Archives of Physiology and Biochemistry最新文献

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.

Introduction: Diabetes abrogates the neuroprotection caused by ischaemic preconditioning (IPC) during cerebral ischaemia-reperfusion (CI/R) injury. The study investigates the involvement of Inositol 1,4,5-trisphosphate (IP3R) receptors in IPC-mediated neuroprotection during C/R injury in hyperglycaemic conditions.

Materials and methods: Swiss Albino mice were administered with streptozotocin (STZ) to induce diabetes. Mice were exposed to CI/R injury via common carotid arteries occlusion (20 min) followed by reperfusion (24 h). For IPC, each mouse was exposed to three-1 min cycles of ischaemia and reperfusion, followed by CI/R injury.

Results: CI/R animals showed behavioural, biochemical, and histopathological alterations. IPC was observed to attenuate the CI/R-induced detrimental effects in the normoglycemic animals; however, IPC failed to provide neuroprotection in the hyperglycaemic mice. 2-Aminoethyl diphenyl borinate (inositol 1,4,5-trisphosphate receptor (IP3R) antagonist) administration in IPC hyperglycaemic mice restored the neuroprotective effects of IPC.

Conclusion: This suggests the possible role of IP3R antagonism in IPC-mediated neuroprotection during CI/R injury in hyperglycaemic conditions.

With the rapid development of Internet of Things (iot) and mobile network technologies, traditional sports training methods are facing challenges in terms of data collection and analysis efficiency. By embedding sensors and cameras in the system, not only can the movements of athletes be monitored in real time, but the data can also be wirelessly transmitted to the cloud for analysis. The experimental results show that the training system based on the Internet of Things and mobile networks significantly improves the agility and training effect of athletes, demonstrating the application potential of mobile networks in sports training. Mobile network technology makes data transmission more efficient and convenient. Patients can access the training system at any time and place and adjust their personalised training plans. Graphic processing technology provides patients with more intuitive training data and simulation feedback, helping them better understand their performance and make adjustments.

Hepatotoxicity is a pathological condition characterised by disrupted biochemical parameters. This study aims to evaluate the hepatoprotective effects of Eriobotrya japonica fruit extract (EJFE) by assessing biochemical endpoints in a rat model of carbon tetrachloride (CCl₄)-induced liver injury. The study was carried out with five experimental groups of Wistar rats (n = 6): I- Control, II- Negative Control, III- EJFE (200 mg/kg b.w.), IV- EJFE (400 mg/kg b.w.), and V- Standard (Silymarin-treated). CCl₄ exposure resulted in a marked reduction in antioxidant potential (p < 0.05) and increases in oxidative stress (p < 0.05), accompanied by detrimental alterations in the lipid, liver-specific enzymes, and biomolecules. Significant (p < 0.05) elevated levels of protein carbonyl (PCO), malondialdehyde (MDA), and low-density lipoprotein (LDL) oxidation susceptibility, along with reduced paraoxonase-1 (PON-1) activity and reduced glutathione (GSH) level, reflect compromised liver function. Treatment with EJFE significantly ameliorated these effects via enhancing PON-1 activity and reducing susceptibility of LDL to oxidation, further supporting the extracts antioxidative and hepatoprotective potential.

Background: Diabetes mellitus (DM) is a chronic metabolic disorder that requires effective treatment strategies with minimal side effects.

Methods: DM was induced by intraperitoneal injection of nicotinamide (NA) at dose 60 mg/kg 15 minutes before streptozotocin (STZ) intraperitoneal injection (60 mg/kg) to 16 hours-fasted Wistar rats. The diabetic rats were treated with xanthine-based dipeptidyl peptidase-4 inhibitor (linagliptin) (1 mg/kg), and diosmin (10 mg/kg) either singly or in combination every other day for 4 weeks via oral gavage in NA/STZ-induced diabetic rats.

Results: Both linagliptin and diosmin potentially lowered the fasting and postprandial blood glucose levels, and fructosamine concentrations, indicating improved glycemic control. The combined treatment effects were the most potent. The treatments also improved serum lipid profile, and cardiac function markers, including AST and CK-MB, suggesting protective effects on the heart. Histopathological analysis demonstrated enhanced adipose tissue integrity and structural improvements. Additionally, inflammatory markers, including TNF-α and IL-1β, were significantly reduced, highlighting the anti-inflammatory properties of linagliptin and diosmin.

Conclusion: the findings suggest that linagliptin and diosmin exert strong anti-hyperglycemic, anti-hyperlipidemic, cardioprotective, and anti-inflammatory effects in diabetic rats; the combined treatment effect was the most potent.

This study aimed to investigate the protective effects of Moringa oleifera (MO) extract against valproic acid (VPA)-induced small intestine damage in rats. Forty-six adult female Sprague-Dawley rats were divided into four groups: Control (saline), MO (300 mg/kg), VPA (500 mg/kg), and VPA + MO. All treatments were administered orally for 15 days. Biochemical oxidative stress analyses revealed that MO treatment mitigated oxidative stress in VPA-treated rats. Molecular docking studies demonstrated that bioactive compounds in MO leaves exhibited potential inhibitory activity against oxidative stress-related enzymes, with high binding affinities. Immunohistochemical results indicated that VPA did not alter antioxidant stress responses such as Nrf2. However, histological examinations showed that VPA caused structural damage to the small intestine, while MO treatment alleviated this effect. Overall, MO exhibited significant protective and antioxidant properties against VPA-induced intestinal injury.

Atherosclerosis, a chronic inflammatory arterial disease, involves lipid deposition and immune cell infiltration, leading to vascular thickening and dysfunction. This study evaluated the protective effects of Pterocarpus marsupium (PM) heartwood extract, rich in polyphenols and flavonoids, in a high-fat diet (HFD)-induced atherosclerosis model in male Wistar rats. Thirty-six rats were divided into six groups (n = 6), receiving either a normal or HFD, with or without atorvastatin or PM extract. After 8 weeks, hemodynamic, biochemical, oxidative stress, and inflammatory parameters were assessed, along with aortic histology. HFD-fed rats showed elevated heart rate, lipids, liver enzymes, and MDA levels, with histological signs of atherosclerosis. PM treatment significantly reduced triglyceride and MDA levels and modestly improved HDL levels. No significant changes were observed in TNF-α or IL-6. Histology revealed reduced lipid infiltration in PM-treated rats. PM extract exhibited anti-atherogenic and antioxidant effects, warranting further studies to explore its therapeutic potential in cardiovascular disease.