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6 mm) chromatographic column ; gradient elution with acetonitrile-0.4% phosphoric acid solution (0.2 : 99. 8 , V/V) , column temperature at 25°C ; detection wavelength at 236 nm; flow rate 1.0 mL/min; using \" Similarity Evaluation System for Chromatographic Fingerprint of Traditional Chinese Medicine\" , to evaluate the similarity of the characteristic chromatogram of erirde drug, standard decoction and formula granules of honeysuckle sem. According to Technical Requirements for Quality Control and Standard Formulation of Traditional Chinese Medicine Formula Granules and the principle of quality consistency, the characteristic chromatogram of raw materials, standard decoction and mass production granules was studied in this research, which systematically and comprehensively reflected the chemical composition and transmission law of honeysuckle stem, standard decoction and granules, in order to provide an experimental basis for the formulation of quality standard of honeysuckle stem formula granules. 2 Materials 2.1 Instruments Agilent 1260 High Performance Liquid Chromatograph (Agilent) ; XPE205/XSE-204 Electronic Analytical Balance (Mettler Toledo); KQ-500DE Numerical Control Ultrasonic Cleaner (Kunshan Ultrasonic Instrument Co. , Ltd.). 2 g-adding 25 mL of 50% ethanol solution-ultrasonic treatment (power 250 W, frequency 40 kHz) for 30 min - cooling- making up for the lost weight with 50% ethanol solution - shaking well- filtering, and taking the filtrate. 3.3 Methodological investigation 3.3.1 Precision test.

Background Micro- and nanoplastic pollution has become a global environmental problem. Nanoplastics in the environment are still hard to detect because of analysis technology limitations. It is believed that when microplastics are found in the environment, more undetected nanoplastics are around. The current “microplastic exposure” is in fact the mixture of micro- and nanoplastic exposures. Therefore, the biological interaction between organisms among different sizes of micro- and nanoplastics should not be neglected. Results We measured the biodistribution of three polystyrene (PS) particles (50 nm PS, PS50; 500 nm PS, PS500; 5000 nm PS, PS5000) under single and co-exposure conditions in mice. We explored the underlying mechanisms by investigating the effects on three major components of the intestinal barrier (the mucus layer, tight junctions and the epithelial cells) in four intestine segments (duodenum, jejunum, ileum and colon) of mice. We found that the amounts of both PS500 and PS5000 increased when they were co-exposed with PS50 for 24 h in the mice. These increased amounts were due primarily to the increased permeability in the mouse intestines. We also confirmed there was a combined toxicity of PS50 and PS500 in the mouse intestines. This manifested as the mixture of PS50 and PS500 causing more severe dysfunction of the intestinal barrier than that caused by PS50 or PS500 alone. We found that the combined toxicity of PS micro- and nanoplastics on intestinal barrier dysfunction was caused primarily by reactive oxygen species (ROS)-mediated epithelial cell apoptosis in the mice. These findings were further confirmed by an oxidants or antioxidants pretreatment study. In addition, the combined toxicity of PS micro- and nanoplastics was also found in the mice after a 28-day repeated dose exposure. Conclusions There is a combined toxicity of PS50 and PS500 in the mouse intestines, which was caused primarily by ROS-mediated epithelial cell apoptosis in the mice. Considering that most recent studies on PS micro- and nanoplastics have been conducted using a single particle size, the health risks of exposure to PS micro- and nanoplastics on organisms may be underestimated.

Background Microplastics and nanoplastics (MNPs) are emerging environmental contaminants detected in human samples, and have raised concerns regarding their potential risks to human health, particularly neurotoxicity. This study aimed to investigate the deleterious effects of polystyrene nanoplastics (PS-NPs, 50 nm) and understand their mechanisms in inducing Parkinson's disease (PD)-like neurodegeneration, along with exploring preventive strategies. Methods Following exposure to PS-NPs (0.5–500 μg/mL), we assessed cytotoxicity, mitochondrial integrity, ATP levels, and mitochondrial respiration in dopaminergic-differentiated SH-SY5Y cells. Molecular docking and dynamic simulations explored PS-NPs' interactions with mitochondrial complexes. We further probed mitophagy's pivotal role in PS-NP-induced mitochondrial damage and examined melatonin's ameliorative potential in vitro. We validated melatonin's intervention (intraperitoneal, 10 mg/kg/d) in C57BL/6 J mice exposed to 250 mg/kg/d of PS-NPs for 28 days. Results In our in vitro experiments, we observed PS-NP accumulation in cells, including mitochondria, leading to cell toxicity and reduced viability. Notably, antioxidant treatment failed to fully rescue viability, suggesting reactive oxygen species (ROS)-independent cytotoxicity. PS-NPs caused significant mitochondrial damage, characterized by altered morphology, reduced mitochondrial membrane potential, and decreased ATP production. Subsequent investigations pointed to PS-NP-induced disruption of mitochondrial respiration, potentially through interference with complex I (CI), a concept supported by molecular docking studies highlighting the influence of PS-NPs on CI. Rescue experiments using an AMPK pathway inhibitor (compound C) and an autophagy inhibitor (3-methyladenine) revealed that excessive mitophagy was induced through AMPK/ULK1 pathway activation, worsening mitochondrial damage and subsequent cell death in differentiated SH-SY5Y cells. Notably, we identified melatonin as a potential protective agent, capable of alleviating PS-NP-induced mitochondrial dysfunction. Lastly, our in vivo experiments demonstrated that melatonin could mitigate dopaminergic neuron loss and motor impairments by restoring mitophagy regulation in mice. Conclusions Our study demonstrated that PS-NPs disrupt mitochondrial function by affecting CI, leading to excessive mitophagy through the AMPK/ULK1 pathway, causing dopaminergic neuron death. Melatonin can counteract PS-NP-induced mitochondrial dysfunction and motor impairments by regulating mitochondrial autophagy. These findings offer novel insights into the MNP-induced PD-like neurodegenerative mechanisms, and highlight melatonin's protective potential in mitigating the MNP’s environmental risk.

Background Oxidative stress plays a critical role in age-related pathophysiology, and postmenopausal women are particularly vulnerable due to hormonal and metabolic changes. Although dietary quality has been implicated in modulating oxidative balance, few studies have explored whether obesity mediates this relationship in this population, representing a novel perspective in dietary-oxidative research. Objectives This study aimed to examine the associations between dietary quality and oxidative stress among postmenopausal women using data from the National Health and Nutrition Examination Survey (NHANES), and to assess whether obesity mediates this relationship. Methods A total of 2,391 postmenopausal women from NHANES 2005–2020 were included. Dietary quality was assessed using the Healthy Eating Index (HEI-2015), Dietary Inflammatory Index (DII), and Composite Dietary Antioxidant Index (CDAI). Oxidative stress was measured using the Oxidative Balance Score (OBS), and obesity was evaluated by body mass index and waist circumference. Multivariable regression and mediation analysis were conducted to explore the relationships. Results Healthier diets (higher HEI and CDAI, lower DII) were significantly associated with better oxidative profiles and lower obesity indicators. Obesity was inversely associated with oxidative stress. Mediation analysis showed that obesity partially explained the association between diet and oxidative stress, indicating an indirect pathway linking dietary quality to oxidative status via adiposity. Conclusions Our findings reveal a significant mediating role of obesity in the relationship between diet and oxidative stress in postmenopausal women. These results underscore the importance of integrated dietary and weight management strategies—such as promoting antioxidant-rich diets and obesity prevention—in mitigating oxidative stress-related health risks in this population.

Exposure to micro‐ and nanoplastics (MNPs) is common because of their omnipresence in environment. Recent studies have revealed that MNPs may cause atherosclerosis, but the underlying mechanism remains unclear. To address this bottleneck, ApoE−/− mice are exposed to 2.5–250 mg kg−1 polystyrene nanoplastics (PS‐NPs, 50 nm) by oral gavage with a high‐fat diet for 19 weeks. It is found that PS‐NPs in blood and aorta of mouse exacerbate the artery stiffness and promote atherosclerotic plaque formation. PS‐NPs activate phagocytosis of M1‐macrophage in the aorta, manifesting as upregulation of macrophage receptor with collagenous structure (MARCO). Moreover, PS‐NPs disrupt lipid metabolism and increase long‐chain acyl carnitines (LCACs). LCAC accumulation is attributed to the PS‐NP‐inhibited hepatic carnitine palmitoyltransferase 2. PS‐NPs, as well as LCACs alone, aggravate lipid accumulation via upregulating MARCO in the oxidized low‐density lipoprotein‐activated foam cells. Finally, synergistic effects of PS‐NPs and LCACs on increasing total cholesterol in foam cells are found. Overall, this study indicates that LCACs aggravate PS‐NP‐induced atherosclerosis by upregulating MARCO. This study offers new insight into the mechanisms underlying MNP‐induced cardiovascular toxicity, and highlights the combined effects of MNPs with endogenous metabolites on the cardiovascular system, which warrant further study. Exposure of ApoE−/− mice to 50 nm polystyrene nanoplastics (PS‐NPs) with a high‐fat diet explores the roles of macrophage and lipid metabolism disruption in micro‐ and nanoplastic‐induced atherosclerosis. Results indicate that long‐chain acyl carnitines (LCACs) aggravate PS‐NP‐induced atherosclerosis by upregulating macrophage receptor with collagenous structure, and highlights the synergistic effects of PS‐NPs with endogenous metabolite LCACs on the cardiovascular system.

Background Obesity is a well-established risk factor for periodontitis, a chronic inflammatory disease with systemic implications. While diabetes has been proposed as a potential mediator in this relationship, its clinical heterogeneity limits its utility in causal modeling. Insulin resistance, quantified by the Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), offers a more mechanistically grounded alternative. Objectives This study aimed to investigate the associations between obesity, insulin resistance, and periodontitis, with a specific focus on the mediating role of HOMA-IR. Methods Data from the National Health and Nutrition Examination Survey (NHANES, 2009–2012) including 8,473 participants were analyzed. Obesity was assessed using body mass index (BMI) and waist circumference (WC), and insulin resistance was measured using HOMA-IR. Periodontitis was evaluated using clinical attachment loss and probing depth. Multivariable logistic regression, restricted cubic splines, and mediation analyses were conducted. Results Both BMI and WC were significantly associated with an increased risk of periodontitis ( P  < 0.05). HOMA-IR was positively associated with periodontitis risk ( P  < 0.01). Mediation analysis revealed that HOMA-IR mediated 63.44% of the association between BMI and periodontitis and 36.77% of that between WC and periodontitis. Nonlinear analyses showed no significant nonlinear trends. Conclusions Insulin resistance, as reflected by HOMA-IR, plays a significant mediating role in the relationship between obesity and periodontitis. These findings underscore the importance of early metabolic regulation in mitigating obesity-related periodontal risk and provide mechanistic insight into the interplay between systemic and oral health.

Novel Ni-PSF@PAO40 microcapsules (NPPMS) with high stability were prepared by using a combined processing method of electroless nickel plating and solvent volatilization. The results indicate that Ni is completely assembled on the surfaces of PSF/PAO40 microcapsules with the encapsulation capacity of NPPMS achieved at 50%. Organic solvents immersion shows that NPPMS have an excellent chemical stability. Macro thermal stability tests reveal that the softening temperature of NPPMS is increased up to over 400 °C while it becomes lower than 200 °C for PSF/PAO40 microcapsules. Furthermore, NPPMS were embedded into polyamide 6 (PA6) to prepare PA6/NPPMS composites. The cross-sectional morphology shows that NPPMS are intact in PA6 matrices. The microhardness of PA6 is effectively improved with the incorporation of NPPMS. As compared with neat PA6, the coefficient of friction (COF) for PA6/NPPMS composites with 10% NPPMS could be reduced by 87.7% (from 0.49 to 0.06) and the wear rate could be decreased by 96.8% (from 1.29×10 −5 to 4.15×10 −7 mm 3 /(N·m)). Further studies confirmed that increasing test loads and test temperatures was beneficial to improve the lubrication performance of NPPMS despite the opposite trend occurred when increasing the sliding speeds. It has been demonstrated that synergistic effects between PAO40 and Ni layer play an important role in improving the tribological properties of PA6. Therefore, NPPMS significantly improve the ability of microcapsules to resist a harsh environment, which has important scientific significance for expanding the use of microcapsules more practically in self-lubricating composites.

To support the 6G vision of seamless “space–air–ground-integrated” global coverage, optical satellite networks must enable high-speed, low-latency, and intelligent data transmission. However, conventional inter-satellite laser link-based optical transport networks suffer from inefficient bandwidth utilization and nonlinear latency accumulation caused by multi-hop routing, which severely limits their ability to support ultra-low-latency and real-time applications. To address the critical challenges of high topological complexity and stringent real-time requirements in satellite elastic optical networks, we propose an asynchronous advantage actor–critic-based quality of service-aware routing optimization mechanism for the optical inter-satellite link (OISL-AQROM). By establishing a quantitative model that correlates the optical service unit (OSU) C value with node hop count, the algorithm enhances the performance of latency-sensitive services in dynamic satellite environments. Simulation results conducted on a Walker-type low Earth orbit (LEO) constellation comprising 1152 satellites demonstrate that OISL-AQROM reduces end-to-end latency by 76.3% to 37.6% compared to the traditional heuristic multi-constrained shortest path first (MCSPF) algorithm, while supporting fine-grained dynamic bandwidth adjustment down to a minimum granularity of 2.6 Mbps. Furthermore, OISL-AQROM exhibits strong convergence and robust stability across diverse traffic loads, consistently outperforming MCSPF and deep deterministic policy gradient (DDPG) algorithm in overall efficiency, load adaptability, and operational reliability. The proposed algorithm significantly improves service quality and transmission efficiency in commercial mega-constellation optical satellite networks, demonstrating engineering applicability and potential for practical deployment in future 6G infrastructure.

Circular RNAs (circRNAs) have been shown to be involved in the development of cancer. The aim of the present study was to investigate the role of circRNA SMARCA5 (cSMARCA5) in human cervical cancer. In the present study, cSMARCA5 expression was upregulated in cervical cancer tissues and cell lines. Furthermore, the proliferation rate of cells transduced with viral plasmids expressing small interfering RNA targeting cSMARCA5 was downregulated. Bioinformatics analysis predicted that microRNA (miR)-432 targeted cSMARCA5, and miR-432 was able to interact with epidermal growth factor receptor (EGFR) by binding to its 3′-untranslated region. The expression levels of EGFR, ERK1 and ERK2 were increased in cervical cancer tissues. Furthermore, correlation analysis revealed that cSMARCA5 levels were positively correlated with ERK1 and ERK2 levels. In conclusion, the present findings suggested that cSMARCA5 may play an important role in the progression of cervical cancer via the ERK signaling pathway by modulating miR-432.

This study aimed to design a novel mouse model of chronic photoaging. We used three different species of mice (C57BL/6J, ICR, and KM) to create a chronic photoaging model of the skin. The irradiation time was gradually increased for 40 consecutive days. The skins of the mice were removed on day 41 and subjected to staining to observe them for morphological changes. Immunohistochemistry was used to detect tumor necrosis factor-α (TNF-α) and p53 expression; superoxide dismutase (SOD) and malondialdehyde (MDA) were measured as well. Compared with C57BL/J mice, which showed hyperpigmentation, the irradiated skin of ICR and KM mice showed more obvious skin thickening and photoaging changes of the collagen and elastic fibers. KM mice had higher levels of inflammation, oxidative stress, and senescent cells. Compared with the 5-month-old KM mice, the photoaging changes of the 9-month-old KM mice were more pronounced, the SOD values were lower, and the MDA values were higher. In summary, KM mice have higher levels of abnormal elastic fibers, inflammation, cellular senescence, and oxidative stress than ICR mice, and are more suitable for studies related to chronic skin photoaging. C57BL/6J mice were found to be suitable for studies related to skin pigmentation due to photoaging.