This study assessed the therapeutic potential of swimming exercise in the curdlan-injected SKG mouse model and investigated the modulatory effects of irisin on inflammation. Curdlan-injected SKG were randomly assigned to either a home-cage group or a swimming group for 6 weeks. Changes in clinical arthritis scores and ankle thickness were measured weekly. Post-swimming program, mice were anesthetized for collection of vastus lateralis muscle and blood, which was followed by histological analysis, micro-CT imaging of the ankle joints, and the measurement of pro-inflammatory cytokines and irisin levels. Additionally, curdlan-injected SKG mice were intravenously injected with recombinant irisin protein and observed. Finally, serum levels of irisin in healthy control and ankylosing spondylitis (AS) patient groups were measured by ELISA. The swimming group of curdlan-injected SKG mice exhibited significant improvements in arthritis and enthesitis compared to the home-cage group. In particular, micro-CT and histological analyses revealed a notable reduction in pathological bone features in the swimming group compared to the home-cage group. Muscle endurance was also enhanced in the swimming group compared to the home-cage group, as determined by the wire-hanging test. Intriguingly, irisin levels not only were statistically increased in the swimming group but, also, TNF-α, IL-1β, and IL-6 levels were decreased. Additionally, injection of irisin protein slightly attenuated both arthritis and enthesitis in curdlan-injected SKG mice. Meanwhile, irisin serum levels were declined in AS patients. Overall, we found that swimming exercise attenuated pathological bone features in an AS animal model, potentially mediated by increased irisin serum levels with associated anti-inflammatory effects.

UNASSIGNED: This study aimed to investigate the effects of chronic swimming exercise and vitamin E administration on elemental levels in the bone tissue of epileptic rats.
UNASSIGNED: Forty-eight rats were divided into six groups: Control, Swimming, Swimming + vitamin E, Swimming + Epilepsy, Swimming + Epilepsy + vitamin E, and Epilepsy. Vitamin E was administered to the animals chronically by gavage at a dose of 500 mg/kg every other day for 3 months. Epileptiform activity was induced with penicillin in animals 24 hours after the last vitamin E intake. The exercise program consisted of daily 30-minute swimming sessions. At the end of the treatment period, the levels of calcium, chromium, copper, iron, magnesium, manganese, lead, and zinc (µg/gram tissue) in bone tissue samples were measured using an atomic emission device.
UNASSIGNED: The results showed that all epileptic groups had significantly lower bone chromium levels compared to the control groups (p<0.05). The epileptic, and epileptic swimming groups had the lowest levels of bone calcium, magnesium, and zinc (p<0.05). Vitamin E administration resulted in a significant increase in bone calcium, magnesium, and zinc levels in the epileptic swimming group with vitamin E compared to the epileptic and epileptic swimming groups. (p<0.05).
UNASSIGNED: The findings of the study show that the administration of vitamin E improves calcium, magnesium, and zinc metabolism in the deteriorated bone tissue of the epileptic rat model.

Exercise has been recognized as an effective intervention in the treatment of pulmonary arterial hypertension (PAH), supported by numerous studies. However, the precise effects of exercise on pulmonary function remain to be fully elucidated. In this study, using a rat model of swimming exercise training and monocrotaline-induced PAH, we aimed to explore its impact on pulmonary morphology and function. Our investigations revealed that MCT-treated rats exhibited augmented mean pulmonary arterial pressure (MPAP) and pulmonary vascular remodeling, which can be attenuated by 4 weeks of swimming exercise training (60 min/day, 5 days/week). Notably, MCT-treated rats showed impaired pulmonary function, as manifested by decreased tidal volume and dynamic compliance, which were reversed by exercise training. Assessment of pulmonary substrate in PAH rats indicated a prominent pro-inflammatory substrate, evidenced by macrophage accumulation through quantitative immunohistological analysis of macrophage-like cell expression (CD68), and extracellular matrix remodeling, evaluated by Masson staining. Importantly, both the pro-inflammatory substrate and extracellular matrix remodeling were ameliorated by swimming exercise training. Additionally, serum biochemical analysis demonstrated elevated levels of low-density lipoprotein cholesterol and Apolipoprotein B following MCT treatment, which were reduced with exercise intervention. Moreover, exercise enhanced systemic insulin sensitivity in both MCT-treated and untreated rats. Notably, MCT and exercise treatment both decreased fasting blood glucose (FBG) levels in rats, whereas exercise training reinstated FBG levels to normal in MCT-treated rats. In summary, our study suggests that swimming exercise confers a pulmonary protective effect in MCT-induced PAH rats, highlighting the potential importance of exercise-based rehabilitation in the management of PAH.

UNASSIGNED: Due to the increasing mortality and morbidity rates in diabetes mellitus (DM), which is one of the biggest health problems of our age, many treatment modalities are still being tried. The positive effects of metformin (MET) and physical exercise (EXE) on the pathophysiology of diabetes are well known. In this study, it was aimed to detail these positive effects of MET and EXE in combination on the basis of inflammation, apoptosis mechanisms, and endogen nesfatin-1 (NES-1) synthesis.
UNASSIGNED: Twenty-seven type 2 DM (DM-2) male Wistar Albino rats were divided into 4 groups, as the high-fat diet (HFD), MET, EXE, and MET+EXE groups. The total duration of the study was 3 months. At the end of the experiment, blood glucose and lipid profiles were measured. Histopathological evaluation was performed on the cardiac and aortic tissues and apoptotic markers were evaluated immunohistochemically. Inflammatory markers and NES-1 levels were analyzed by enzyme-linked immunosorbent assay.
UNASSIGNED: The plasma glucose, homeostatic model evaluation-insulin resistance (HOMA-IR), low-density lipoprotein (LDL) levels increased, and high-density lipoprotein (HDL) levels decreased significantly in the HFD group. In the treatment groups, the glucose, HOMA-IR, LDL, NES-1 levels in the plasma, as well as tumor necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), IL-6, caspase-3 (Cas-3), Bcl-2-associated X protein (Bax), and histopathological findings of inflammation in tissues were decreased. Additionally, there was an increase in plasma insulin, HDL, and tissue B-cell lymphoma-2 and levels.
UNASSIGNED: It was observed that the MET and EXE treatments in the DM-2 model reduced cellular damage mechanisms such as inflammation and apoptosis. The decrease in NES-1 levels was thought to be secondary to this antiinflammatory effect. In conclusion, the results demonstrated the effectiveness of EXE in reducing DM-2 and the NES-1 levels. Further studies are needed to evaluate the effect in different EXE models and treatment durations.

Hypertension, characterized by persistent and uncontrolled high blood pressure, is one of the most common significant causes of mortality worldwide. Lifestyle modifications such as exercise and antioxidant intake have showed beneficial effects on hypertensive conditions. Adropin and endothelin-1 (ET-1) have important vasoregulatory functions in the endothelium. However, the underlying mechanisms linking exercise- and/or antioxidant intake-mediated improvement of hypertension are not fully understood. In this study, it was hypothesized that swimming exercise and pomegranate juice (PJ) (as an antioxidant) administration might have protective effects on hypertension development and possible involvements of serum adropin and ET-1. To test the hypothesis, the rats with hypertension, induced by Nω-nitro-L-arginine methyl ester hydrochloride, were subjected to swimming exercise and received PJ for 8 weeks. Weekly systolic and diastolic pressures, serum concentrations of adropin and ET-1, and oxidant/antioxidant parameters in various tissues were measured. The obtained data show that swimming exercise leads to complete protection against hypertension within the 8-week duration, whereas the PJ administration causes an ameliorative effect. In addition, the combination of swimming exercise and PJ administration do not have additive effects in protection against hypertension. Notably, the 8-week swimming exercise restores the diminished serum adropin concentration in rats with hypertension to the control level. Serum adropin significantly correlated with systolic and diastolic pressures, depending on swimming exercise, but not PJ administration. Serum ET-1 concentration inconsistently fluctuates in response to Nω-nitro-L-arginine methyl ester hydrochloride, swimming exercise, and PJ intake. In addition, swimming exercise and/or PJ administration lead to a complete normalization in liver malondialdehyde concentrations of rats with hypertension, whereas these interventions cause slight or no improvements in superoxide dismutase, catalase, and glutathione in the heart, liver, and kidney. In conclusion, 8-week swimming exercise modulates hypertension, possibly by influencing adropin concentration and oxidative stress.

The objective of this study was to evaluate the combined and independent effects of exercise training and L-Arginine loaded chitosan nanoparticles (LA CNPs) supplementation on hippocampal Tau, App, Iba1, and ApoE gene expression, oxidative stress, β-secretase enzyme activity, and hippocampus histopathology in aging rats. Thirty-five male Wistar rats were randomly assigned to five groups (n = 7 in each): Young (8 weeks old), Old (20 months old), old + L-arginine supplementation (Old Sup), old + exercise (Old Exe) and old + L-arginine supplementation + exercise (Old Sup + Exe). LA CNPs were administered to the supplement groups through gavage at a dosage of 500 mg/kg/day for 6-weeks. Exercise groups were subjected to a swimming exercise program five days/week for the same duration. Upon the completion of their interventions, the animals underwent behavioral and open-field task tests and were subsequently sacrificed for hippocampus genetic and histopathological evaluation. For histopathological analysis of brain, Cresyl violet staining was used. Congo Red staining was employed to confirm amyloid plaques in the hippocampus. Expressions of Tau, App, Iba1, and ApoE genes were determined by real-time PCR. In contrast to the Old group, Old Exe and Old Sup + Exe groups spent more time in the central space in the open field task (p < 0.05) and have more live cells in the hippocampus. Old rats (Old, Old Sup and Old Exe groups) exhibited a significant Aβ peptide accumulation and increases in APP, Tau, Iba1, APOE-4 mRNA and MDA, along with decreases in SOD compared to the young group (p < 0.05). However, LA CNPs supplementation, exercise, and their combination (Old Sup, Old Exe and Old Sup + Exe) significantly reduced MDA, Aβ plaque as well as APP, Tau, Iba1, and APOE-4 mRNA compared to the Old group (p < 0.05). Consequently, the administration of LA CNPs supplements and exercise might regulate the risk factors of hippocampus cell and tissue.

BACKGROUND: The benefits of physical activity for the overall well-being of elderly individuals are well-established, the precise mechanisms through which exercise improves pathological changes in the aging lens have yet to be fully understood.
METHODS: 3-month-old C57BL/6J mice comprised young sedentary (YS) group, while aging mice (18-month-old) were divided into aging sedentary (AS) group and aging exercising (AE) group. Mice in AE groups underwent sequential stages of swimming exercise. H&E staining was employed to observe alterations in lens morphology. RNA-seq analysis was utilized to examine transcriptomic changes. Furthermore, qPCR and immunohistochemistry were employed for validation of the results.
RESULTS: AE group showed alleviation of histopathological aging changes in AS group. By GSEA analysis of the transcriptomic changes, swimming exercise significantly downregulated approximately half of the pathways that underwent alterations upon aging, where notable improvements were \'calcium signaling pathway\', \'neuroactive ligand receptor interaction\' and \'cell adhesion molecules\'. Furthermore, we revealed a total of 92 differentially expressed genes between the YS and AS groups, of which 10 genes were observed to be mitigated by swimming exercise. The result of qPCR was in consistent with the transcriptome data. We conducted immunohistochemical analysis on Ciart, which was of particular interest due to its dual association as a common aging gene and its significant responsiveness to exercise. The Protein-protein Interaction network of Ciart showed the involvement of the regulation of Rorb and Sptbn5 during the process.
CONCLUSIONS: The known benefits of exercise could extend to the aging lens and support further investigation into the specific roles of Ciart-related pathways in aging lens.

BACKGROUND: Recent findings elucidated hepatic PPARγ functions as a steatogenic-inducer gene that activates de novo lipogenesis, and is involved in regulation of glucose homeostasis, lipid accumulation, and inflammation response. This study delved into a comprehensive analysis of how PPARγ signaling affects the exercise-induced improvement of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD), along with its underlying mechanism.
METHODS: Chronic and acute swimming exercise intervention were conducted in each group mice. IR status was assessed by GTT and ITT assays. Serum inflammatory cytokines were detected by Elisa assays. PPARγ and its target genes expression were detected by qPCR assay. Relative protein levels were quantified via Western blotting. ChIP-qPCR assays were used to detect the enrichment of PPARγ on its target genes promoter.
RESULTS: Through an exploration of a high-fat diet (HFD)-induced IR and NAFLD model, both chronic and acute swimming exercise training led to significant reductions in body weight and visceral fat mass, as well as hepatic lipid accumulation. The exercise interventions also demonstrated a significant amelioration in IR and the inflammatory response. Meanwhile, swimming exercise significantly inhibited PPARγ and its target genes expression induced by HFD, containing CD36, SCD1 and PLIN2. Furthermore, swimming exercise presented significant modulation on regulatory factors of PPARγ expression and transcriptional activity.
CONCLUSIONS: The findings suggest that swimming exercise can improve lipid metabolism in IR and NAFLD, possibly through PPARγ signaling in the liver of mice.

The aim of this study was to demonstrate that swimming exercise combined with silymarin and vitamin C supplementation improves hepatic inflammation, oxidative stress, and liver histopathology in elderly rats with high-fat diet-induced liver damage.
Forty elderly male Wistar rats were randomly assigned to five groups (n = 8 in each): a normal diet (control), a high-fat diet (HFD), HFD + silymarin and vitamin C supplementation (HFD+Sup), HFD + swimming exercise (HFD+Exe), and HFD+Sup+Exe group (HFD+Sup+Exe). The non-alcoholic fatty liver model was induced for 6 wk in the HFD groups. After 6 wk of consuming an HFD, a daily supplemental gavage was administered to rats as an intervention along with HFD in the supplement groups for 8 wk. Moreover, rats in the exercise groups were subjected to swimming exercise training 5 d/wk for the same period.
The combination of swimming training and supplementation caused significant decreases in liver inflammatory biomarkers tumor necrosis factor-α and interleukin-1β while increasing total antioxidant capacity and peroxisome proliferator-activated receptor α (P < 0.05).
In elderly rats with liver injury caused by an HFD, the combination of exercise and silymarin with vitamin C supplementation effectively reduced oxidative stress, liver inflammation, fat accumulation, and regulated liver enzymes.

OBJECTIVE: Hepatic damage caused by oxidative stress is one of the problems associated with the emission of electromagnetic radiation (EMR). In this study, the effects of swimming exercise (SE) on oxidative stress and liver cell damage caused by EMR emission in rats were investigated.
METHODS: Thirty-two rats (8 weeks old) were randomly divided into four groups, including control (C), EMR, SE, and EMR + SE. During four weeks, the animals engaged in SE (30 min/session, 5session/week) and were also exposed to EMR (4 h/day, seven days/week) emission from a Wi-Fi 2.45GHZ router. The liver and blood samples were collected at 48 h after completing four weeks of SE to assess histopathological damage, oxidative stress, and liver enzymes.
RESULTS: Tissue sections showed severe liver damage in the EMR group compared to the C group, while the SE attenuated the liver damage. In the EMR group, compared to the C, SE and EMR + SE groups, the activity of superoxide dismutase (SOD) and catalase (CAT) decreased significantly, and the concentration of malondialdehyde (MDA) and liver enzymes (AST, ALT, and ALP) increased significantly (P < 0.05). Swimming exercise in the SE and EMR + SE groups compared to EMR led to a significant increase in the activity of SOD and CAT and a significant decrease in the concentration of MDA and liver enzymes (P < 0.05).
CONCLUSIONS: The study findings showed that the SE is beneficial in attenuating the harmful effects of RF-EMR emitted from the Wi-Fi on the liver.