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Hyperglycemia can exacerbate cerebral ischemia/reperfusion (I/R) injury, and the mechanism involves oxidative stress, apoptosis, autophagy and mitochondrial function. Our previous research showed that selenium (Se) could alleviate this injury. The aim of this study was to examine how selenium alleviates hyperglycemia-mediated exacerbation of cerebral I/R injury by regulating ferroptosis. Middle cerebral artery occlusion (MCAO) and reperfusion models were established in rats under hyperglycemic conditions. An in vitro model of hyperglycemic cerebral I/R injury was created with oxygen-glucose deprivation and reoxygenation (OGD/R) and high glucose was employed. The results showed that hyperglycemia exacerbated cerebral I/R injury, and sodium selenite pretreatment decreased infarct volume, edema and neuronal damage in the cortical penumbra. Moreover, sodium selenite pretreatment increased the survival rate of HT22 cells under OGD/R and high glucose conditions. Pretreatment with sodium selenite reduced the hyperglycemia mediated enhancement of ferroptosis. Furthermore, we observed that pretreatment with sodium selenite increased YAP and TAZ levels in the cytoplasm while decreasing YAP and TAZ levels in the nucleus. The Hippo pathway inhibitor XMU-MP-1 eliminated the inhibitory effect of sodium selenite on ferroptosis. The findings suggest that pretreatment with sodium selenite can regulate ferroptosis by activating the Hippo pathway, and minimize hyperglycemia-mediated exacerbation of cerebral I/R injury. [ABSTRACT FROM AUTHOR]

Hyperglycemia aggravates cerebral ischemia/reperfusion (I/R) injury via vascular injury. There is still a lack of effective pharmaceutical preparations for cerebral I/R injury under hyperglycemia. This study aimed to investigate the effects of oxymatrine (OMT) on hyperglycemia-exacerbated cerebral I/R injury in vitro and in vivo. The middle cerebral artery occlusion (MCAO) and reperfusion was established in the rats under hyperglycemia. Meanwhile, oxygen–glucose deprivation and reoxygenation (OGD/R) with high glucose was used as an in vitro model of hyperglycemic cerebral I/R injury. The results showed that the neurological deficit score, mortality, infarct volume and penumbra apoptosis in hyperglycemia group were significantly higher than those in normal glucose group. OMT pre-treated obviously reduced the degree of neurological deficit, mortality, infarct volume, improve cerebral blood flow after I/R in rats with hyperglycemia, and increase the survival rate of human brain microvascular endothelial cells (HBMECs) in high glucose and OGD/R group. OMT significantly improved the ultrastructure changes of endothelial cells, and maintain the migration and angiogenesis potency of HBMECs in high glucose and OGD/R group. OMT obviously alleviated the down-regulating CD31 and CD105 expression in cerebral microvessels caused by hyperglycemia. It is concluded that OMT treatment might alleviate cerebral I/R injury under hyperglycemia via protecting microvessels. [ABSTRACT FROM AUTHOR]

Selenium has been shown to possess antioxidant and neuroprotective effects by modulating mitochondrial function and activating mitochondrial biogenesis. Our previous study has also suggested that selenium protected neurons against glutamate toxicity and hyperglycemia-induced damage by regulating mitochondrial fission and fusion. However, it is still not known whether the mitochondrial biogenesis is involved in selenium alleviating hyperglycemia-aggravated cerebral ischemia reperfusion (I/R) injury. The object of this study is to define whether selenium protects neurons against hyperglycemia-aggravated cerebral I/R injury by promoting mitochondrial biogenesis. In vitro oxygen deprivation plus high glucose model decreased cell viability, enhanced reactive oxygen species production, and meanwhile stimulated mitochondrial biogenesis signaling. Pretreated with selenium significantly decreased cell death and further activated the mitochondrial biogenesis signaling. In vivo 30 min of middle cerebral artery occlusion in the rats under hyperglycemic condition enhanced neurological deficits, enlarged infarct volume, exacerbated neuronal damage and oxidative stress compared with normoglycemic ischemic rats after 24 h reperfusion. Consistent to the in vitro results, selenium treatment alleviated ischemic damage in hyperglycemic ischemic animals. Furthermore, selenium reduced the structural changes of mitochondria caused by hyperglycemic ischemia and further promoted the mitochondrial biogenesis signaling. Selenium activates mitochondrial biogenesis signaling, protects mitochondrial structure integrity and ameliorates cerebral I/R injury in hyperglycemic rats. [ABSTRACT FROM AUTHOR]

Overexpression of extracellular signal-regulated kinase ½ (ERK ½) signaling pathway leads to overproduction of reactive oxygen species (ROS) which induces oxidative stress. Coenzyme Q10 (CoQ10) scavenges ROS and protects cells against oxidative stress. The present study was designed to examine whether the protection of Coenzyme Q10 against oxidative damage in astrocytes is through regulating ERK 1/2 pathway. Ultraviolet B (UVB) irradiation was chosen as a tool to induce oxidative stress. Murine astrocytes were treated with 10 μg/ml and 25 μg/ml of CoQ10 for 24 h prior to UVB and maintained during UVB and 24 h post-UVB. Cell viability was evaluated by counting viable cells and MTT conversion assay. ROS production was measured using fluorescent probes. Levels of p-ERK 1/2, ERK 1/2, p-PKA, PKA were detected using immunocytochemistry and/or Western blotting. The results showed that UVB irradiation decreased the number of viable cells. This damaging effect was associated with accumulation of ROS and elevations of p-ERK 1/2 and p-PKA. Treatment with CoQ10 at 25 μg/ml significantly increased the number of viable cells and prevented the UVB-induced increases of ROS, p-ERK 1/2, and p-PKA. It is concluded that suppression of the PKA-ERK 1/2 signaling pathway may be one of the important mechanisms by which CoQ10 protects astrocytes from UVB-induced oxidative damage. [ABSTRACT FROM AUTHOR]

Background: Previous studies have indicated that selenium supplementation may be beneficial in neuroprotection against glutamate-induced cell damage, in which mitochondrial dysfunction is considered a major pathogenic feature. However, the exact mechanisms by which selenium protects against glutamate-provoked mitochondrial perturbation remain ambiguous. In this study glutamate exposed murine hippocampal neuronal HT22 cell was used as a model to investigate the underlying mechanisms of selenium-dependent protection against mitochondria damage.Results: We find that glutamate-induced cytotoxicity was associated with enhancement of superoxide production, activation of caspase-9 and -3, increases of mitochondrial fission marker and mitochondrial morphological changes. Selenium significantly resolved the glutamate-induced mitochondria structural damage, alleviated oxidative stress, decreased Apaf-1, caspases-9 and -3 contents, and altered the autophagy process as observed by a decline in the ratio of the autophagy markers LC3-I and LC3-II.Conclusion: These findings suggest that the protection of selenium against glutamate stimulated cell damage of HT22 cells is associated with amelioration of mitochondrial dynamic imbalance. [ABSTRACT FROM AUTHOR]

We developed an environmentally benign, convenient microwave-assisted process for the construction of 1,3,5-trisubstitued pyrazolines ( 10a∼ 10f, 11a∼ 11f, 12a∼ 12f, 13a∼ 13f). Chalcones, as the key intermedi- ates, were obtained by the condensation of each of appropriately substituted aromatic aldehydes ( 1∼ 4) with 4-substituted acetophenones ( 5a∼ 5f) via a Claisen-Schmidt reaction under the action of microwave irradiation. Cyclization of the chalcones ( 6a∼ 6f, 7a∼ 7f, 8a∼ 8f, 9a∼ 9f) with p-toluene sulfonhydrazide af- forded 1,3,5-trisubstitued pyrazoline derivatives using microwave-assisted process in 25 min and 140 watt power in glycol. The structures of targeted compounds were established by IR, 1H NMR, MS and ele- mental analysis. The results indicate that microwave-assisted synthetic process presents advantages in terms of enhancement in rate, decrease in reaction time, clean reaction and convenient operation. [ABSTRACT FROM AUTHOR]

Aims and objectives To provide a theoretical basis for the clinical care of patients with late stomach cancer, we investigated the life quality and analysed its related factor in the patients with late stomach cancer. Background Due to the lack of effective screening methods, stomach cancer usually has been in the advanced stage when patients are diagnosed. However, the treatment for late stomach cancer is a tough problem in today's medicine. Chemotherapy or radiotherapy brings patients physiological and psychological distress and heavy financial burden, affecting patients' therapeutic effects, prognosis and life quality. Design The patients with late stomach cancer were included, and then, questionnaires about the life quality were completed. Methods Questionnaires including European Organisation for Research on Treatment of Cancer Quality of Life Questionnaire-Core 30, Social Support Rating Scale, Medical Coping Modes Questionnaire and Self-rating Anxiety Scale were completed by 173 patients with late stomach cancer who received treatment in our hospital between May 2010 and May 2011. Correlation analyses were performed. Results The overall score of the life quality of the patients with late stomach cancer was only 29·54 ± 12·21. The social support, medical coping modes, anxiety and patients' clinical data (except radiotherapy) markedly affected the overall life quality of the patients with late stomach cancer ( p < 0·05). Conclusion The life quality of the patients with late stomach cancer is poor and is associated with many factors. Relevance to clinical practice This study provides a theoretical basis for better nursing the patients with late stomach cancer and improving their life quality. [ABSTRACT FROM AUTHOR]

Structural and spectroscopic properties of Sr2ZnTeO6 (SZTO) were investigated by angle-dispersive synchrotron X-ray powder diffraction and Raman spectroscopy in a diamond anvil cell up to 31 GPa at room temperature. Although SZTO remained stable up to the highest pressure, the different pressure coefficients of the normalized axial compressibility were obtained as βab=8.16x10-3 GPa-1 and βc=7.61x10-3 GPa-1. The bulk modulus B0 was determined to be 190(1) GPa by fitting the pressure--volume data using the Birch--Murnaghan equation of state. All the observed Raman modes exhibited a broadening effect under high pressure. The vibrational band ν1 around 765 cm-1, which is associated with the Te-O stretching mode in the basal plane of the TeO6 octahedron had the largest pressure coefficient, and the Grüneisen parameters for all the observed phonon modes were also calculated and presented. These parameters could be used to measure the amount of uniaxial or biaxial strain, providing a fundamental tool for monitoring the magnitude of the shift of phonon frequencies with strains. [ABSTRACT FROM AUTHOR]