Huntington’s disease (HD) is an autosomal-dominant inherited neurological disorder caused by a genetic mutation in the IT15 gene. This neurodegenerative disorder is caused by a polyglutamine repeat expansion mutation in the widely expressed huntingtin (HTT) protein. HD is characterized by the degeneration of basal ganglia neurons and progressive cell death in intrinsic neurons of the striatum, accompanied by dementia and involuntary abnormal choreiform movements. Animal models have been extensively studied and have proven to be extremely valuable for therapeutic target evaluations. They reveal the hallmark of the age-dependent formation of aggregates or inclusions consisting of misfolded proteins. Animal models of HD have provided a therapeutic strategy to treat HD by suppressing mutant HTT (mHTT). Transgenic animal models have significantly increased our understanding of the molecular processes and pathophysiological mechanisms underlying the HD behavioral phenotype. Since effective therapies to cure or interrupt the course of the disease are not yet available, clinical research will have to make use of reliable animal models. This paper reviews the main studies of rodents as HD animal models, highlighting the neurological and behavioral differences between them. The choice of an animal model depends on the specific aspect of the disease to be investigated. Toxin-based models can still be useful, but most experimental hypotheses depend on success in a genetic model, whose choice is determined by the experimental question. There are many animal models showing similar HD symptoms or pathologies. They include chemical-induced HDs and genetic HDs, where cell-free and cell culture, lower organisms (such as yeast, Drosophila, C. elegans, zebrafish), rodents (mice, rats), and non-human primates are involved. These models provide accessible systems to study molecular pathogenesis and test potential treatments. For developing more effective pharmacological treatments, better animal models must be available and used to evaluate the efficacy of drugs.

Obesity is a risk factor for cardiovascular diseases, frequently related to oxidative stress and inflammation. Dietary antioxidant compounds improve heart health. Here, we estimate the oxidative grade and inflammation in the heart of dietary-induced obese (DIO) rats after exposure to a high-fat diet compared to a standard diet. The effects of tart cherry seed powder and seed powder plus tart cherries juice were explored. Morphological analysis and protein expressions were performed in the heart. The oxidative status was assessed by the measurement of protein oxidation and 4-hydroxynonenal in samples. Immunochemical and Western blot assays were performed to elucidate the involved inflammatory markers as proinflammatory cytokines and cellular adhesion molecules. In the obese rats, cardiomyocyte hypertrophy was accompanied by an increase in oxidative state proteins and lipid peroxidation. However, the intake of tart cherries significantly changed these parameters. An anti-inflammatory effect was raised from tart cherry consumption, as shown by the downregulation of analyzed endothelial cell adhesion molecules and cytokines compared to controls. Tart cherry intake should be recommended as a dietary supplement to prevent or counteract heart injury in obese conditions.

The enteric nervous system (ENS) constitutes a highly organized and intricate neuronal network comprising two principal plexuses: myenteric and submucosal. These plexuses consist of neurons and enteric glial cells (EGCs). Neurons ensure innervation throughout the intestinal wall, whereas EGCs, distributed within the mucosa, contribute to epithelial barrier integrity and modulation of local inflammatory responses. The ENS orchestrates essential gastrointestinal functions, including motility, secretion, absorption, vascular regulation, and immune interactions with gut microbiota. Under physiological conditions, intestinal homeostasis involves moderate generation of reactive oxygen species (ROS) through endogenous processes such as mitochondrial oxidative phosphorylation. Cellular antioxidant systems maintain redox equilibrium; however, excessive ROS production induces oxidative stress, promoting EGCs activation toward a reactive phenotype characterized by pro-inflammatory cytokine release. This disrupts neuron–glia communication, predisposing to enteric neuroinflammation and neurodegeneration. Obesity, associated with hyperglycemia, hyperlipidemia, and micronutrient deficiencies, enhances ROS generation and inflammatory cascades, thereby impairing ENS integrity. Nevertheless, non-pharmacological strategies—including synthetic and natural antioxidants, bioactive dietary compounds, probiotics, and prebiotics—attenuate oxidative and inflammatory damage. This review summarizes preclinical and clinical evidence elucidating the interplay among the ENS, obesity-induced oxidative stress, inflammation, and the modulatory effects of antioxidant interventions.

Obesity has a great impact on adipose tissue biology, based on its function as a master regulator of energy balance. Brown adipose tissue (BAT) undergoes remodeling, and its activity declines in obese subjects due to a whitening process. The anti-obesity properties of fruit extracts have been reported. The effects of tart cherry against oxidative stress, inflammation, and the whitening process in the BAT of obese rats were investigated. Intrascapular BAT (iBAT) alterations and effects of Prunus cerasus L. were debated in rats fed for 17 weeks with a high-fat diet (DIO), in DIO supplemented with seed powder (DS), and with seed powder plus the juice (DJS) of tart cherry compared to CHOW rats fed with a normo-caloric diet. iBAT histologic observations revealed a whitening process in DIO rats that was reduced in the DS and DJS groups. A modulation of uncoupling protein-1 (UCP-1) protein and gene expression specifically were detected in the obese phenotype. An upregulation of UCP-1 and related thermogenic genes after tart cherry intake was detected compared to the DIO group. Metabolic adjustment, endoplasmic reticulum stress, protein carbonylation, and the inflammatory microenvironment in the iBAT were reported in DIO rats. The analysis demonstrated an iBAT modulation that tart cherry promoted. In addition to our previous results, these data confirm the protective impact of tart cherry consumption on obesity.

The kidney plays a crucial role in the complex inter-organ communication that occurs during obesity, leading to the development of oxidative stress, inflammation, and fibrosis. Dysfunction of the transient receptor potential (TRP) ion channels contributes to this pathophysiology. This study was designed to evaluate the effects of antioxidant-rich fruit tart cherry (Prunus cerasus L.) on kidney morphology and protein expression in rats with diet-induced obesity (DIO). Methods include histological staining and immunohistochemical and Western blot assays. Obese rodents were fed with seed powder (DS) and seed powder plus juice (DJS) of the tart cherry. Results demonstrated that rats fed a high-fat-diet (HFD) showed a significant reduction in renal expression of the pro-inflammatory cytokines interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) following tart cherry supplementation. Furthermore, the study provided evidence that TRP channels, specifically TRP canonical 1 (TRPC1) and TRP melastatin 2 (TRPM2), were significantly upregulated in obese animals (p < 0.05 vs. CHOW rats) and markedly downregulated following tart cherry supplementation (p < 0.05 vs. DIO rats). In conclusion, these TRP proteins offer new insights for identifying targets and biomarkers for developing therapeutic strategies against HFD-induced renal damage, characterized by glomerulosclerosis, fibrosis, and inflammation. Tart cherries supplementation exerted a protective effect on the kidneys by reducing protein oxidation and pro-inflammatory cytokine expression.

Background: Sleep bruxism involves repetitive jaw-muscle activity, including teeth clenching, grinding, or mandibular bracing. Despite the growing interest in botulinum toxin type A (BTX-A) as a therapeutic intervention for bruxism, evidence remains limited, particularly regarding studies using portable electromyography (EMG) monitoring devices. This study evaluated the effects of BTX-A injections into the masseter muscle on the reduction of bruxism activity, as measured using the portable electromyographic Holter Bruxoff system. Methods: Adult patients with diagnosed sleep bruxism were monitored for two nights using the Bruxoff device to record masseter EMG activity, respiratory rate, and heart rate. After receiving standardized bilateral masseter BTX-A injections, participants underwent the same monitoring protocol 40 days later. Statistical analyses compared pre- and post-treatment values, and effect sizes were calculated. Results: Ten participants (60% women; mean age 47.6 ± 4.4 years) completed the study. The Bruxism Index showed a marked reduction, dropping from 12.2 ± 1.32 at baseline to 7.4 ± 1.35 after 40 days, a statistically significant change (t (9) = 10.23, p < 0.001; Cohen’s d = 3.25). Average heart rate also decreased significantly, from 64.4 ± 2.99 to 62.6 ± 2.63 (t (9) = 2.86, p = 0.018; Cohen’s d = 0.91). However, the respiratory rate measurement remains stable. Conclusions: BTX-A injections into the masseter muscles produced a marked reduction in sleep-related bruxism activity as measured by portable EMG. These findings support BTX-A as a promising and effective treatment option for sleep bruxism.