bioRxiv Science⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2025.05.21.655247

Impact of a standardized Tetradesmus obliquus Mi175.B1.a extract on gut function and physiology in inflammatory conditions: in vitro and in vivo insights

MAURY, J.·Albina, P.·Pradelles, R.
View original source ↗Export metadata ↓

Abstract

Microalgae have emerged as a promising source of natural nutraceuticals, which may play a critical role in maintaining the structural integrity of the gut mucosal barrier and modulating immune responses. Extracts from Tetradesmus obliquus have demonstrated potential benefits for gut health in humans. This study aimed to evaluate the efficacy of Tetradesmus obliquus Mi175.B1.a through two complementary approaches: (1) an in vitro model using the HT-29 cell line to assess cytotoxicity, intestinal permeability, immunomodulatory properties, and gut barrier function, and (2) an in vivo mouse model of dextran sodium sulfate (DSS)-induced colitis to examine parameters relevant to digestive physiology. In the in vitro model, HT-29 cells were pretreated with two selected doses of T. obliquus (Mi175.B1.a) extract for 72 hours prior to stress induction with lipopolysaccharide (LPS). Parameters assessed included gene expression, paracellular permeability, and immunomodulatory properties. For the in vivo model, forty (40) male mice were randomly allocated to receive daily oral administration of either vehicle or T. obliquus extract at two different doses for 21 days. Colitis was induced from Day 14 to Day 21 using 3% DSS, and macroscopic and gut motility parameters were subsequently evaluated. Key findings revealed that T. obliquus (Mi175.B1.a) significantly reduced FITC-dextran permeability, restored physiological expression of Zonula occludens-1 (a tight junction protein), and attenuated TNF- release and Cox2 gene expression in comparison to the LPS-only condition. In the in vivo model, T. obliquus extract significantly reduced the daily disease activity index and colitis score compared to DSS-only condition. Importantly, the two evaluated doses of T. obliquus (Mi175.B1.a) were well-tolerated, demonstrating no toxic effects. These results highlight the potential of T. obliquus extract to enhance intestinal barrier integrity by regulating inflammatory and oxidative stress pathways opening promising research perspectives to determine the benefits in human application.

Explore related subjects

physiologyPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

MAURY, J., Albina, P., Pradelles, R.. 2025-05-26. Impact of a standardized Tetradesmus obliquus Mi175.B1.a extract on gut function and physiology in inflammatory conditions: in vitro and in vivo insights. https://doi.org/10.1101/2025.05.21.655247

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Stress-induced Metabolic Remodeling of Adipose and Brain Tissue revealed by Positron Emission Tomography

Stress impacts our health and triggers physiological adaptations, yet the metabolic programs engaged during stress remain incompletely understood. To fill this knowledge gap, we utilized total-body positron emission tomography (PET), multi-OMICS, and endocrine profiling to assess how various murine stress models affect systemic metabolic remodeling. We found that acute immobilization and surgery activate brown adipose tissue as part of the stress response, independently of hypothermia, thereby acting as a highly stress-sensitive metabolic hub. Additionally, we identified stress-specific hypo- and hypermetabolic signatures in different brain regions, and distinguished networks between brain and adipose tissue depots across the different stress groups. Our work presents a novel perspective on stress and its mobilization of metabolic resources and identifies PET imaging of brain and adipose tissue as a valuable, minimally invasive technique for tracking metabolic stress responses in mice, with relevance for animal welfare and disease models, and translational impact for mental health studies and preventive medicine.

physiology↗
bioRxiv2026

Multiparametric in vivo mapping reveals tissue-specific mitochondrial aging trajectories

Mitochondrial dysfunction is a hallmark of aging, yet how mitochondrial states are remodeled across tissues and subcellular compartments in vivo remains elusive. Progress has been limited, in part, because mitochondrial physiology is highly sensitive to experimental perturbations, underscoring the need for minimally disruptive measurement strategies. Here, we establish a tissue-resolved, in vivo framework for the quantitative analysis of mitochondrial states in live, intact Caenorhabditis elegans without confounding effects from mounting-induced hypoxia. This platform couples two-photon fluorescence lifetime imaging microscopy (2p-FLIM) with a custom segmentation pipeline, MitoSLIT, to track functional and structural features across multiple tissues and single neurons. By integrating membrane potential-associated TMRM intensity, lifetime-based microenvironmental metrics, and morphological descriptors, we uncover localized metabolic heterogeneity masked by conventional intensity analysis. Leveraging this framework, we mapped physiological aging against mitochondrial shifts induced by acute stress and fission-fusion mutations. Our analyses reveal that mitochondrial aging is highly tissue-specific, executing distinct trajectories across cell types. Extending the framework to genetically identified neurons revealed age-dependent divergence between somatic and axonal mitochondrial states, accompanied by structural remodeling and a late shift in optical redox ratio. Together, our findings demonstrate that mitochondrial populations do not converge on a uniform bioenergetic endpoint during aging, but rather follow highly compartmentalized, tissue-specific spatiotemporal trajectories in vivo.

physiology↗
bioRxiv2026

Arginine methyltransferase signalling is hyperactive in conditions of neuromuscular junction instability and muscle atrophy

Background: The neuromuscular junction (NMJ) is the site of communication between myofibers and a-motor neurons. Cellular and molecular mechanisms that determine, maintain, and remodel the neuromuscular synapse are poorly understood. Coactivator-associated arginine methyltransferase 1 (CARM1) post-translationally modifies target proteins by methylating arginine residues and has emerged as a key determinant of skeletal muscle biology. Methylarginine signalling is required for the maintenance and repair of the NMJ, but the direct role of CARM1 on the NMJ in health and disease remains unexplored, particularly in humans. Methods: We generated Carm1 skeletal muscle-specific knockout-out (mKO) mice to gain a basic understanding for the role of the enzyme in NMJ biology under homeostatic and denervated conditions. Additionally, we investigated CARM1 activity in severe mouse models of neuromuscular disorders (NMDs) including D2.mdx and Smn2B/- mice, which replicate Duchenne's muscular dystrophy (DMD) and spinal muscular atrophy (SMA), respectively, and exhibit chronic remodelling of the NMJ. Lastly, to evaluate if methylarginine signalling is implicated during NMJ instability in human skeletal muscle, we obtained samples from healthy volunteers before and after 14 days of single leg immobilization as well as from patients with myotonic dystrophy type 1. Results: Our results demonstrated that Carm1 mRNA expression and activity are elevated (P<0.05) in NMJ-enriched regions of healthy murine skeletal muscle. Carm1 muscle-specific deletion reduced NMJ compactness (-9.3%; P<0.05), increased fragmentation (+33%; P<0.05), and disrupted the expression of synapse-specific transcripts basally and following sciatic nerve transection. In skeletal muscle from pre-clinical models of NMDs, we observed a compensatory upregulation in CARM1-dependent arginine methylation as evident by +54% and +71 increases (P<0.05) in asymmetric dimethylarginine (ADMA)-marked CARM1 substrates in DMD and SMA mice, respectively. Similarly, muscle CARM1 was hyperactive with increased NMJ instability during neuromuscular disuse (+22%; P<0.05), and disease (+30%; P<0.05), in humans. In a cohort of muscular dystrophy patients and healthy volunteers, elevated CARM1 signalling was negatively correlated with clinical metrics of skeletal muscle health including grip strength (r = -0.583; P<0.05) as well as positively correlated with mRNA expression of NMJ machinery such as CHRNA1 (r = 0.578; P<0.05). Conclusion: In summary, we highlight that muscle-specific CARM1 is required for maintaining NMJ morphology and transcriptional regulation. Insults to NMJ stability during muscle disuse or in myopathic conditions were associated with enhanced CARM1-mediated methylarginine signalling in mice and humans. Collectively, our findings demonstrate CARM1 as a key mediator of NMJ biology and plasticity in health and disease.

physiology↗