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Mitochondria play a key role in the cerebral ischemia-reperfusion injury. Although the extracellular signal-regulated kinase 1/2 inhibitor PD98059 (PD) is a selective and reversible flavonoid that can protect the mitochondria in a rat model of cardiac arrest/cardiopulmonary resuscitation, its role requires further confirmation. In this study, we investigated whether PD could maintain mitochondrial homeostasis and decrease reactive oxygen species (ROS) production in neuroblastoma (SH-SY5Y) cells exposed to oxygen-glucose deprivation/reperfusion (OGD/R). PD improved the mitochondrial morphology and function, reversed the increase in ROS production and cell apoptosis, and reduced total-superoxide dismutase and Mn-superoxide dismutase activities induced by OGD/R. PD decreases ROS production and improves mitochondrial morphology and function, protecting SH-SY5Y cells against OGD/R-induced injury.

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Background: In cardiac accident/cardiopulmonary resuscitation (CA/CPR) rat model, oxidative stress occurs during cerebral ischemia/reperfusion injury (CIRI), and antioxidative treatment has a neuroprotective effect. The antioxidant capabilities of pomelo peel essential oil (PPEO) have mostly been investigated in vitro, with little convincing data in vivo, particularly whether PPEO has a neuroprotective role against CIRI. Methods: In this investigation, a CA/CPR SD rat model and an oxygen-glucose deprivation/reperfusion (OGD/R) SH-SY5Y cell model were used to imitate the CIRI, and the neuroprotective role of PPEO was discovered in both. The morphological changes of neurons after PPEO treatment were observed using Nissl staining and transmission electron microscopy, while biochemical markers such as MDA, GSH, and Fe2+ were evaluated. Furthermore, western blot, immunofluorescence, and immunohistochemistry were used to examine the proteins GPX4, SLC7A11, ACSL4, and Nrf2. Results: Significant morphological alterations were identified during the pathological progression of CIRI. The neurologic deficit scores improved after PPEO therapy, and the expression of GPX4 and SLC7A11 increased, while the levels of intracellular Fe2+, ROS, and ACSL4 declined. PPEO also prevented CIRI caused by erastin (a specific inhibitor of SLC7A11) or RSL3 (inhibitor of GPX4). Furthermore, PPEO-induced increases in SLC7A11 and GPX4 may be related to Nrf2 translocation to the nucleus. Conclusions: In vitro and in vivo, we verified and investigated the neuroprotective effects of PPEO on CIRI. The underlying process may be connected to redox homeostasis regulation, which enhances antioxidative capacity through upmodulation of SLC7A11 and GPX4. It implies that PPEO will be considered as a source of potential adjuvant therapeutic agents for improving CIRI outcomes.

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To obtain the influence of the Bi2O3 particle content of a PTFE/Al/Bi2O3 reactive material (later referred to as PAB) on its shock-induced chemical reaction (SICR) characteristics, five kinds of PAB with different Bi2O3 contents were prepared; the reaction process in a drop-hammer test, recorded using a high-speed camera, was analyzed. The ignition and reaction mechanisms of PAB under mechanical impact were analyzed based on the thermochemical reaction characteristics and the microstructure. The results show that with an increase in Bi2O3 content, the shock-induced chemical reaction duration and the sensitivity of PAB increase, and then decrease. When the Bi2O3 content is 9%, the impact sensitivity is the highest and the reaction duration is the longest. The heating at the crack tip is responsible for PAB ignition under long-pulse low-velocity impact. During ignition, PAB undergoes several physicochemical changes such as the melting of PTFE, a PTFE/Bi2O3 reaction, an Al/Bi2O3 reaction, pyrolysis of the melted PTFE, and a C2F4/Al reaction; moreover, the presence of Bi2O3 decreases the excitation threshold of the reactive material, which facilitates the propagation of the reaction and improves the degree of the reaction and overall energy release of the reactive material.

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Polytetrafluoroethylene (PTFE)/Al reactive material with different aluminum particle sizes were prepared by molding and sintering, and the effect of aluminum particle size on the impact behavior of PTFE/Al reactive material with a mass ratio of 50:50 was investigated. The results show that aluminum particle size has significant effects on the shock-reduced reaction diffusion, reaction speed, and degree of reaction of the PTFE/Al reactive material. At a moderate strain rate, the reaction delay of PTFE/Al increased, and the reaction duration and degree decreased, with the increase of aluminum particle size. Under the strong impact of explosive loading, aluminum particle size has little effect on the reaction delay, which maintains at about 1.5 µs-2.5 µs, but the reaction durability and degree of reaction of PTFE/Al decrease with increasing aluminum particle size. There is also a strain rate threshold for the shock-induced reaction of PTFE/Al reactive material, which is closely related to aluminum particle size. The shock-induced reaction occurs when the strain rate threshold is exceeded.

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CONTEXT: Pomelo peel oil (PPO) [Citrus maxima (Burm.) Merr. (Rutaceae)] is reported to possess antioxidant and antimelanogenic activities. OBJECTIVE: To investigate the effect of PPO [Citrus maxima (Burm.) Merr. cv. Shatian Yu] on tumour necrosis factor-α (TNF-α)-induced necroptosis in cerebral ischaemia-reperfusion injury (CIRI) after cardiac arrest (CA). MATERIALS AND METHODS: Male Sprague Dawley rats were randomly assigned to six groups: sham group, PP0-L (10 mg/kg), PPO-M (20 mg/kg), PPO-H (40 mg/kg) and two control groups (CA, 0.9% saline; Gly, 10% glycerol). All drugs were administered intravenously to the CA/CPR rats within 10 min after return of spontaneous circulation (ROSC). After 24 h, rats were assessed for neuronal injury via the neurological deficit score (NDS), cerebral cortex staining and transmission electron microscopy (TEM) and expression levels of TNF-α and necroptosis-related proteins by immunoreactivity staining and western blotting. RESULTS: Compared to those in the sham group (survival rate, 100% and NDS, 80), the survival rate and NDS were significantly reduced in the model groups (CA, 56.25%, 70; Gly, 62.5%, 71; PPO-L, 75%, 72; PPO-M, 87.5%, 75; PPO-H, 81.25%, 74). In the PPO-M group, Nissl bodies were significantly increased (43.67 ± 1.906 vs. 17 ± 1.732), the incidence of pathomorphological injury was lower and the necroptosis markers (TNF-α, RIPK1, RIPK3, p-MLKL/MLKL) expression was downregulated compared to those in the CA group (p < 0.05). DISCUSSION AND CONCLUSIONS: The neuroprotective effects of PPO in the CA rats suggested that PPO possibility as a health product enhances the resistance ability against brain injury for humans.

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BACKGROUND: Reducing cerebral ischemia-reperfusion injury is crucial for improving survival and neurologic outcomes after cardiac arrest/cardiopulmonary resuscitation (CA/CPR). The purpose of this study is to investigate the neuroprotective effects of green tea polyphenols (GTPs) concern with the modulation of endogenous antioxidation and endoplasmic reticulum stress. METHODS: After subjecting to CA/CPR, rats were randomized into the saline group (NS, n = 40) and the GTPs group (GTPs, n = 40) and the GTPs group (GTPs, n = 40) and the GTPs group (GTPs. RESULTS: Comparing with that in NS group, GTPs increased the expression of SOD1 and SOD2 at 12 h, 24 h, 48 h, 72 h, and the expression of GRP78 at 24 h and 48 h (p < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (p < 0.05) butdecreased caspase-12, CHOP, caspase-3 level, and apoptotic number of neurons (. CONCLUSION: GTPs exert neuroprotective effects via mechanisms that may be related to the enhancement of endogenous antioxidant capacity and inhibition of endoplasmic reticulum stress in CA/CPR rat models.

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Physical activity could be an effective way to prevent obesity and cardiovascular disease. OBJECTIVE: The aim of our study was to evaluate physical performance in Chinese university students to offer a basis for preventing obesity. METHODS: A cross-sectional study was conducted for evaluate physical performance, including the standing long jump, 50-meter dash, and pull-up/sit-up test. RESULTS: The overall mean time of the 50-meter dash, standing long jump distance, and mean number of pull-ups was 7.98 seconds, 2.2773 meters, and 4.1041, respectively. For female students, the overall mean time for the 50-meter dash, standing long jump distance, and mean number of sit-ups was 9.89 seconds, 2.6191 meters, and 26.7997, respectively. CONCLUSION: Our study suggests that physical performance in Chinese university students is poor; related departments should pay more attention to the physical health of university students.

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Antiflammin-1 (AF-1) is a synthetic nonapeptide with a similar sequence to the conserved sequence of CC10 secreted by lung Clara cells. Studies suggest that it is potent inhibitor of inflammation. We investigated the effects and possible mechanisms of AF-1 on LPS-induced alveolar macrophage (AM) activation in vitro. AMs harvested from the BALF of Sprague-Dawley (SD) rat were treated with various concentrations of AF-1 both simultaneously and after LPS stimulation. The concentrations of the cytokines IL-1beta, IL-6, and IL-10 in the supernatant were detected by an enzyme-linked immunosorbent assay. The mRNA expression levels of these cytokines in AMs were analyzed using quantitative RT-PCR. To investigate more fully the possible mechanisms by which AF-1 modulates the expression of cytokines, cells were pretreated with anti-IL-10 antibody. Toll-like receptor-4 (TLR-4) expression on the cell surface was also detected using flow cytometry. The results showed that AF-1 suppressed mRNA expression and protein production of IL-1beta and IL-6, while it promoted IL-10 expression in LPS-stimulated AMs, in a dose-dependent manner. The inhibitory effects of AF-1 on IL-1beta were significantly decreased when endogenous production of IL-10 was blocked. AF-1 also showed an effect on downregulated TLR-4 expression in LPS-stimulated AMs. The data show for the first time that AF-1 modulates the AM response to LPS by regulating TLR-4 expression and upregulating IL-10 secretion, which could be another important mechanism in the AF-1 inhibiting effect on inflammation.

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