Objective To evaluate the effect of microinvasive puncturatio in therapy of hypertensive intracerebral hemorrhage. Methods In 112 cases of hypertensive intracerebral hemorrhage,with CT orientation, the appropriate length of YL-1 type of intracranial hematoma puncture needle was penetrated into the hematoma. Washing, drainage and Urokinase were applied. Results 21 patients died, 91 patients' consciousness and physical function got better in 1-5 days, and 2 patients were in a vegetable state. Conclusion In therapy of hypertensive intracerebral hemorrhage, microinvasive puncturation can improve efficiency of clinical treatment, recovery of nerve function and daily living of patients,with advantages of safety,convenience,cheaper costs and minimal trauma.

Objective To evaluate the role of c-AMP-protein kinase A (cAMP-PKA) on the up-regulation of heme oxygenase-1 (HO-1) expression during lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats.Methods Forty-eight healthy male Sprague-Dawley rats,weighing 180-220 g,aged 2.5-3.0 months,were randomly divided into 4 groups (n =12 each)∶ normal control group (group C),ALI group (group ALI),H89 +ALI group (group H + ALI) and H89 group (group H).In group C,normal saline (solvent for LPS) 0.5 ml was injected via the femoral vein and normal saline (solvent for H89) 0.5 ml was injected subcutaneously 2 h later.In group ALI,10 mg/kg LPS 0.5 ml was injected via the femoral vein and normal saline 0.5 ml was injected subcutaneously 2 h later.In group H +ALI,10 mg/kg LPS 0.5 ml was injected via the femoral vein and 5 mg/kg H89 0.5ml was injected subcutaneously 2 h later.In group H,normal saline 0.5 ml was injected via the femoral vein and 5 mg/kg H89 0.5 ml was injected subcutaneously 2 h later.The rats were then sacrificed at 6 h after iv injection of LPS and the lungs were removed for microscopic examination and lung water content.The pathological changes of the lung were scored.The expression of HO-1 and PKA (by Western blot) and HO-1 mRNA (by RT-PCR) was detected.Results Compared with group C,the pathological score and lung water content were significantly increased,and the expression of HO-1,PKA and HO-1 mRNA was up-regulated in groups ALI and H +ALI (P ＜0.05),and no significant change was found in the parameters mentioned above in group H (P ＞ 0.05).The pathological score and lung water content were significantly higher,and the expression of HO-1,AP-1 and HO-1 mRNA was significantly lower in group H + ALI than in group ALI (P ＜ 0.05).Conclusion Activation of signaling pathway c-AMP-PKA is involved in the up-regulation of HO-1 expression during LPS-induced ALI in rats.

Objective To evaluate the effect of electro-acupuncture (EA) at Zusanli and Feishu on endotoxin shock-induced acute lung injury in rabbits.Methods Sixty healthy male New Zealand white rabbits aged 2 months weighing 1.5-2.0 kg were randomly divided into 6 groups (n =10 each):group sham operation (group S); group zinc protoporphyrin-Ⅸ (ZnPP-Ⅸ) (group Z); group lipopolysaccharide (LPS) (group L); group LPS + EA (group EL) ; group LPS + sham EA (group SEL) and group LPS + EA + ZnPP-Ⅸ (group ELZ).The animals were anesthetized with intraperitoneal 10％ chloral hydrate 400 mg/kg and tracheostomized.The animals kept spontaneous breathing.Right internal carotid artery was cannulated for BP monitoring.Ear vein was cannulated for drug administration.LPS 5 mg/kg was injected iv in groups L,EL,SEL,ELZ.Endotoxin shock was confirmed by decrease in BP by 20 ％ of the baseline value and PaO2/FiO2 ≤ 300.ZnPP-Ⅸ (heme oxygenase (HO-1 ) inhibitor)10μmol/kg was injected intraperitoneal at 2 h after LPS injection in groups Z and ELZ.Bilateral 15 min EA stimulation of Zusanli and Feishu ( according to atlas of animal acu-points) was performed once a day for 5 days before LPS administration in groups EL and ELZ.The animals were sacrificed by blood-letting at 6 h after LPS administration.The lungs were removed for microscopic examination (0 =no injury,4 =most severe injury),detection of alveolar epithelial cell apoptosis (by TUNEL) and determination of HO-1 protein and mRNA expression.Results LPS significantly increased lung injury scores,alveolar epithelial cell apoptosis index (the number of apoptotic cells/total cells) and HO-1 protein and mRNA expression.EA significantly attenuated lung injury and alveolar epithelial cell apoptosis induced by LPS and further increased the expression of HO-1 protein and mRNA in group EL as compared with group L.The protective effects of EA was counteracted by ZnPP- Ⅸ in group ELZ.Conclusion EA at Zusanli and Feishu can attenuate endotoxin shock-induced lung injury by up-regulation of HO-1 expression and inhibiting alveolar epithelial cell apoptosis in the lung.

Objective To investigate the effects of CORM-2 via p38 mitogeu-activated protein kinase (p38MAPK) signaling pathway on the expression of the mitochondrial fission protein 1 (Fisl) in lipopolysaccharide (LPS)-induced mouse pulmonary macrophages.Methods The rat subculture alveolar macrophages were seeded on 96 well plates with 2 × 105/ml densities.After 24 hours of culture,it was divided into 4 groups by random number table method:normal control group (group C),group LPS (group L),CO releasing agent CORM-2 + LPS group (group LC),p38MAPK inhibitor SB203580 + CORM-2 + LPS group (group LCS).When the cells were incubated for 24 hours,the mitochondrial MDA content and SOD activity were determined by ELISA kit,the levels of HO-1、mitochondrial fission protein Fis1 and p38 were determined by Western blot,the expressions of HO-1 and mitochondrial fission protein Fis1 were detected by RT-PCR.Results Compared with the C group,the levels of MDA [(2.43 ±0.12) vs.(3.59 ±0.07)],HO-1 [(1.31±0.27) vs.(1.65±0.41)],Fis1 [(1.27±0.23) vs.(1.65±0.41)] andp38 [(1.01 ±0.24) vs.(1.36 ±0.17)] in group L were increased,and the activity of SOD [(81.7 ± 1.62) vs.(54.7 ± 1.62)] was decreased (P ＜ 0.05);Compared with the group L,the MDA content [(3.59 ± 0.07) vs.(3.08 ±0.52)] and the level of Fis1 [(2.01 ±0.35) vs.(1.48 ±0.39)] in group LC were down-regulated,and the levels of SOD [(54.7 ± 1.62) vs.(67.4 ± 1.32)]、and the expressions of HO-1 [(1.65±0.41)vs.(2.25±0.18)] andp38 [(1.36±0.17) vs.(1.78±0.23)] wereup-regulated (P ＜0.05).Compared with the group LC,the MDA content [(3.08 ±0.52) vs.(4.16 ±0.19)] and the expression of Fis1 [(1.48 ±0.39) vs.(1.96 ±0.31)] in group LCS were increased,and the level of SOD [(67.4±1.32)vs.(45.9±1.52)]、and the expressions of HO-1 [(2.25±0.18)vs.(1.78± 0.19)] and p38 [(1.78 ±0.23) vs.(1.12 ±0.29)] were decreased (P ＜0.05).Conclusions HO-1/CO system inhibits the expression of Fis1 in LPS-induced lung macrophages,which may be regulated by p38MAPK signaling pathway.

OBJECTIVETo evaluate the effects of copper-phenanthroline (CuOP) on pentachlorophenol (PCP)-induced adaptation and cell death of Escherichia coli.

METHODSBacterial growth and adaptation to PCP were monitored spectrophotometrically at 600 nm. Inactivation of bacterial cells was determined from colony count on agar dishes. Cellular ATP content and accumulation of PCP were assessed by chemiluminescence and HPLC analysis respectively. The formation of PCP-Cu-OP complex was shown by UV-visible spectra.

RESULTSEscherichia coli (E. coli) could adapt to PCP, a wood preservative and insecticide used in agriculture. The adaptation of E. coli to PCP prevented its death to the synergistic cytotoxicity of CuOP plus PCP and declined cellular accumulation and uncoupling of oxidative phosphorylation of PCP. Furthermore, CuOP and PCP neither produced reactive oxygen species (ROS) nor had a synergistic effect on uncoupling of oxidative phosphorylation in E. coli. The synergistic cytotoxicity of CuOP and PCP in E. coli might be due to the formation of lipophilic PCP-Cu-OP complex.

CONCLUSIONOur data suggested that adaptation of E. coli to PCP decreased the synergistic effects of CuOP and PCP on prokaryotic cell death due to the formation of lipophilic PCP-Cu-OP complex, but it had no effect on the uncoupling of oxidative phosphorylation and production of reactive oxygen species in E. coli.

Adaptation, Physiological ; Adenosine Triphosphate ; metabolism ; Antioxidants ; metabolism ; Apoptosis ; drug effects ; Copper ; pharmacology ; Cytotoxins ; pharmacology ; Drug Resistance, Bacterial ; Drug Synergism ; Escherichia coli ; drug effects ; metabolism ; Pentachlorophenol ; pharmacology ; Phenanthrolines ; pharmacology

Objective To evaluate the role of mitochondrial fusion?fission in endotoxin?induced a?cute lung injury in rats. Methods Twenty healthy male Sprague?Dawley rats, weighing 160-180 g, were e?qually and randomly divided into either control group ( group C ) or endotoxin?induced acute lung injury group (group L) using a random number table. Lipopolysaccharide 5 mg∕kg was injected intravenously in group L, while the equal volume of normal saline 0?5 ml was given instead in group C. The animals were sacrificed at 6 h after administration of lipopolysaccharide or normal saline. The lungs were immediately re?moved for measurement of wet to dry lung weight ratio ( W∕D ratio) , superoxide dismutase ( SOD) activity and malondialdehyde ( MDA) content. The mitochondrial fusion proteins mitofusin 1 ( Mfn1) , Mfn2 and op?tic atrophy 1 ( OPA1) mRNA and protein expression was detected, and mitochondrial fission proteins dy?namin?related protein 1 (Drp1) and fission 1 (Fis1) mRNA and protein expression was also detected in lung tissues. Results Compared to group C, the W∕D ratio and MDA contents in lung tissues were signifi?cantly increased, SOD activity was decreased, Mfn1, Mfn2 and OPA1 mRNA and protein expression in lung tissues was down?regulated, and Drp1 and Fis1 mRNA and protein expression was up?regulated in group L. The pathological damage to lung tissues was obviously aggravated in group L when compared to group C. Conclusion The mechanism underlying endotoxin?induced acute lung injury is related to enhanced oxidative stress responses caused by decreased mitochondrial fusion and increased mitochondrial fission in rats.

Animals ; Dose-Response Relationship, Drug ; Guinea Pigs ; Heart Ventricles ; Ion Channels ; antagonists & inhibitors ; physiology ; Male ; Myocytes, Cardiac ; drug effects ; physiology ; Promethazine ; pharmacology ; Terfenadine ; pharmacology ; Time Factors

Objective To optimize the process conditions of the oil extraction ofseabuckthorn oil and to evaluate its antioxidant activity by anti-free radical action.Methods The extraction time and particle size of sea-buckseed oil were optimized by using the response surface software design-expert.Its antio xidant activity was studied through its anti-dpph free radical reaction.Results The best process of seabuckthorn seed oil was extracting time 3 h,material liquid than 1:8,extraction temperature 80 C,about 30 mesh size,the yield is highest at 11.13％.The optimum reaction time was 8 min in control,and with the increase of concentration,seabuckthorn oil antioxidant activity increased,when the addition amount of 4.00 ml sample,clearance rate as high as 77.62％.Conclusions This method is simple and reliable,the extraction rate is high,and the test results show that the oil has obvious anti-oxidative effect,which can be used as whitening and wrinkling products to delay the aging of human body.

OBJECTIVETo investigate the clinical characteristics of anti-HBc IgM positive chronic hepatitis B patients and the relation of anti-HBc IgM development to serum HBV DNA load and the state of HBeAg/anti-HBe.

METHODSThe clinical data were collected from patients with chronic hepatitis B hospitalized in the Infectious Diseases Hospital, Zhangjiakou city, and in Ditan Hospital, some of whom were anti-HBc IgM positive and some others were negative. Their HBV DNA load was examined by real-time PCR, and HBeAg/anti-HBe was detected by AXSYM auto-enzyme analyzer with the third generation EIA regent.

RESULTSTotally 200 patients were enrolled in this study. The number of patients with mild, moderate and severe hepatitis was 71, 83 and 46. The anti-HBc IgM positive patients were older and had longer course of disease than those of anti-HBc IgM negative patients. Of the anti-HBc IgM positive group, 45.71 percent and 54.29 percent had mild and moderate hepatitis, which were significantly different from those in the anti-HBc IgM negative patients (30.00 percent and 70.00 percent). But there was no difference between anti-HBc IgM positive and negative patients in serum HBV DNA level, the state of HBeAg/anti-HBe and outcome.

CONCLUSIONThe anti-HBc IgM state of chronic hepatitis B patients was related to the severity of hepatitis, but not with virus load and state of HBeAg/anti-HBe.

Adult ; DNA, Viral ; blood ; genetics ; Female ; Hepatitis B Antibodies ; blood ; Hepatitis B Core Antigens ; immunology ; Hepatitis B virus ; genetics ; immunology ; physiology ; Hepatitis B, Chronic ; immunology ; virology ; Humans ; Immunoglobulin M ; blood ; Male ; Middle Aged ; Viral Load ; Young Adult

OBJECTIVETo study the effect of crocin on rat experimental hyperlipemia and its mechanisms.

METHODHyperlipemia model was established by feeding heavy cholesterol for 2 months and the effect of crocin on blood lipid in experimental hyperlipemia rats was observed. Aortic smooth muscle cells were cultured in different culture media and proliferation was measured by MTT assay. Western blotting was used to detect the effect of crocin on phosphorylation of p38 MAPK.

RESULTCrocin not only decreased greatly the content of cholesterol, triglyceride and density lipoprotein in blood, but also increased the content of high density lipoprotein. In addition, the proliferation of smooth muscle cells and the activation of p38MAPK were inhibited by Crocin.

CONCLUSIONCrocin prevents atherosclerosis in hyperlipemia, which may be mediated by the inhibition of both proliferation of smooth muscle cells and activation of p38MAPK.

Animals ; Aorta, Thoracic ; cytology ; Carotenoids ; isolation & purification ; pharmacology ; Cell Proliferation ; drug effects ; Cholesterol ; blood ; Crocus ; chemistry ; Hyperlipidemias ; etiology ; metabolism ; pathology ; Hypolipidemic Agents ; pharmacology ; Lipoproteins, HDL ; blood ; Lipoproteins, LDL ; blood ; Male ; Myocytes, Smooth Muscle ; cytology ; enzymology ; Plants, Medicinal ; chemistry ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; blood ; p38 Mitogen-Activated Protein Kinases ; metabolism