Diabetic cardiomyopathy (DCM) is a chronic cardiac disorder that develops independently of coronary artery disease or hypertension in individuals with diabetes. Despite being identified over fifty years ago, it remains poorly recognized, and its management lacks standardization. The rising global prevalence of diabetes has amplified the incidence of DCM, underscoring the urgent need to clarify its molecular underpinnings and clinical progression. To provide a comprehensive review of the molecular and physiological mechanisms underlying diabetic cardiomyopathy, elucidating how metabolic dysregulation contributes to cardiac structural and functional alterations. This study also aims to highlight the potential therapeutic targets involved in the key signaling pathways of DCM pathogenesis. A systematic literature review was conducted using major scientific databases, including PubMed, Scopus, and Web of Science, covering studies published between 2000 and 2025. Keywords used included "diabetic cardiomyopathy," "hyperglycemia," "insulin resistance," "oxidative stress," "inflammation," "mitochondrial dysfunction," and "therapeutic targets." Peer-reviewed articles, original research papers, and review articles focusing on molecular mechanisms, signaling pathways, and therapeutic interventions related to DCM were included. Studies involving both experimental models and human subjects were considered. Data were extracted regarding metabolic alterations, key signaling cascades (NF-κB, PARP1, GLUT4, AT1R), and their association with cardiac remodeling, fibrosis, and functional impairment. The information was synthesized to illustrate the progression from metabolic imbalance to clinical manifestations and to identify promising molecular targets for therapy. Diabetic Cardiomyopathy is a critical metabolic and cardiac disorder. The IDF Diabetic Atlas 2021 reported that 537 million people are living with diabetes in the world and will peak at 643 million by 2030 (Magliano & Boyko, 2021). It is startling that 12% of diabetic patients develop cardiomyopathy, and the cause of mortality is predominantly heart failure (Lorenzo-Almorós et al., 2017). The disease remains asymptomatic and, therefore, is not well diagnosed in earlier stages. There is an obvious lack of in-depth understanding of the mechanism and pathophysiology in this regard. Through our review, we try to understand the symptoms through the underlying mechanism of pathophysiology. We also review crucial potential therapeutic moieties like NFKB, PARP, AT1R, and GLUT4 for alleviating Diabetic Cardiomyopathy.
Narcotic drugs, psychotropic drugs and toxic drugs are categories of drugs strictly controlled, and their use and management must strictly comply with relevant laws and regulations. This study aims to explore the application effect of the PDCA cycle method in the management of anaesthetics, psychotropic and toxic drugs in primary-level traditional Chinese medicine hospitals, and to analyse its mechanism of action in optimising drug management in combination with the theoretical basis of nervous system regulation. After two rounds of PDCA cycle management, the management deficiencies of anaesthetics, psychotropic and toxic drugs were significantly reduced, and the rationality rate of prescriptions was significantly improved. The PDCA cycle method, combined with the theoretical basis of nervous system regulation, can effectively enhance the management level of anaesthetics. The application of this method in drug management has significant theoretical and practical value and is worthy of promotion and application in primary medical institutions.
Chronic sinusitis with nasal polyps (CRSwNP) has a relatively high recurrence rate, seriously affecting the quality of life of patients. Neuroinflammation interacts with the persistent inflammatory state of the nasal mucosa. This study aims to explore the application value of medical thermal imaging technology in predicting postoperative recurrence of nECRSwNP, and to evaluate potential biomarkers and efficacy assessment methods for neuroinflammation treatment, with the expectation of providing new strategies for reducing postoperative recurrence rates and improving the quality of life. Medical thermal imaging technology can monitor the temperature changes of nasal mucosa in real time and promptly detect alterations in inflammatory activity. The levels of EOS and cytokines in peripheral blood can serve as potential biomarkers for evaluating the status of neuroinflammation, which is helpful for identifying patients with a higher risk of recurrence, thereby enabling timely adjustment of treatment plans and improving the pertinence and effectiveness of neuroinflammation treatment.
As people pay more and more attention to health management and exercise, the demand for monitoring fat metabolism and sports injuries is increasing day by day. Fat metabolism, as an important component of human energy metabolism, is closely related to athletic performance, weight management and the prevention of chronic diseases. Through high-precision optical sensors and advanced data analysis algorithms, this method can capture the changes in human physiological signals in real time, thereby reflecting the state of fat metabolism and the occurrence of sports injuries. This research provides new ideas and methods for fat metabolism monitoring and sports injury prevention and is expected to be widely applied in fields such as sports health management, sports training guidance. Through this real-time monitoring technology, people can better understand their own fat metabolism, formulate scientific exercise and diet plans, effectively prevent and promptly handle sports injuries, and improve exercise effectiveness and health levels.
The objective of this study was to assess the protective effects of melatonin (Mel) and selenium nanoparticles (SeNPs) against cisplatin (Cis)-induced nephrotoxicity in rats. Sixty male rats were categorised into five groups: Control, Cis, Cis + Mel, Cis + SeNPs, and Cis + Mel + SeNPs. Kidney injury was evaluated at 5 and 11 days using biochemical markers, oxidative stress indicators, gene expression analysis as well as histopathological and immunohistochemical assessments. The combined treatment of Mel + SeNPs significantly improved kidney function biomarkers, reduced MDA levels, increased the activities of SOD, CAT, and GSH, decreased the expression of Bax and IL-6, and increased the expression of Bcl-2, Nrf2, and HO-1 compared to Cis group (p < 0.05). The histological structure and protein expression profiles indicated the most significant enhancement in the combined therapy group, especially on day 11. The co-administration of Mel and SeNPs demonstrated a significant synergistic effect in protecting the kidneys from Cis-induced nephrotoxicity.
Urotensin II (U-II) is one of the most potent endogenous vasoconstrictors, with its vascular effects tightly regulated by endothelial function and ion channel activity. The impact of diabetes mellitus on the signalling mechanisms underlying U-II-induced vascular reactivity remains insufficiently understood. This study systematically investigated how diabetes alters U-II-induced vasoconstriction by dissecting the contributions of endothelial integrity, potassium channel subtypes, calcium influx, and gap junction communication in the thoracic aorta of normoglycemic and streptozotocin-induced diabetic rats. Isolated aortic rings with intact or denuded endothelium were exposed to cumulative concentrations of U-II (1 0 -11-1 0 -8 M). Pharmacological inhibitors-including L-NAME (NOS inhibitor), indomethacin (COX inhibitor), TEA (Kv channel blocker), BaCl2 (Kir channel blocker), clotrimazole (IKCa channel blocker), nifedipine (L-type Ca2+ channel blocker), and GAP27 (gap junction inhibitor) were employed to delineate mechanistic pathways. Endothelial removal significantly potentiated U-II-induced contractions in both non-diabetic and diabetic vessels, affirming the critical modulatory role of endothelium-derived vasodilators. Diabetic vessels exhibited marked reductions in maximal contraction (Emax) and sensitivity (pD2) to U-II. In non-diabetic aorta, Kir and IKCa channel blockade robustly suppressed U-II-induced contraction, whereas these effects were diminished or reversed in diabetic tissue, indicating functional channel dysregulation. L-NAME potentiated U-II responses selectively in diabetes, implicating impaired nitric oxide bioavailability. Strikingly, nifedipine enhanced U-II-mediated contraction in diabetic rats, suggesting maladaptive remodelling of calcium influx. GAP27 reduced U-II responses, with a more pronounced inhibitory effect in diabetic vessels, highlighting disease-specific alterations in gap junction signalling. Diabetes markedly impairs urotensin II-induced vascular contractility by disrupting Kir and IKCa potassium channel function, alongside distinct changes in calcium channels, gap junctions, and prostanoids. Restoring Kir and IKCa  may offer an effective therapeutic strategy to reverse vascular dysfunction in diabetic vascular myopathy.
Moyamoya disease is a chronic progressive cerebrovascular disease, characterised by stenosis or occlusion of the ends and branches of bilateral internal carotid arteries, accompanied by the formation of abnormal vascular networks at the base of the skull. Through non-invasive detection techniques such as magnetic resonance spectroscopy (MRS), diffusion tensor imaging (DTI). It provides important basis for clinical treatment. This study aims to explore the characteristics of three-dimensional pseudo-continuous arterial spin labelling (3D-pCASL) parameters in patients with moyamoya disease and their predictive value for the improvement of cognitive function after revascularization, and to investigate the potential application value of 3D-pCASL parameters in evaluating neuronal injury and predicting the improvement of postoperative cognitive function. This study further confirmed the application value of 3D-pCASL parameters in the examination of neuronal injury and the prediction of postoperative cognitive function improvement, providing an objective imaging basis for the early clinical identification of patients.
Background: Hierarchical medical treatment is the core system of China's medical reform. The medical alliance model, as an important carrier, has been promoted nationwide. Purpose: This study aims to comprehensively assess the current status of pharmaceutical services in the medical alliance of Shaoxing City, with a focus on the application of metabolic abnormality tests, providing a basis for improving service homogeneity. Methods: The study adopted the cross-sectional survey method. Questionnaires were distributed to the heads of the pharmacy departments of 4 general hospitals of the medical alliance and 23 branch hospitals in Shaoxing from April to May 2021. Discussion: Measures such as optimising the allocation of testing resources, improving unified standards and mutual recognition mechanisms, and strengthening the collaboration between testing and pharmaceutical services should be taken to enhance the homogenisation level of metabolic abnormality tests, thereby comprehensively improving the pharmaceutical service capabilities of the medical alliance and promoting implementation of hierarchical medical treatment.
With the intensification of population ageing, the incidence of bone metabolism-related diseases such as osteoporosis has significantly increased, becoming an important factor affecting the quality of life of the elderly. A total of 120 patients with rotator cuff tear (RCT) were selected as the research subjects. There were 65 male patients and 55 female patients. The aim of this study was to explore the predictive value of bone metabolism disease examinations and changes in proximal humeral bone density for intraoperative anchor loosening. The predictive value of proximal humeral bone density for intraoperative anchor loosening was analysed using the ROC curve. The increase in age and the decrease in bone density are closely related to risk of intraoperative anchor loosening. The combination of bone metabolism disease examinations and proximal humeral bone density detection can provide important basis for clinical preoperative prediction of anchor loosening risk and formulation of individualised treatment plans.
Context: Paraoxonase 1 (PON1) is a crucial antioxidant enzyme involved in the hydrolysis of organophosphates and the prevention of oxidative damage to lipoproteins. Objective: This study aimed to purify PON1 using a newly synthesised hydrophobic interaction chromatography gel and to investigate the inhibitory effects of selected emergency cardiac drugs on PON1 activity through in vitro and in silico approaches. Materials and methods: PON1 was purified using a Sepharose-4B-L-tyrosine-6-aminochrysene hydrophobic interaction chromatography gel. The inhibitory effects of deslanoside, digitoxin, esmolol, and adenosine were evaluated via kinetic inhibition assays, molecular docking, molecular dynamics simulations, and MMPBSA calculations. Results: Among the tested compounds, esmolol exhibited the strongest inhibition of PON1 activity (IC50 = 0.131 ± 0.071 μM, Ki = 0.044 ± 0.009 μM) via a competitive mechanism. Molecular docking revealed strong binding affinity of esmolol to the PON1 active site, which was further supported by molecular dynamics simulations over 150 ns. Discussion and conclusion: The findings indicate a potential interaction between commonly used emergency cardiac drugs and PON1, highlighting the importance of evaluating off-target effects on critical metabolic enzymes in cardiovascular therapy.
Diabetes mellitus (DM) is a chronic metabolic disorder that requires effective treatment strategies with minimal side effects. 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. 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. 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.
Post-thrombotic syndrome (PTS), a chronic complication of deep vein thrombosis, causes pain, swelling, and ulcers, impairing quality of life. This study explores the role of lipid peroxidation and chronic inflammation in PTS. Oxidative stress and chronic inflammation damage the endothelium, increase venous pressure, and induce fibrosis, driving PTS progression. A biomarker-based ELISA approach is proposed to measure plasma lipid peroxidation products (e.g. MDA) and pro-inflammatory cytokines (e.g. IL-6, TNF-α). This method detects early biochemical changes in post-DVT patients and tracks PTS risk. Elevated oxidative and inflammatory markers are strongly linked to PTS, supporting their use as diagnostic and therapeutic targets. Screening may improve prediction (98.7%), prevention (97.3%), and management (99.4%), while reducing MDA (95.6%), IL-6 (93.4%), and TNF-α (97.45%). Observational NHS data support symptom-biomarker correlations. Preliminary values for MDA (14.3 ± 4.1 nmol/mL), IL-6 (2.3 ± 1.1 pg/mL), and TNF-α (1.5 ± 0.7 pg/mL) are included to clearly present and support the research hypothesis.
Context: With the continuous development of sports science, the importance of lipid metabolism control in athletes' physical training and evaluation has become increasingly prominent. Objective: Lipid metabolism, as a key link in human energy metabolism, its reasonable regulation has a profound impact on athletes' endurance, physical recovery and sports performance. Methods: By rationally regulating lipid metabolism, the endurance and exercise efficiency of athletes can be effectively enhanced. In the design of the physical fitness assessment system, the addition of the lipid metabolism monitoring module makes the physical fitness assessment more comprehensive and scientific. Results: This system can monitor the lipid metabolism status of athletes in real time and conduct comprehensive analysis in combination with other physical fitness indicators, providing more accurate feedback information for coaches and athletes. Conclusion: The application of artificial intelligence algorithms has further enhanced the accuracy and personalisation of physical fitness assessment.
Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme with many essential biochemical functions. However, in various cancer diseases, increased activity of G6PD causes cancer cells to grow, so G6PD inhibitors have become a significant area of research in cancer treatment. Here, G6PD was purified 4530-fold with affinity chromatography using 2',5'-ADP Sepharose 4B from sheep liver. The effects of reduced glutathione (GSH) and ascorbic acid (vitamin C) on G6PD activity were explored. GSH and ascorbic acid showed a significant inhibitory effect on G6PD, and IC50 values were found as 0.37 µM and 34.66 µM, respectively. The inhibition type from Lineweaver-Burk plots of these compounds was identified as non-competitive inhibition. The Ki values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively. In this study, it was observed that GSH and ascorbic acid antioxidant compounds exhibit an inhibitory effect on G6PD and may be protective and preventive against cancer.
Traditional cancer diagnosis methods include imaging examinations, biopsy, etc., but these methods are often invasive, time-consuming, and costly. This study aims to explore the application effect of infra-red thermography technology in cancer diagnosis and analyse the coping experience of primary caregivers during patient diagnosis and treatment. The data collection methods include semi-structured interviews, observations, and questionnaire surveys. The research results show that infra-red thermography technology has high sensitivity and specificity in cancer diagnosis, which can assist doctors in detecting early signs of tumours. Therefore, cancer diagnosis technology based on infra-red thermography has shown great potential in early detection and is expected to become a beneficial supplement to traditional diagnostic methods. At the same time, caregivers' coping experiences during cancer diagnosis and treatment are complex and diverse, requiring the healthcare system to provide more support and resources to help them better adapt and cope.
Context: Lipid peroxidation (LPO) causes oxidative stress and neuroinflammation in eye diseases. Malondialdehyde and 4-hydroxy-2-nonenal are produced in the eye via polyunsaturated fatty acid oxidation. Objective: Electrophiles damage biological components. LPO damages the retina and optic nerve, causing age-related macular degeneration, diabetic retinopathy, and glaucoma. Materials and Methods: LPO also causes cataracts and dry eye in the anterior area. It also stimulates NLRP3 and NF-κB pathways, causing inflammation. Results: Electrophiles damage biological components. LPO damages the retina and optic nerve, causing age-related macular degeneration, diabetic retinopathy, and glaucoma. LPO also causes cataracts and dry eye in the anterior area. It also stimulates NLRP3 and NF-κB pathways, causing inflammation. Conclusion: Understanding how lipid peroxidation, oxidative stress, and neuroinflammation interact is crucial to developing effective eye health and vision loss therapies.
Context: Sirtuin-2 (SIRT2) is a longevity-related protein implicated in apoptosis, metabolic regulation and oxidative stress; however, its role in ageing pancreas remains unclear. Objective: This study investigated the effects of the selective SIRT2 inhibitor, Arabidopsis guanylate kinases-2 (AGK-2) on oxidative stress and apoptosis in aged rat pancreatic tissue. Methods: Young (3-month) and aged (22-month) Wistar albino rats were divided into control and AGK-2-treated groups (10 μM, 30 days). Total oxidant status (TOS) and total antioxidant status (TAS) used commercial kits, then calculated Oxidative stress index (OSI). For detecting nitrosative stress, we determined nitrite-nitrate levels using the Griess test. SIRT2 and caspase-3 were evaluated by ELISA and Western blot. Discussion and conclussion: Our findings showed that ageing increased SIRT2 expression, oxidative stress and caspase-3 protein compared to young rats. AGK-2 treatment reduced SIRT2, TOS, OSI and caspase-3, and increased TAS particularly in aged rats. AGK-2 reverses ageing-associated changes in pancreatic oxidative stress and apoptosis. SIRT2 modulation may represent a potential therapeutic target against age-related pancreatic degeneration.
The NLRP3 protein plays a crucial role in the occurrence and development of various diseases. Research has shown that arthritis caused by sports injuries is closely related to the activation of NLRP3. This study aims to explore the molecular structure of NLRP3 protein and its role in sports induced arthritis, and evaluate the effectiveness of nutritional and exercise interventions in combating sports induced arthritis. In sports induced arthritis, NLRP3 expression is significantly upregulated, indicating its importance in the inflammatory process. Nutritional intervention showed effective inhibition of NLRP3 inflammasome activation. Stability intervention analysis shows that long-term adherence to exercise and nutritional interventions can sustainably reduce the activation level of NLRP3. Therefore, appropriate nutrition and exercise interventions can significantly reduce the activation of NLRP3, alleviate joint inflammation, and help protect joint health. It is recommended to introduce such intervention strategies in clinical practice to improve the consequences of joint injuries.
Cellular ageing is closely related to various age-related diseases, and Klotho protein, as an anti-ageing related factor, plays an important role in delaying ageing by regulating cellular function and metabolism. This study aims to explore the role of Klotho protein in exercise intervention and its relationship with age-related metabolism. Study the effects of exercise intervention on serum Klotho protein levels, Klotho gene methylation status, ageing related β - galactosidase (SA - β - Gal) activity, and ageing metabolic indicators, revealing the molecular mechanism of exercise delaying cellular ageing. The experiment was divided into a control group and an exercise intervention group, with an intervention period of 12 weeks. Exercise intervention significantly improved oxidative stress indicators and blood lipid metabolism. Exercise intervention delays cellular ageing by upregulating serum Klotho protein levels and reducing gene methylation levels, inhibiting SA - β - Gal activity, improving oxidative stress and lipid metabolism.
Schwannoma of the ulnar nerve is often closely related to cubital tunnel syndrome. Neuroinflammation plays a significant role in the pathogenesis of ulnar schwannoma and cubital tunnel syndrome. This study aims to explore the application value of thermal radiation imaging technology in the diagnosis of ulnar schwannoma combined. After neuroinflammatory intervention, the patient's pain and numbness symptoms were significantly alleviated. Thermal radiation images show that the state of neuroinflammation is closely related to the improvement of neurological function. Thermal radiation imaging technology holds significant clinical importance in the diagnosis and treatment evaluation of ulnar schwannoma combined with cubital tunnel syndrome. It can provide real-time monitoring data of neuroinflammation and assist doctors in formulating more effective treatment plans. Neuroinflammatory intervention has shown good effects in alleviating patients' symptoms and promoting the recovery of neurological function, providing new ideas and methods for the treatment of ulnar schwannoma combined with cubital tunnel syndrome.