Advancements in Ti3C2Tx MXene Stability: Synergistic Antioxidant Strategies and Their Impact on Long-Lasting Flexible Sensors.

Two-dimensional (2D) transition metal carbides (Ti3C2Tx MXene) have demonstrated substantial application potential across various fields, owing to their excellent metallic conductivity and solution processability. However, the rapid oxidation of Ti3C2Tx in aqueous environments, leading to a loss of stability within mere days, poses a significant obstacle for its practical applications. Herein, we introduce an antioxidant strategy that combines free radical scavenging with surface passivation, culminating in the design and synthesis of imidazolium-based ionic liquids (ILs) incorporating siloxane groups. By deploying a straightforward hydrolysis-addition reaction, we successfully fabricated IL-modified Ti3C2Tx materials (Ti3C2Tx-IL). The Ti3C2Tx -IL not only displayed exceptional conductivity exceeding 3.85 × 104 S/m and hydrophilic contact angles below 45° but also showcased its superior chemical stability and antioxidation mechanisms through various analyses, including visual color change experiments, spectroscopic and energy spectrum characterization, free radical scavenging tests, and density-functional-theory-based molecular simulations. Furthermore, when utilized as a conductive filler in the fabrication of a poly(vinyl alcohol)/nanocellulose fiber (PVA/CNF) composite hydrogel (PCMIL), the resultant sensors exhibited remarkable mechanical performance with up to 535% strain, 1.59 MPa strength, 4.35 MJ/m3 toughness, and a conductivity of 3.40 mS/cm, as well as a high sensitivity gauge factor of 3.3. Importantly, even after 45 days of storage, the PCMIL retained most of its functionalities, demonstrating superior performance in human-machine interaction applications compared to hydrogels made from unmodified Ti3C2Tx. This research establishes a robust antioxidant protection strategy for Ti3C2Tx, offering substantial technical reinforcement for its prospective applications in the realm of flexible electronics and sensing technologies.

Caulophine protects cardiomyocytes from oxidative and ischemic injury.

Caulophine is a new fluorenone alkaloid isolated from the radix of Caulophyllum robustum MAXIM and identified as 3-(2-(dimethylamino) ethyl)-4,5-dihydroxy-1,6-dimethoxy-9H-fluoren-9-one. Due to its new chemical structure, the pharmacological activities of caulophine are not well characterized. The present study evaluated the protective effect and the primary mechanisms of caulophine on cardiomyocyte injury. Viability of cardiomyocytes was assayed with the MTT method, and cell apoptosis was detected by flow cytometry. Myocardial infarction was produced by ligating the coronary artery, and myocardial ischemia was induced by isoproterenol in rats. Myocardial infarction size was estimated with p-nitro-blue tetrazolium staining. Lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD), malondialdehyde (MDA), and free fatty acid (FFA) were spectrophotometrically determined. Histopathological and ultrastructural changes of ischemic myocardium were observed. The results showed that pretreatment with caulophine increased the viability of H(2)O(2)- and adriamycin-injured cardiomyocytes; decreased CK, LDH, and MDA; increased SOD; and inhibited H(2)O(2)-induced cellular apoptosis. Caulophine reduced myocardial infarct size and serum CK, LDH, FFA, and MDA; raised serum SOD; and improved histopathological and ultrastructural changes of ischemic myocardium. The results demonstrate that caulophine has the ability to protect cardiomyocytes from oxidative and ischemic injury through an antioxidative mechanism that provides a basis for further study and development of caulophine as a promising agent for treating coronary heart disease.

Effects of caulophine on caffeine-induced cellular injury and calcium homeostasis in rat cardiomyocytes.

Caulophine is a novel fluorenone alkaloid isolated from the radix of Caulophyllum robustum Maxim. Caulophine showed high affinity for the rat myocardial cell membrane as assessed by cell membrane chromatography, suggesting that the compound may exert bioactivity in the heart. It is known that calcium plays an important role in the pathogenesis of ischaemic heart disease, and caffeine can cause calcium overload in cardiomyocytes by inducing calcium release from the sarcoplasmic reticulum. Therefore, the present study evaluated the effects of caulophine on caffeine-induced injury and calcium homeostasis in cardiomyocytes. Cardiomyocytes were pre-treated with caulophine before exposure to caffeine or potassium chloride (KCl). Cell viability was assayed using the MTT method, and lactate dehydrogenase (LDH) and malondialdehyde (MDA) were measured spectrophotometrically. Caulophine-pre-treated cardiomyocytes were incubated with Fluo-3/AM, and then caffeine or KCl was used to induce Ca(2+) overload. The total intracellular Ca(2+) concentration was measured by flow cytometry. Fluorescence densities of single cardiomyocytes were detected using a confocal microscope. Caulophine increased the viability of caffeine-injured cardiomyocytes and decreased LDH activity and MDA level in cardiomyocytes. Furthermore, caulophine significantly decreased the total intracellular free Ca(2+) concentration and intracellular calcium release in cardiomyocytes in response to caffeine. However, the same concentrations of caulophine did not affect KCl-induced calcium influx. Our results suggest that caulophine protects cardiomyocytes from caffeine-induced injury as a result of calcium antagonism. This finding provides a basis for further study and development of caulophine as a new calcium antagonist for treating ischaemic cardiovascular diseases.

[Study on anti-atherosclerotic mechanisms of divided functional recipes of dahuang zhechong pill in rabbits].

OBJECTIVE: To study anti-atherosclerotic mechanisms of divided functional recipes of Dahuang Zhechong pill (DHZCP) in rabbits. METHOD: The atherosclerotic rabbit model was established by high fat feeding combined with immune endothelial injury. Male New Zealand rabbits were divided into 9 groups: normal control group, model control group, Danshen positive control group, and 6 DHZCP-divided groups including divided functional recipes No. 1, 2, 3 with low and high doses for each divided recipe. After intragastric administration for 60 days, blood lipids and serum MDA and NO levels and SOD activity and plasma ET concentration, and contents of hydroxyproline and proteins in the vascular wall were determined. RESULT: Compared with the model group, the level of blood lipids did not significantly change, serum MDA and ET levels, and the contents of hydroxyproline and proteins in the vascular wall significantly decreased (P < 0.05), and SOD activity and NO level increased in the divided functional recipes (all P < 0.05). CONCLUSION: The divided functional recipes of DHZCP can inhibit development of atherosclerosis via a non-lowering lipid mechanisms, including anti-peroxidation of lipids, protection of endothelial function, and decrease of formation of extracellular matrix by reducing synthesis of collage and protein on the vascular wall. Among them, the divided functional recipe No. 1 exhibits the most obvious effect.

[Protective effect of total flavonoid of Herba Pyrolae on acute myocardial ischemic injury in rats].

OBJECTIVE: To investigate the protective effect of Total Flavonoid of Herba Pyrolae(TFHP) on acute myocardial ischemic injury in rats. METHODS: Acute myocardial ischemic models were established by i. v. injection of pituitrin and the ligation of left descending coronary artery in rats. ECG of the rat was recorded, myocardial ischemic size was evaluated, and activites of creatine phosphokinase( CK), lactate dehydrogenase (LDH) and superoxide dismutase (SOD), level of malondialdehyde (MDA) in the rat serum were determined. RESULTS: In comparison with the model control, TFHP significantly reduced the incidence of ischemic arrhythmia induced by pituitrin, size of myocardial infarction, release of myocardial CK and LDH caused by the ligation of left descending coronary artery in rats. The primary study of action mechanism showed that TFHP decreased MDA level and increased SOD activity in the rat serum. CONCLUSION: TFHP provide a protective effect on acute myocardial ischemic injury via antioxidation.