Death of nerve cells after cerebral ischemia have a variety of forms,including cell necrosis occurs immediately in ischemic core area and the subsequent apoptosis and autophagy induced by oxidative stress and inflammatory response in the course of reperfusion.After cerebral ischemia,a variety of different molecular mechanisms eventually lead to cell death,and the process involves several signaling pathways.Intervention of different forms and mechanisms of cell death may alleviate cell death after cerebral ischemia.

Bone Diseases, Metabolic ; physiopathology ; Bone and Bones ; metabolism ; physiopathology ; Child ; Child Nutrition Disorders ; physiopathology ; Child Nutritional Physiological Phenomena ; physiology ; Humans ; Infection ; physiopathology ; Kidney Failure, Chronic ; physiopathology

As an intracellular energy sensor, AMP-activated protein kinase (AMPK) plays an important role in maintaining the energy balance of the cells and organisms. Initially, the effects of AMPK on the processes of pathophysiology in diabetes, obesity and other metabolic diseases were well studied. In recent years, the roles of AMPK in the pathophysioiogical processes, including distribution and acidosis, oxidative stress injury and apoptosis in brain tissue have received increasing attention. At the same time, it also found that artificially regulates the AMPK activity after stroke may change the outcome of neurons. Therefore, AMPK is expected to become a new target in the treatment of ischemic cerebrovascular disease.

As an important component of the “neurovascular unit”,astrocytes provide protective effect for nervous through intaking excessive excitatory amino acids,providing energy substances,maintaining extracellular K + and water balance,scavenging oxygen free radicals and secreting neurotrophic factor during ischemic stroke.This article elaborates the mechanisms of astrocytes participating in ischemic stroke in recent years.

Objective To investigate the effects of adenosine monophosphate-activated protein kinase (AMPK) on high-mobility group box 1 (HMGB1) release from PC12 cells after oxygen-glucose deprivation and reoxygenation (OGD/R) and its mediated inflammatory response in BV2 cells.Methods PC12 and BV2 cells were cultured,respectively.The PC12 cells were used to induce a model of oxygen glucose deprivation for 12 h and reoxygenation for 24 h.After giving 5-aminoimidazole-4-carboxamide (AICAR) 5,50 and 100 μmol/L as well as Compound C 0.1,1 and 10 μmol/L activation or inhibition of AMPK phosphorylation,respectively,methyl thiazolyl tetrazolium (MTT) was used to detect the PC12 cell activity.Enzyme-linked immunosorbent assay was used to detect the HMGB1 release level in the PC12 cell culture media.After OGD/R in each group,the PC12 culture media were acted on normal cultured BV2 cells for 24 h respectively.Westem blotting and Enzyme-linked immunosorbent assay were used to detect the NFκB inhibitory protein (inhibitor of NFκB,IκB) phosphorylation level and TNF-α release level in BV2 cells,respectively.Results After OGD/R,the PC12 cell activity was decreased significantly (68.84％±6.60％ vs.100.04％ ± 8.82％;P ＜ 0.01);the AMPK phosphorylation level was increased significantly (1.95 ±0.39 vs.1.00 ±0.20;P＜0.05),and the extracellular HMGB1 release was increased significantly (287.66 ± 26.42 pg/μl vs.53.05 ± 9.11 pg/μl;P ＜ 0.01).Compared with the OGD/R group,AICAR 100 μmol/L significantly increased the survival rate of PC12 cell after OGD/R (78.6％ ± 3.75％ vs.68.84％ ± 6.60％;P ＜ 0.05),promoted AMPK phosphorylation (3.32 ± 0.66 vs.1.95 ± 0.39;P ＜ 0.01),and reduce the release of extracellular HMGB1 (164.06 ± 12.77 pg/μl vs.287.66 ± 26.42 pg/μl;P ＜0.01).In contrast,Compound C 10 μmol/L significantly reduced the cell survival rate of PC12 (40.44％ ±3.79％ vs.68.84％ ±6.60％;P ＜0.01),inhibited AMPK phosphorylation (1.07 ± 0.21 vs.1.95 ± 0.39;P＜0.05),and increased the release of HMGB1 (337.97 ± 18.9 pg/μlvs.287.66 ± 26.42 pg/μl;P＜0.01).The conditioned medium from the AICAR 100 μmol/L group significantly inhibited IκB phosphorylation (1.68 ±0.51 vs.3.09 ± 0.10;P ＜ 0.05) and reduced the release of TNF-α (669.53 ±38.58 pg/μlvs.841.76 ± 45.82 pg/μl;P＜ 0.05) in BV2 cells.The conditioned medium from the compound C 10 μmol/L group significantly promoted IκB phosphorylation (4.98 ± 1.24 vs.3.09 ± 0.10;P ＜0.01) and increased the release of TNF-α (1 035.32 ± 128.06 pg/μl vs.841.76 ± 45.82 pg/μl;P ＜0.05) in BV2 cells.Conclusions Promoting AMPK phosphorylation activation may reduce the release of HMGB1 from PC12 cells after OGD/R,and inhibit its mediated NF-κB inflammatory pathway and reduce the release of TNF-αin BV2 cells,and thus reducing neuroinflammatory injury.On the contrary,inhibiting AMPK phosphorylation may promote the release of HMGB1 from PC12 cells after OGD/R and aggravate its mediated inflammatory reaction in BV2 cells.

AAIM:To investigate the effect of atorvastatin ( ATO) on electrical remodeling, atrial ion channel protein expression and cardiac function in atrial tachypacing rabbits, and to explore the potential electrical mechanism of ATO in the prevention of atrial fibrillation.METHODS:The rabbits were subjected to atrial tachypacing at 600 min-1 in the absence or presence of treatment with atorvastatin (ATP and ATO groups) for 48 h, and the other 10 as sham group without pacing ( NP group) .The tachypacing model was performed by attaching pacing and testing electrodes to left atrial and connecting with custom animal cardiac pacemaker in the open-chest situation.The animals in ATO group were pretrea-ted with ATO for 7 d and continued during tachypacing.Serial atrial effective refractory period ( AERP) was measured in each rabbit at baseline, 8 h, 16 h, 24 h, 32 h, 40 h and 48 h with different cycle lengths.The changes of cardiac func-tions and cardiac structure were observed by cardiac ultrasonic cardiogram before and after atrial tachypacing.The expres-sion of atrial ion channel proteins CaLα1 and Kv4.3 was detected by Western blotting.RESULTS:Compared with NP group, AERP at cycle lengths of 150 and 200 ms, the adaption of AERP, and the levels of CaLα1 and Kv4.3 expression were all decreased in ATP and ATO group, especially in ATP group.Left atrial dimension ( LAD) was increased in pacing groups as compared with NP group (P<0.05) after pacing delivery for 48 h, while no difference between the formers was observed.No significant change of the left ventricular dimension ( LVD) and ejection fraction ( LVEF) among groups be-fore and after pacing was found.CONCLUSION:Atrial tachypacing significantly shorten AERP, resulting in poor adap-tion of AERP, while ATO pretreatment significantly attenuates the atrial electrical remodeling in rabbits, but had no effect on cardiac structure.ATO suppresses the down-regulation of atrial ion channel proteins CaLα1 and Kv4.3 expression after 48 h, which may be the potential ionic mechanism of atrial electrical remodeling for ATO.

Objective To investigate the changes in the concentration of myocardin in children with lupus nephritis (LN) under different degree of vessel damage.Methods Forty-nine children diagnosed with LN by routine tissue immunolfuorescence, light microscope, and electron microscope were included, and 30 healthy children were included as control group. The pathological classiifcations were performed according to the ISN/RPS 2003 LN pathological classiifcation criterion. According to the Katafuchi evaluation method, the semi quantitative assessment of glomerular and kidney tubule damage was carried out, and the degree of vascular damage was evaluated at the same time. Double antibody sandwich method was used to detect the concentration of serum myocardin.Results The glomerular and kidney tubules damage in children with LN were signiifcantly aggravated with higher pathological classification (P<0.05). Glomerular damage was positively correlated with renal interstitial damage (r=0.96, P<0.01). The degree of vascular damage was related to the degree of glomerular injury and renal interstitial injury, while it was no related with the results of clinical tests. There were different concentrations of myocardin among mild-, moderate-, severe-vessel damage and control groups (F=378.61,P<0.001), and the concentration of myocardin in moderate- and severe-vessel damage groups were obviously lower than those in control group and mild-vessel damage group (P<0.01) while there was no difference between control group and mild-vessel damage group (P>0.05). According to pathological type, there were signiifcant differences in the concentration of myocardial between control group and different pathological types (F=626.793,P<0.01). FromⅡ,Ⅲ,Ⅲ+Ⅴ,Ⅳ toⅣ+Ⅴ, the concentrations of myocardial were decreased systematically, and there were statistic differences between groups (P all<0.05).Conclusion The concentration of myocardin in children with LN can relfect the renal vascular damage to a certain extent. Elevation of myocardin concentration may be helpful for the repair of vascular damage.

Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms ; genetics ; metabolism ; pathology ; MicroRNAs ; genetics ; metabolism ; Paraffin Embedding ; RNA, Neoplasm ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; methods

Objective To research Henoch-Schonlein purpura purpura (HSP) and renal pathology in children.Methods 31 hospitalized HSP children that with normal urine routine and accepted renal biopsy in our hospital.Results There were different levels of kidney pathological damage in this group of 31 cases,the results of light microscope were from grade Ⅱ to grade Ⅵ The proportion was grade Ⅱ(35.48％,11 of 31),grade Ⅲ (54.83％,17 of 31),and grade Ⅳ,Ⅴ and Ⅵ (each 1 case of 31,3.23％ ).lmmunofluorescence pathology results were showed as following:merely IgA depositional (48.38％,15 of 31 ),IgA + IgG depositional ( 19.36％,6 of 31 ),IgA + IgM depositional ( 19.36％,6of 31 ),IgA + igG + IgM depositional ( 12.90％,4 of 31 ).Microalbuminuria had been founded in 14 cases,and the microalbuminuria level of 10 cases were higher than normal value( 10 of 14,71.43％ ).Conclusions HSP children had renal pathologic dysfunction,even the urine routine were normal,and the detection of urine microalbumin was a significant marker in the early stage.

Objective To establish a cell line with overexpression of rat serotonin1A receptor (5-HT1AR).Methods Human neuroblastoma cells-SH-SY5Y were donated by cancer institute attached to the 4 th Affiliated Hospital, Hebei Medical University. Total RNA was extracted from brain tissues of male SD rats and rat 5-HT1A R was obtained by RT-PCR. Plasmid pc-DNA3. 1/hisC containing the rat 5-HT1AR (pc-DNA3.1/hisC-Rat-5-HT1AR)was constructed and transfected into SH-SY5Y cells. The transfected cells were isolated by G418 selection and SH-SY5Y-Rat-5-HT1A R cells were obtained. Expression of 5-HT1A R was detected by Western blot analysis. Cell viability was evaluated by MTT assay. SH-SY5Y-Rat-5-HT1AR cells were further observed for 5-HT1AR by immuno-fluorescence staining. Results Plasmid pc-DNA3. 1/hisC-Rat-5-HT1AR was successfully constructed by linking Rat-5-HT1A R with pc-DNA3.1/hisC and transfected into SH-SY5Y. The SH-SY5Y-Rat-5-HT1A R cells were more slender than SH-SY5Y cells with less and longer processes. MTT showed that the viability of SH-SY5Y-Rat-5-HT1A R cells was much lower than SH-SY5Y. Rat 5-HT1A R was expressed efficiently on the membrane of SH-SY5Y-Rat-5-HT1A R cells. Conclusion A cell line with overexpress of rat 5-HT1A R is successfully established.