[Construction and evaluation of a gradient stress model of PC12 cells induced by corticosterone].

Objective: A gradient stress model of PC12 cells induced by corticosterone was established to provide a basis for the evaluation and regulation of cell stress. Methods: The effect of corticosterone on cell viability was observed by measuring PC12 cell viability at different concentrations of corticosterone (0~1 000 µmol/L) after different intervention times (8~48 h) to screen the cell models for optimal intervention conditions. Key stress indicators (MDA, SOD, NADH, LDH) were measured spectrophotometrically and microscopically to evaluate the models. Results: When the concentration of corticosterone was below 200 µmol/L and the intervention time was 12 h, the cell viability was below half inactivation rate, which could reduce the confounding factors due to the decrease of cell viability in each group. Compared with the blank control group, corticosterone increased the levels of MDA, NADH and LDH,and decreased the levels of SOD in the model group in a concentration-dependent manner (P＜0.01), which was consistent with the construction of the gradient stress model. Conclusion: A gradient stress injury model of PC12 cells was successfully established, with intervention concentrations of 0 µmol/L, 25 µmol/L, 50 µmol/L, 100 µmol/L, 150 µmol/L and 200 µmol/L corticosterone at an intervention time of 12 h. The degree of stress injury of the cell model was increased gradually, which could be used as a basis and object for conducting cell stress injury assessment and regulation experiments.

Does Advanced Human Capital Structure Provide Positive Feedback on Public Health? Evidence From China.

This paper explores the relationship of advanced human capital structure with public health applying the panel threshold regression model in China. The empirical results highlight that the advanced human capital structure has a non-linear single threshold effect on population health indicators. The health-promoting effect of advanced human capital structure is significantly weaker when exceeding the threshold. These asymmetric effects are strongly related to the response of China's health policies. The promotion effect of the advanced human capital structure on public health has significant heterogeneity in different regions. There is a single threshold value in the eastern and central regions, but the threshold value and facilitation effect are different. However, the western region has no threshold. The heterogeneity effects are caused by the different levels of advanced human capital structure. Governments should adopt appropriate public health policies according to the development characteristics of different regions.

[Establishment and evaluation of oxidative stress injury model of in vitro rat aortic endothelial cells].

OBJECTIVE: To establish a model of oxidative stress injury in cultured rat aortic endothelial cells, and to provide a basis for the research of cell injury and apoptosis. METHODS: The rats were decapitated to get the aorta in thoracic operation under aseptic conditions. By subculture after tissue block culture method to get sufficient aortic endothelial cells, cultured in 96-well plates or grow on cover glass for the following test. Without H2O2 group as a control group, with different doses of H2O2 (100,200,300,400,500 µmol/L) treated endothelialcells in 12 h to screen the optimal dose. Based on the results, with the same dose of H2O2 (100 or 200 µmol/L) acted on endothelial cells respectively in different time (3, 6, 9, 12 and 24 h) to screen the optimal duration. Each group was made in sextuplicate. The establishment of the model was evaluated by immunofluorescence,cell viability testing, biochemical indicators detection (lactate dehydrogenase(LDH), nitric oxide(NO), malondialdehyde(MDA), superoxidedismutase(SOD))and apoptosis index testing. RESULTS: Endothelial cells were cultured successfully and verified by immunofluorescence staining of intracellular antigen Ⅷ collagen. With the increase of H2O2 doses at the same action time 12 h, the cell viability was significantly decreased (77.63%±5.20% to 40.90%±2.10%). The same dose(100 µmol/L group and 200 µmol/L group)with the action time increasing, the cellviability was significantly decreased (100 µmol/L group was 86.83%±12.11% to 44.26%±5.70%, 200 µmol/L group was 78.28%±11.98% to 34.45%±5.87%). At dose of H2O2 was 100 µmol/L and treated in 3,6,9,12 and 24 h, LDH-L and MDA were significantly increased after 9 h while NO and SOD were significantly decreased. In H2O2 dose of 100 µmol/L and action time 12 h, flow cytometry showed endothelial cellapoptosis rate was 16.92%±2.37%, significantly higher than the control group of 2.68%±0.47%(P<0.01); TUNEL detected endothelial cell apoptosis index was17.65%±2.36%, which was significantly higher than that in the control group of 3.23%±0.57%(P<0.01). CONCLUSIONS: The method was successfullyestablished a model of oxidative stress injury in cultured rat aortic endothelial cells, explore the moderate conditions that induced cells injury and apoptosis which could be a basis for the research.

[Protective effects of histone deacetylase inhibitor on stress-induced myocardial injury in rats].

OBJECTIVE: To observe the protective effects of histone deacetylase inhibitor on stress-induced myocardial injury. METHODS: Healthy male Wistar rats were randomly divided into 3 groups( n = 6), and the stress-induced myocardial injury model was established with chronic restraint stress method. The protective effects of histone deacetylase inhibitor on stress-induced myocardial injury were observed with Trichostatin A (TSA) intervention. Histone acetylation levels in myocardium of rats were detected by Western blot method, spectrophotometry method was used to dynamically determine the activity of rat serum lactate dehydrogenase (LDH), serum creatine kinase isoenzyme-MB (CK-MB) and Caspase 3, and nagar Olsen staining were used to observe the early myocardial damage. RESULTS: Restraint stress could significantly reduce the level of histone acetylation of myocardium in rats, and TSA intervention could inhibit the stress-induced reduction of myocardial levels of histone acetylation. Restraint stress could cause the significant increase of serum LDH activity ( P < 0.05), serum CK-MB activity ( P < 0.05), and the Caspase 3 activity of myocardial tissue (P < 0.05), and early myocardial damage also occurred during restraint stress. ISA intervention could significantly reduce the serum LDH activity (P < 0.05), the serum CK-MB activity (P < 0.05), the activity of myocardial tissue caspase 3 induced by restraint stress (P < 0.05), and the stress-induced myocardial injury was also attenuated by TSA intervention. CONCLUSION: The histone deacetylase inhibitor TSA can protect stress-induced myocardial injury.

ZFP580, a novel zinc-finger transcription factor, is involved in cardioprotection of intermittent high-altitude hypoxia against myocardial ischemia-reperfusion injury.

BACKGROUND: ZFP580 is a novel C2H2 type zinc-finger transcription factor recently identified by our laboratory. We previously showed that ZFP580 may be involved in cell survival and growth. The aim of this study was to elucidate whether ZFP580 is involved in the cardioprotective effects of intermittent high-altitude (IHA) hypoxia against myocardial ischemia-reperfusion (I/R) injury. METHODS AND RESULTS: After rats were subjected to myocardial ischemia for 30 min followed by reperfusion, ZFP580 expression in the left ventricle was measured. ZFP580 protein expression was found to be up-regulated within 1 h and decreased at 2 h after reperfusion. Comparing normoxic and IHA hypoxia-adapted rats (5000 m, 6 h day-1, 6 weeks) following I/R injury (30 min ischemia and 2 h reperfusion), we found that adaptation to IHA hypoxia attenuated infarct size and plasma leakage of lactate dehydrogenase and creatine kinase-MB. In addition, ZFP580 expression in the myocardium was up-regulated by IHA hypoxia. Consistent with this result, ZFP580 expression was found to be significantly increased in cultured H9c2 myocardial cells in the hypoxic preconditioning group compared with those in the control group following simulated I/R injury (3 h simulated ischemic hypoxia and 2 h reoxygenation). To determine the role of ZFP580 in apoptosis, lentivirus-mediated gene transfection was performed in H9c2 cells 72 h prior to simulated I/R exposure. The results showed that ZFP580 overexpression significantly inhibited I/R-induced apoptosis and caspase-3 activation. H9c2 cells were pretreated with or without PD98059, an inhibitor of ERK1/2 phosphorylation, and Western blot results showed that PD98059 (10 µM) markedly suppressed I/R-induced up-regulation of ZFP580 expression. CONCLUSIONS: Our findings demonstrate that the cardioprotective effect of IHA hypoxia against I/R injury is mediated via ZFP580, a downstream target of ERK1/2 signaling with anti-apoptotic roles in myocardial cells.

Tetra-aqua-(1,10-phenanthroline)nickel(II) 3,6-dicarboxy-bicyclo-[2.2.2]oct-7-ene-2,5-dicarboxyl-ate.

In the title compound, [Ni(C(12)H(8)N(2))(H(2)O)(4)](C(12)H(10)O(8)), the Ni(II) ion is six-coordinated by two N atoms from one phenanthroline ligand and by the O atoms of four water mol-ecules in a distorted octa-hedral geometry. In the crystal, inter-molecular O-H⋯O hydrogen bonds form an extensive three-dimensional network, which consolidates the crystal packing.

[Soil moisture and interspecific relationships between grass and legume on mixed grassland: a research review].

From the viewpoints of plant morphology and physiology, this paper discussed the survival strategy of grass and legume on mixed grassland under water stress, their competition for water and the hydraulic facilitation effects of legumes on water resource utilization, and the impact of drought on biological nitrogen fixation and nitrogen transfer of legume. It was indicated that to promote the productivity of grassland in arid area, the mechanisms of competition and coexistence between grass and legume should be further studied, and one of the main aspects should be the effects of water stress on their aboveground and belowground competitions and their feedback on the competitions.

[The delayed protection of exercise preconditioning from the relative myocardial ischemia-reperfusion injury.].

OBJECTIVE: To explore the delayed protection of exercise preconditioning from the relative myocardial ischemia-reperfusion injury. METHODS: The experiment included the vivo experiment and the vitro experiment, 32 Wistar rats in each experiment were divided into 4 groups randomly: control group (CN), relative ischemia reperfusion group (IR), exercise preconditioning group (EP) and Exercise preconditioning + relative ischemia-reperfusion group (EI). We detected the third loading exercise time, the levels of MDA in serum in vivo experiment and the Cardiac function parameter, the levels of MDA in coronary effluent in vitro experiment. RESULTS: (1) The vivo experiment: The third loading exercise time of EI group [(71.67 +/- 9.00) min] increased significantly compared with that of IR group [(58.67 +/- 4.13) min] (P < 0.05); The levels of MDA in serum of EP group (107.00 +/- 35.99) micromol/L and EI group [(152.23 +/- 29.94) micromol/L] decreased significantly contrasted to IR group (313.20 +/- 43.40 micromol/L) (P < 0.05). (2) The vitro experiment: The PRP (heart rate * left ventricular developed pressure) in reperfusion period of CN group and EP group were stable relatively, while it reached the peak after 30 minutes and almost recovered to the level before ischemia in EI group. The parameter of IR group recovered slightly but was lower significantly than that before ischemia. There was significant difference between the recovery rate of Cardiac function of EI group and that of IR group. The increase of MDA in coronary effluent after Ischemia-reperfusion of EP group (0.34 +/- 0.24 micromol/L) and EI group [(0.41 +/- 0.26) micromol/L] decreased significantly contrasted to that of IR group [(1.27 +/- 0.52) micromol/L] (P < 0.05). CONCLUSION: EP has the obvious delayed protection from the relative myocardial ischemia-reperfusion injury.

[Study of the protective effect of L-arginine on relative ischemic/reperfusion injury in myocardium of rat].

AIM: To explore the protective effect of L-arginine on isolated rat heart with ischemia/reperfusion injury. METHODS: 24 wistar rats were randomly divided into 3 groups (each 8): control group, ischemia group, L-arginine group. The myocardiac relatively ischemia/reperfusion models in vitro were set up by using weak current stimulating isolated rat hearts. During the pre-ischemia, post-ischemia 15 min and post-ischemia 30 min, the coronary fluid was collected for testing contents of MDA and activities of both CK and LDH. Cardiac functional indexes were recorded through Pclab. At the time of 5 min, 10 min, 20 min, 30 min after ischemia, the recovery of PRP, + DP/dt(max) and - DP/dt(max) were calculated. RESULTS: (1) During the reperfusion, L-arginine group achieved better recovery of cardiac function than that of the ischemia group. (2) MDA content, CK and LDH activities both in the coronary fluid and in the myocardium of L-arginine group were lower than those of the ischemia group, while SOD activities in the myocardium of L-arginine group were higher than that of the ischemia group. CONCLUSION: To some extent, L-arginine could protect the myocardium from ischemia/reperfusion injury.