrier permeability, and strong interactions with adenosine monophosphate kinase (AMPK). In vivo, oral administration of leaf extracts for four weeks in high-fat diet-induced obese rats significantly reduced obesity and MASLD-related changes by improving adipocyte function and decreasing hepatic steatosis. These effects were achieved through increased phosphorylation of AMPK and decreased activity of Peroxisome proliferator-activated receptor gamma (PPAR-γ) in the liver and adipose tissue, thereby enhancing lipid and carbohydrate metabolism disrupted by high-fat diet feeding. Additionally, the leaf extracts enhanced endogenous antioxidant defences and lowered oxidative stress. Overall, these results show that Bambusa vulgaris leaf extract has strong therapeutic effects against obesity and MASLD, underscoring its potential as a natural hepatoprotective and metabolic regulator.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-026-04735-w.

Exercise-induced ionic changes can modulate the interaction between liraglutide and the glucagon-like peptide-1 receptor (GLP-1R). To investigate this, molecular dynamics simulations and in vivo experiments using streptozotocin-induced diabetic rats were performed. Under exercise-mimicking ionic conditions (NaCl 129 mM, KCl 8.5 mM), the simulations revealed enhanced stability of the liraglutide-GLP-1R complex, evidenced by reduced interatomic distances, a lower radius of gyration, increased ligand flexibility (as indicated by RMSF), higher solvent-accessible surface area, and stronger binding energy. Structural analysis using PDBsum identified one salt bridge, two hydrogen bonds, and eighty-nine non-bonded contacts between liraglutide and key receptor residues, confirming a robust and stable interaction. In diabetic rats, the combined treatment with liraglutide and exercise significantly decreased body weight and plasma glucose levels (P < 0.001), improved lipid profiles, and enhanced insulin sensitivity. These effects were accompanied by a significant increase in the expression of mitochondrial regulators PGC-1α and UCP-1 (P < 0.01), indicating enhanced mitochondrial biogenesis and thermogenic capacity.

The global surge in plastic production and inadequate waste management have resulted in widespread environmental contamination with microplastics (MPs). Derived either as primary particles from consumer products or as secondary fragments from the degradation of larger plastics, MPs are now omnipresent in terrestrial, aquatic, and atmospheric ecosystems. Their small size, durability, and surface reactivity enable biofilm formation, heavy metal adsorption, and easy entry into food chains, ultimately posing significant risks to human health. This review outlines the sources, types, human exposure, including dietary intake, inhalation, and dermal contact, and their toxicological impacts on multiple organ systems. MPs can cross biological barriers, including the gastrointestinal epithelium, blood-brain barrier, and placenta, leading to distribution and bioaccumulation. Mechanistically, they induce oxidative stress, inflammation, immune dysregulation, and disruption of the gut microbiota. In the digestive system, MPs impair intestinal integrity, inhibit digestive enzymes, and promote hepatic inflammation. Inhalation alters pulmonary surfactant function, triggers cytokine release, and is implicated in asthma, fibrosis, and chronic obstructive pulmonary disease. MPs also function as endocrine-disrupting chemicals, interfering with hypothalamic-pituitary axes and reproductive hormones, thereby affecting fertility and development. Neurological consequences include oxidative stress-mediated neurotoxicity, neuroinflammation, and potential links to neurodegenerative disorders. Additionally, chronic exposure to MPs and associated additives may promote carcinogenesis by inducing DNA damage, persistent inflammation, and immune evasion. Collectively, these findings highlight MPs as emerging environmental toxins with wide-ranging adverse effects on human health. Further mechanistic studies and regulatory interventions are essential to mitigate exposure and address this growing global health threat.

We conducted an integrated pan-cancer analysis to characterize the expression profile, clinical relevance, immune associations, and cellular localization of glutathione peroxidase 4 (GPX4) across human cancers by integrating transcriptomic, proteomic, clinical, immune, and single-cell datasets. GPX4 was frequently upregulated at the mRNA level across multiple solid tumors, whereas proteomic analyses revealed reduced expression in primary tumors but progressive upregulation with advancing pathological stage in selected cancer types. Elevated GPX4 expression was significantly associated with adverse overall or disease-free survival in colorectal, stomach, adrenocortical, prostate, and uveal cancers, while an opposite prognostic pattern was observed in thyroid cancer. Immune deconvolution analyses demonstrated that GPX4 expression correlated positively with cancer-associated fibroblast infiltration and distinct immune checkpoint and T/NK-cell contexts across cancers. Single-cell transcriptomic analyses consistently localized GPX4 expression predominantly to malignant epithelial cells, with secondary expression in stromal fibroblasts and minimal expression in immune compartments. In vitro experiments further confirmed increased GPX4 expression and enhanced proliferative capacity in tumor cell lines compared with normal epithelial counterparts. Collectively, these results identify GPX4 as a context-dependent, tumor-cell-intrinsic regulator with prognostic and immunological relevance across cancers, supporting its potential as a biomarker and therapeutic vulnerability in selected tumor types.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-026-04733-y.

Breast cancer progression is increasingly recognized as an immunometabolic disorder in which tumor-intrinsic metabolic reprogramming and microenvironmental stress converge to impair innate immune surveillance. Beyond its established role in glycemic control, metformin has emerged as a promising immunometabolic modulator with anticancer potential. Accumulating evidence indicates that metformin suppresses breast tumor growth by targeting key metabolic vulnerabilities, including dysregulated glycolysis, lipid metabolism, and mitochondrial energetics, while simultaneously restoring the functional competence of innate immune effectors, particularly natural killer (NK) and natural killer T (NKT) cells. At the molecular level, metformin engages AMP-activated protein kinase (AMPK)-centered signaling and mitochondrial complex I-associated energetic stress, leading to downstream modulation of mTOR activity, redox balance, autophagy, and RNA-mediated regulatory networks. These coordinated effects reduce tumor cell plasticity and enhance immune permissiveness. Within the tumor microenvironment, metformin attenuates hormone-dependent stromal support, disrupts immunosuppressive myeloid networks, normalizes chemokine and cytokine profiles, and promotes antigen presentation and innate immune cell recruitment. Preclinical studies consistently demonstrate delayed tumor onset, suppression of aggressive breast cancer subtypes, impairment of cancer stem cell maintenance, and reinforcement of NK/NKT-mediated antitumor surveillance following metformin treatment. However, emerging clinical and translational evidence suggests that therapeutic efficacy is context dependent, influenced by tumor molecular subtype, host metabolic status, immune composition, and pathway-specific biomarker engagement. This review critically synthesizes mechanistic, preclinical, and clinical findings to position metformin as a host-directed immunometabolic adjuvant in breast cancer. Integrating insights from metabolism, innate immunology, pharmacology, and biotechnology, this work highlights opportunities for biomarker-guided stratification and rational combination strategies aimed at enhancing NK/NKT-cell-driven antitumor immunity in breast cancer therapy.

This study explores the multifunctional plant beneficial traits of the endophytic bacterium Enterobacter sp. P1P isolated from the indigenous rice varieties of Kerala, India. Among the fifty seed-borne bacterial isolates screened, P1P exhibited the highest antifungal effect against the rice pathogen Rhizoctonia solani, with 55.29% fungal mycelial growth inhibition. Chemical profiling by using GC-MS has also identified several bioactive metabolites in the prepared extract of P1P, including the 2,4-di-tert-butylphenol and didemnin B which are known for their antifungal properties. In controlled pot experiments, P1P significantly enhanced the rice seedling growth, demonstrating a shoot length (20.5 ± 3.4 cm) and root length (14.3 ± 2.7 cm) which were higher when compared to the untreated control (17.9 ± 2.9 cm and 11.9 ± 1.7 cm, respectively). Moreover, P1P has also been demonstrated to have the phosphate and zinc solubilization properties along with the indole-3-acetic acid (IAA) production, the key factors contributing to plant growth promotion. Whole genome sequencing, revealed that P1P has a genome size of 4.84 Mb containing 5045 protein-coding genes, including the six biosynthetic gene clusters related to the secondary metabolites and antimicrobial peptides, such as enterobactin and saquayamycin. Genes implicated in the IAA biosynthesis (ipdc, aldH, and patA1) and mineral solubilization (gcd, gad, and pqq operon) could also be identified, highlighting its genetic basis for both the biocontrol and growth-promoting functions. By the comparative genome analysis, P1P was shown to have 99.2% average nucleotide identity with Enterobacter cloacae strains which have been previously isolated from maize. Collectively, these findings underscore the Enterobacter sp. P1P to be an eco-friendly candidate with the potential to be explored for the integrated disease management and growth enhancement for the sustainable rice cultivation.

Supplementary information: The online version contains supplementary material available at 10.1007/s13205-026-04696-0.

Pinus morrisonicola Hayata, also known as Taiwan white pine or Taiwan short-leaf pine, is an endemic species to Taiwan. In Asia, particularly Taiwan, China, and Korea, P. morrisonicola needles have been used as a functional beverage for many years. In this study, we investigated the anti-cancer potential of P. morrisonicola leaves and barks against human lung adenocarcinoma (A549) in vitro. Three different extracts, including supercritical CO₂ extract, ethanol extract, and steam-distilled essential oils of leaves and barks were obtained. Among them, ethanol extract of P. morrisonicola leaves (PMLE) displayed the strongest cytotoxicity on A549 cells. Next, we found that PMLE treatment arrested lung adenocarcinoma cells induced a pronounced G1/S cell-cycle arrest without triggering apoptosis. Treatment with PMLE resulted in a down regulation of cyclin D1 and phosphorylation of Cdc-2 in A549 cells. In addition, this effect was associated with down regulation of cyclin-dependent kinase 2 (CDK2) and up regulation of CDK inhibitors p21^Cip1 and p27^Kip1. Moreover, cyclin B1, cyclin D1, and cyclin E expression levels were reduced, which corresponds to a decreased distribution of cells in the S and G₂/M phases. Furthermore, PMLE treatment significantly activated p53 in A549 cells, followed by increased nuclear translocation, which may account for the up regulation of p16^INK4a, p21^Cip1, and p27^Kip1 proteins. Taken together, our results indicate that PMLE exerts anti-cancer activity in human lung adenocarcinoma by arresting the cell cycle through activation of the p53-dependent pathway.