ABSTRACT
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.
ABSTRACT
Cerebral ischemia-reperfusion injury (CIRI) is associated with a poor neurological prognosis in patients who have experienced cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). The aim of the current study was to investigate the potential role of a calpain inhibitor in CIRI using a rat model of CA. CA was induced in adult male Sprague-Dawley rats, and MDL28170 (a calpain inhibitor) was administered to the rats within 30 min after the return of spontaneous circulation. Differences between groups were evaluated by measuring survival rate, CPR duration and neurological deficit score. Hematoxylin-eosin staining and Nissl staining were performed to assess cerebral injury, and microstructure and autophagy were assessed by transmission electron microscopy. The levels of calpain-1, calpain-2, calpastatin, interleukin (IL)-1ß, tumor necrosis factor (TNF)-α, P62, beclin-1 and LC3 in the brain tissues were determined using western blotting and double immunofluorescence staining. There was no significant difference in CPR duration or survival rate among the groups. At 24 h after CPR, the CA group demonstrated damaged tissue morphology; decreased neurological deficit scores, and P62 expression; and upregulated calpain-2, IL-1ßp17, TNF-α, beclin-1 and LC3 levels in the cortex. However, MDL28170 improved neuronal function and suppressed inflammation and autophagy by inhibiting calpain-2 level, but there were no differences in the calpain-1 and calpastatin levels. These results suggest that calpain-2, inflammation and autophagy are involved in CA-induced CIRI. MDL28170 inhibited calpain-2 expression, inflammation and autophagy, which suggests its potential efficacy in treating post-CA nerve damage.
ABSTRACT
Soils and sediments of different origins were collected, which included the cropland soils surrounding Dishui Lake, the sediments from rivers, the sediments of wetland and the sediments in Dishui Lake. These samples were used for the experiment of phosphorus isothermal adsorption. The results of this experiment were analyzed and fitted. It shows that, the adsorption-desorption equilibrium mass concentration (EPC(0) value) of the sediments in Dishui Lake (0.11-0.63 mg x L(-1)) is higher than that of the soils and sediments from other sources, which indicates that it is easier to release phosphorus to overlying water. Both the Langmuir model and Freundlich model have a high fitting degree to the isothermal adsorption of phosphorus. The maximum adsorption capacity (Q(m)) calculated by Langmuir model demonstrate that the adsorption capacity of soils and sediments from different sources follows the order: sediments from rivers (1 003.05-2977.65 mg x kg(-1)) > sediments in Dishui Lake (669.77-1 717.94 mg x kg(-1)) > sediments of wetland (368.60-1 145.51 mg x kg(-1)) > cropland soils(441.36-702.30 mg x kg(-). It shows that the adsorption capacity of cropland soils is the weakest. Cropland soils can be a source of phosphorus in Dishui Lake when extra fertilizer is used.
