Objective To investigate the mechanism of protective effects of 17-β estradiol on the experimental model of spinal cord injury (SCI) rats.Methods First,the primary astrocytes were cultured and identified.When the third generation astrocytes were cultured,they were induced by H202 whose concentrations were established by the method of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT).The cells were randomly divided into five groups:control group; the group of treatment with 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 2 hours prior to exposure to 400 μmol/L H2O2 for 24 hours; the group of treatment with 20 nmol/L estrogen for 26 hours and the group of treatment with dimethyl sulfoxide for 26 hours.The proteins which were extracted from these cells after treatments with H2O2 for 24 hours were detected by Western blotting.Results The absorbances of the astrocytes of treatments with H2O2 were reduced( q' =-11.45,P =0.001 ).But exposure to estrogen prior to exposure to H2O2 provided partial restoration of the absorbances (q' =7.025,P =0.0025 ).The absorbances of the astrocytes among different groups showed significant differences( F =69.69,P =0.0025 ).The results suggested that estrogen might increase the cell viability in astrocytes.Compared with the group of treatment cells with H2O2,treatment cells with 17-β estradiol prior to H2O2 exposure down-regulated the expressions of both phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) ( F =290.003,P =0.001 ) and caspase-3 ( F =46.158,P =0.023 ).And,17-β estradiol treatment of cells increased the levels of p-Akt ( F =49.173,P =0.033 ) and Bcl-2 ( F =115.916,P =0.001 ) when compared with the group of treatment astrocytes with H2O2.Conclusion These findings suggest that the attenuation of PTEN expression mediated by estrogen is associated with an increase in phosphorylation/activation of the Akt and the Bel-2 expressions.These results suggest that the protective effects of 17-β estradiol on the experimental model of SCI rats may depend on the estrogen protection to the astrocytes which may be mediated by decreasing the PTEN expression.

Objective To investigate pathogenic bacteria distribution and its effect on the expression of apoptosis protein in patients with acute cerebral infarction (ACI) complicated with pulmonary infection. Methods A retrospective analysis was conducted. From January 2014 to October 2017, the clinical data of 178 patients suffered from ACI hospitalized in Department of Neuromedical Center of Affiliated Hospital of the Chinese People's Armed Police Force Logistics Academy were collected, including 86 cases with ACI complicated with pulmonary infection selected as the observation group, and 92 cases with ACI without pulmonary infection assigned in the control group. The identification and classification of pathogenic bacteria were carried out by using the French BioMieux microorganism fully automatic identification instrument; the contents of serum interleukins (IL-8, IL-17), soluble intercellular adhesion molecule-1 (sICAM-1) and B type lymphocyte tumor-2 related X protein (Bax), B lymphocyte tumor-2 protein (Bcl-2) in two groups were detected by enzyme-linked immunosorbent assay (ELISA). Pearson correlation analysis was used to observe the correlations between sICAM-1 and Bax, Bcl-2 protein expression. Results From the bacterial cultures of 86 patients with ACI complicated with pulmonary infection, 86 strains of pathogenic bacteria were isolated, including 41 strains of gram positive (G+) bacteria (47.67%), mainly Staphylococcus aureus (25.58%); 37 strains of gram negative (G-) bacteria (43.02%), mainly Acinetobacter baumannii (11.63%); 8 strains of fungi (9.30%). The serum levels of IL-8 (μg/L: 0.72±0.15 vs. 0.68±0.09), IL-17 (μg/L: 9.31±3.58 vs. 8.12±2.76), sICAM-1 (ng/L: 421.36±39.74 vs. 385.13±28.59) and Bax (μg/L: 4.52±0.47 vs. 3.86±0.34) in the observation group were significantly higher than those in the control group, while the level of Bcl-2 in the observation group was significantly lower than that in the control group (μg/L: 0.84±0.26 vs. 1.13±0.31), all the differences were statistically significant (all P ＜ 0.05). In the observation group, sICAM-1 was significantly positively correlated with Bax protein (r = 0.401, P ＜ 0.001), while sICAM-1 was significantly negatively correlated with Bcl-2 (r = -0.447, P ＜ 0.001). Conclusion The pathogenic bacteria of ACI patients complicated with pulmonary infection is mainly G+bacteria, the infection can induce elevation of serum pro-inflammatory factors and sICAM-1 levels in the patients, and the mechanisms may be related to the up-regulation of Bax protein expression and down-regulation of Bcl-2 protein expression.

Sodium prasterone sulfate (DHEAS) and dehydroepiandrosterone (DHEA) are endogenous steroid compounds, which are synthesized and secreted by adrenal gland.They are the precursors of steroid hormones,including sex hormone.Based on intracrine theory,the majority of postmenopausal women will have vaginal atrophy,which is caused by the absence of endogenous hormones,DHEAS or DHEA.Moderate supplementation of DHEAS can relieve the associated symptoms of vaginal atrophy.Many clinical researches have demonstrated that DHEAS can efficiently alleviate the related symptoms of vaginal atrophy.The concentration of androgen and estrogen in patients with long term use of DHEAS are still in the normal intracrine physiological range.Therefore,DHEAS may become the first drug for the treatment of vaginal atrophy in the future.

In order to investigate the effects of electric pulses on cancer cells, we carried out the experiments with exposing HepG2 and L02 to electric pulses (1 kV/cm, l00 micros, 1 Hz) for different lengths of time (8 s, 15 s, 30 s, 60 s). Annexin V-FITC Kit and Flow cytometry were used to study the apoptosis of treated cells. The results showed that the electric pulses of 1 kV/cm, l00 micros, 1 Hz for 8 s could not induce tumor cells apoptosis. Apoptosis was observed when tumor cells were stimulated for 15 s and longer, and the apoptosis percentage increased with the increase of stimulation time. Furthermore, tumor cells were more sensitive than normal cells in response to electrical pulses. Rhodamine 123 and Laser Scanning Confocal Microscope (LSCM) were used to make a real-time study of mitochondrial transmembrane potential (Deltapsim) when the tumor cells were exposed to electric pulses for 60 s. No significant change of Deltapsim was observed within 30 s stimulation. After that, the Deltapsim increased sharply and declined later, suggesting that the mitochondrial pathway may be one of the apoptosis mechanism induced by electric pulses.
Apoptosis ; radiation effects ; Electromagnetic Fields ; Hep G2 Cells ; Humans ; Membrane Potential, Mitochondrial ; physiology ; radiation effects ; Time Factors