Archives of Physiology and Biochemistry最新文献

Background: Parkinson's disease is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra. Although the exact cause of Parkinson's disease is still unknown, neuroinflammation and mitochondrial dysfunction have been identified as essential factors in the disease's pathophysiology.

Methods: Coenzyme Q10 has gathered considerable attention as a potential therapeutic agent due to its dual function in antioxidant defense and mitochondrial bioenergetics. It is an essential electron carrier in the mitochondrial electron transport chain and plays a crucial role in reducing oxidative stress, a primary cause of neuronal degeneration in Parkinson's disease.

Results: Coenzyme Q10 supplements can enhance mitochondrial activity, reduce oxidative stress, and protect dopaminergic neurons from degeneration. To improve Coenzyme Q10 formulations and ascertain its effectiveness in slowing the progression of Parkinson's disease, more study is required.

Conclusion: This review examines the neuroprotective mechanisms of Coenzyme Q10 and its potential as a therapeutic option for Parkinson's disease.

This study evaluates the protective effects of Iris germanica (I. germanica) methanolic extract against L-arginine-induced acute pancreatitis in male rats. The extract's antioxidant potential was confirmed by in vitro assays, revealing 30.76 mg/g of phenolics, 15.86 mg/g of flavonoids, and strong antioxidant activity. HPLC analysis identified catechin and chlorogenic acid as major components. In vivo, rats were divided into five groups: control, L-arginine-only, two I. germanica-treated groups (100 and 400 mg/kg), and a melatonin-treated group. L-arginine elevated serum amylase and lipase levels, while I. germanica extract significantly reduced them, particularly at 24 hours post-treatment. The extract also increased total antioxidant capacity and reduced malondialdehyde and myeloperoxidase levels dose-dependently. Histological analysis showed decreased pancreatic necrosis and edema in treated groups. However, no significant differences were found in cytokine levels (TNF-α, IL-6, IL-10). These findings suggest I. germanica extract may alleviate acute pancreatitis primarily through antioxidant mechanisms.

Context: Physical exercise is one of many environmental variables that may affect an organism through epigenetic mechanisms, and thus, it may be passed on to the offspring.

Objective: We assessed the effect of resistance training by the parents on mice offspring.

Materials and methods: Training protocol lasted eight weeks, being males and females paired for mating. After birth, the litters were adjusted to eight pups, organised into four groups: sedentary parents (SS), trained parents (TT), sedentary fathers and trained mothers (ST), and trained fathers and sedentary mothers (TS). Male and female pups were analysed separately at the age of 21 days. One-way ANOVA or Kruskal-Wallis was applied when appropriate at the significance level of p < 0.05.

Results: Resistance training improved the strength of both male and female parents. HOMA-IR index of the female offspring of groups ST and TS was improved, as well as that of the male offspring of groups TT and ST. In addition, there was a discrete reduction of adiposity in the offspring when at least one of the parents was trained.

Conclusion: Therefore, parental resistance training improved insulin sensitivity and adiposity of male and female offspring suggesting resistance training as a beneficial preconception health strategy for better metabolic outcomes in future generations.

The present study examined the effects of Tartrazine, a common industrial food colourant, on the pancreas and the protective role of Thymoquinone. Thirty-two Wistar albino male rats were randomly divided into four equal groups: Control, Tartrazine, Thymoquinone, and Tartrazine + Thymoquinone. The rats received Tartrazine and Thymoquinone treatments for 21 days. At the end of this period, pancreatic tissues and blood samples were collected for analysis. Tartrazine administration elevated malondialdehyde (MDA), total oxidant status (TOS), and oxidative stress index (OSI) levels, while decreasing glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase (CAT), and total antioxidant status (TAS) in pancreatic tissue. It increased glucose, total cholesterol, triglycerides, and LDL levels, while decreasing insulin and HDL levels in blood samples. Tartrazine administration aggravated pancreatic histopathology and enhanced Caspase-3 positive immunoreactivity. Thymoquinone administration reduced the harmful effects of Tartrazine on biochemical and histopathological parameters. Tartrazine administration negatively impacted pancreatic tissue and blood samples. The increased oxidant capacity and oxidative stress led to these harmful effects. Conversely, Thymoquinone alleviated oxidative stress by increasing antioxidant capacity and could act as a protective agent.

Background: Chemotherapeutics target cancerous cells, but they also have unavoidable toxicities in healthy tissues.

Aim: In this study, the effects of the commonly used chemotherapeutic 5-fluorouracil (5FU) on lung tissue were investigated, along with the possible protective benefits of apigenin (API), hesperidin (HES), and their combination.

Methodology: The study consisted of control, 5FU, API + 5FU, HES + 5FU, and API+HES + 5FU groups. API 50 mg/kg and HES 200 mg/kg were administered for 7 days. On the 8th day, 5FU was administered a dose of 100 mg/kg.

Results: Analyses showed that API and HES were effective in preventing oxidative stress induced by 5FU in lung tissue, attenuating inflammation and apoptosis by suppressing MAPK/NFκB and Caspase-3/Bax/Bcl-2 pathways, suppressing autophagy by decreasing LC3B expression, and regulating Sigmar1 expression.

Conclusion: These results suggest that the two flavonoids, when administered separately or in combination, may be useful in reducing side effects that often occur during the use of chemotherapeutics.

Background: We investigated whether the probiotic yeast Saccharomyces boulardii confers cardiometabolic protection and prevents diabetic cardiomyopathy by modulating inflammation, cardiac remodelling, cardiovascular function, and autonomic regulation.

Methods: Male C57BL/6 mice were allocated into four groups: Control (C), Diabetes (DM), Control+Saccharomyces boulardii (CSb), and Diabetes+Saccharomyces boulardii (DMSb). Diabetes was induced with intraperitoneal streptozotocin (STZ), and treatments (sterile water or Saccharomyces boulardii) were administered orally for 8 weeks. Blood glucose, cytokines, and nitric oxide levels were measured, along with cardiac function via echocardiography and direct blood pressure recordings.

Results: Saccharomyces boulardii reduced blood glucose and increased cardiac IL-10 in diabetic mice, restoring nitric oxide levels. These effects were associated to reduced collagen deposition, preventing vascular damage and ventricular fibrosis, and were accompanied by improved systolic/diastolic function and autonomic control.

Conclusion: Saccharomyces boulardii improved cardiac structure, function, and autonomic control in diabetic mice, supporting its potential as adjunct therapy for diabetic cardiomyopathy.

This study explored the neuroprotective effects of honokiol against oxidative stress, neuroinflammation and transforming growth factor-beta1 (TGF-β1) pathways in kainic acid (KA)-induced neurodegeneration in rats. The animals were divided into: control [Honokiol solvent (dimethyl sulphoxide), intraperitoneal for 7 days]; sham [single-dose KA solvent (saline, intracerebroventricular)]; KA (0,5 μg/μl, single-dose, intracerebroventricular); Honokiol [5 mg/kg-intraperitoneal) for 7 days]; and KA+Honokiol [KA single dose and Honokiol (for 7 days)]. Cerebral cortex and hippocampus tissues of the right hemispheres of rat brains were removed and examined biochemically and histopathologically. KA administration caused an increase in malondialdehyde levels and a decrease in reduced glutathione (GSH) and superoxide dismutase (SOD) levels. In addition, interleukin-1β levels and TGF-β1 expression were increased. Honokiol treatment decreased malondialdehyde levels, increased SOD and GSH levels, increased interleukin-1β levels and improved TGF-β1 expression in rats. Our data showed Honokiol has a protective potential against kainic acid-induced neurodegeneration by suppressing oxidative stress, inflammation and TGF-β1 expression.

Background: The effect of halophyte plant "Salicornia arabica" decocted extract (HDE) on histological damage and metabolic disorders induced by a High-Caloric Diet (HCD) in Psammomys obesus (P. obesus) was investigated.

Methods: Forty P. obesus were divided into two groups: receiving a natural Low-Caloric Diet (LCD) or a high-caloric diet (HCD). On day 90, each group was further subdivided into two groups, with or without a daily oral administration of HDE at 300 mg/kg body weight for one month. Body weight, glycaemia, and serum lipid profile were assessed. Histopathological analyses on retinal, pancreatic, renal, and adipose tissues were conducted on day 120.

Results: HDE administration markedly alleviates the HCD-induced metabolic disorder and histopathological alterations, restoring tissue integrity compared to the untreated HCD group. ATR-FTIR and micronutrient analyses showed HDE contains antioxidant minerals, soluble dietary fibers, and phenolic compounds likely responsible for its effects.

Conclusion: HDE may protect against HCD-induced metabolic disorders and tissues alteration in P. obesus.

Introduction: One of today's major health threats is brain tumours, yet current systems focus mainly on diagnostic methods and medical imaging to understand them. Here, the Shepard Quantum Dilated Forward Harmonic Net (ShQDFHNet) is developed for brain tumour detection using MRI scans.

Methods: It starts by enhancing images with high boost filtering to highlight key features, then uses Log-Cosh Point-Wise Pyramid Attention Network (Log-Cosh PPANet) for accurate tumour segmentation, guided by a refined Log-Cosh Dice Loss. To capture texture details, features like Spatial Grey-Level Dependence Matrix (SGLDM) and Gray-Level Co-occurrence Matrix (GLCM) are extracted. The final detection uses ShQDFHNet, combining Shepard Convolutional Neural Network (ShCNN) and Quantum Dilated Convolutional Neural Network (QDCNN), with layers enhanced by a Forward Harmonic Analysis Network.

Results: ShQDFHNet achieved strong performance on the Brain Tumour MRI dataset, with 90.69% accuracy, 91.14% True Positive Rate (TPR), and 90.61% True Negative Rate (TNR) using K-fold of 9.

Discussion: The use of high boost filtering, Log-Cosh PPANet, and texture-based features improves the input data quality and enables accurate tumor segmentation in MRI scans. The proposed ShQDFHNet model improves feature learning and achieves strong performance on brain tumor MRI data.

Background: Tangeretin (TAN) has antioxidant and anti-inflammatory characteristics. This study aims to investigate its effects on neurological recovery following spinal cord injury (SCI).

Methods: A mouse SCI model and a lipopolysaccharide (LPS)-induced BV-2 cell model were constructed. BV-2 cell proliferation was evaluated by CCK-8 assay and EdU staining. LDH kit and flow cytometry were used to detect BV-2 cell damage, different kits to detect ferroptosis-related indicators. Histopathological damage was observed by pathological staining. The Nrf2/GPX4 pathway and ferroptosis-related proteins were examined using Western blot.

Results: TAN treatment attenuated LPS-induced BV-2 cell injury while reduced lipid peroxidation and ROS content. TAN improved behavioural scores, attenuated histopathological damage, and promoted neurofilament regeneration in SCI mice. Notably, TAN reduced mitochondrial damage and ferroptosis in SCI model, activated the Nrf2/GPX4 pathway, whereas Nrf2 inhibitor attenuated the protective effect of TAN.

Conclusion: TAN inhibits ferroptosis in SCI model through activating Nrf2/GPX4 pathway.