Type-1 Diabetes Mellitus (T1DM) is regarded as a multifunctional, immune-related disease which causes massive destruction of islet β-cells in pancreas resulting in hyperglycemic, hypoinsulinemia and hyperlipidimic conditions. The aim of the present study, was to investigate the hypothesis that streptozotocin (STZ)-induced T1DM in Balb/c mice when treated with crude polysaccharide from seaweed, Dictyopteris divaricata (CDDP) depicts improvement in diabetes-related symptoms. Treatment with CDDP resulted in decreased body weight loss, improved food consumption and water intake disbalances. The CDDP effectively improved fasting blood glucose, oral glucose tolerance (OGTT), serum insulin, insulin secretion, rejuvenation of β-cells mass, serum lipid profile and pro-inflammatory cytokines levels. Additionally, treatment with CDDP increased the population of beneficial bacteria such as Firmicutes, Bacteroidetes and Lactobacillus at phylum, family and genus levels by 16S rRNA sequencing. Furthermore, immunohistological examination confirmed that CDDP reduces the inflammation and restored the structural morphology of colon and upraised the levels of insulin receptor substrate-1 (IRS-1), Mucin-2 (MUC-2) and tight-junction proteins (TJs) whereby maintaining the gut structures and barrier permeability. Thus, the above presented data, highlights the safe and therapeutic effects of crude polysaccharide (CDDP) from D. divaricata in the treatment and restoration of T1DM disorders and can be used as a food supplement alternative to diabetes medicine.

Stroke remains a leading cause of long-term disability and mortality worldwide, necessitating novel therapeutic strategies to enhance recovery. Traditional rehabilitation approaches, including physical therapy and pharmacological interventions, often provide limited functional improvement. Neuromodulation has emerged as a promising strategy to promote post-stroke recovery by enhancing neuroplasticity and functional reorganization. Among various neuromodulatory techniques, chemogenetics, particularly Designer Receptors Exclusively Activated by Designer Drugs (DREADDs), offers precise, cell-type-specific, and temporally controlled modulation of neuronal and glial activity. This review explores the mechanisms and therapeutic potential of chemogenetic modulation in stroke recovery. Preclinical studies have demonstrated that activation of excitatory DREADDs (hM3Dq) in neurons located within the peri-infarct area or contralateral M1 has been shown to enhance neuroplasticity, facilitate axonal sprouting, and lead to improved behavioral recovery following stroke. Conversely, stimulation of inhibitory DREADDs (hM4Di) suppresses stroke-induced excitotoxicity, mitigates peri-infarct spreading depolarizations (PIDs), and modulates neuroinflammatory responses. By targeting specific neuronal and glial populations, chemogenetics enables phase-specific interventions-early inhibition to minimize damage during the acute phase and late excitation to promote plasticity during the recovery phase. Despite its advantages over traditional neuromodulation techniques, such as optogenetics and deep brain stimulation, several challenges remain before chemogenetics can be translated into clinical applications. These include optimizing viral vector delivery, improving ligand specificity, minimizing off-target effects, and ensuring long-term receptor stability. Furthermore, integrating chemogenetics with existing stroke rehabilitation strategies, including brain-computer interfaces and physical therapy, may enhance functional recovery by facilitating adaptive neuroplasticity. Future research should focus on refining chemogenetic tools to enable clinical application. By offering a highly selective, reversible, and minimally invasive approach, chemogenetics holds great potential for revolutionizing post-stroke therapy and advancing personalized neuromodulation strategies.

The gut–heart axis plays a role in cardiac injury due to the disruption of barriers, endotoxemia, and inflammatory signaling; yet, it is not clear whether sodium butyrate (SB) is capable of alleviating isoprenaline-induced myocardial injury through coordinated intestinal, microbial, and metabolic restoration. This study used male Sprague-Dawley rats, which were grouped into control, control + SB, isoprenaline (ISO)-induced myocardial injury, and ISO + SB groups. We evaluated cardiac biomarkers of injury, oxidative stress, histopathologic, intestinal barrier (16S rRNA sequencing), and serum metabolomics (LC-MS). SB treatment decreased serum cardiac troponin I, creatine kinase-MB, and lactate dehydrogenase; relieved oxidative stress; and lowered myocardial necrosis and fibrosis. It re-established colonic architecture, upregulated the expression of ZO-1 (zonula occludens-1) and claudin-1, and reduced endotoxin in the bloodstream. SB also prevented the production of proinflammatory cytokines such as TNF-α, IL-6, and IL-1β; cardiac TLR4; IκBα degradation; and NF-κB p 65 phosphorylation. In addition, SB altered the gut microbiota in favor of beneficial commensals, including Ligilactobacillus and Bifidobacterium, and reduced Desulfovibrio. It normalized key circulating metabolites and enriched cardiometabolic pathways, and the patterns of correlation suggested the coordinated remodeling of the microbiome–metabolome. These findings reveal that SB prevents myocardial injury caused by ISO through strengthening gut barrier protection, alleviating endotoxemia, inhibiting TLR4/NF-κB, and remodeling the microbiome–metabolome axis, indicating its potential for use as a gut-targeted cardioprotective intervention.