Aconitum ; poisoning ; Animals ; Disease Models, Animal ; Female ; Hemoperfusion ; methods ; Male ; Plant Poisoning ; therapy ; Rabbits

Animals ; Diazepam ; pharmacology ; Drug Antagonism ; Electroencephalography ; Female ; Male ; Pyrazoles ; poisoning ; toxicity ; Rats ; Rats, Sprague-Dawley

Objective To evaluate the perioperative period safety of improved transurethral plasma kinetic enucleation of prostate (TUPKEP) in high-risk benign prostatic hyperplasia (BPH) patients with coronary heart disease (CHD).Methods One hundred and twenty-eight BPH patients were selected,24 patients had CHD (with CHD group),among whom 10 patients were given transurethral vapor-resection of prostate (TUVP),and 14 patients were given improved TUPKEP; 104 patients didn't have CHD,among whom 22 patients were given TUVP,and 82 patients were given improved TUPKEP.The serum endothelin (ET)-1 was measured by specific radioimmunoassay at preoperative 2 h and postoperative 1,2,6 d,and complication was observed.Results All the patients were cured by operation,and left hospital smoothly.There were no statistical differences in the preoperative 2 h serum ET-1 in with CHD group and without CHD group (including all TUVP patients and improved TUPKEP patients) (P ＞ 0.05).The postoperative 1 and 2 d serum ET-1 levels of TUVP patients were significantly higher than those of improved TUPKEP patients,in with CHD group:(114.09 ± 15.33) ng/L vs.(94.77 ± 12.14) ng/L and (99.67 ± 9.87) ng/L vs.(88.21 ± 9.55) ng/L; in without CHD group:(70.21 ± 12.44) ng/L vs.(53.67 ± 9.02) ng/L and (61.18 ± 9.52) ng/L vs.(48.54 ± 9.15) ng/L,and there were statistical differences (P ＜ 0.05).There were no statistical differences in postoperative 6 d serum ET-1 in TUVP patients and improved TURKEP patients (P ＞ 0.05).In with CHD group,5 patients had ischemic ST-T change in the early postoperative period,and 3 patients had angina pectoris.They all were promptly treated,and the events were controlled.Serious complications did not present such as acute myocardial infarction (AMI),acute heart failure and sudden cardiac death,etc.Conclusions The postoperative BPH patients have vascular endothelial injury catholically,especially the high-risk patients with CHD.Furthermore,it might be one of the causes of the postoperative adverse cardiovascular events.Compared with TUVP,improved TUPKEP has a minor impact on vascular endothelial function,and it can reduce the postoperative adverse cardiovascular events in the BPH patients with CHD.Improved TUPKEP is a relatively safer surgical method for high-risk BPH with CHD.

Acute Disease ; Animals ; Behavior, Animal ; drug effects ; Female ; Male ; Mice ; Mice, Inbred ICR ; Nitriles ; poisoning ; Rabbits

Objective To observe the poisoning components in plasma and histological changes of rabbits with acute toxicity of aconitum kusnezoffii (草乌).Methods Eight rabbits were garaged with aconitum kusnezoffii liquor,aconitum poisoning model was reproduced,electrocardiogram (ECG) and blood pressure were recorded,the concentrations of aconitine,hypaconitine and mesaconitine in plasma after 0.5,1, 2,3 and 6 hours were measured,and the pathological changes of heart,liver and cerebral cortex were observed.Results After garage with poisoning liquor,arrhythmias and the declination of blood pressure, presenting a tendency of progressive aggravation [before garage:(121.98?16.77)/(110.66?8.78) mm Hg, 1 hour after garage:(102.98?8.34)/(90.22?5.85) mm Hg,2 hours after garage:(66.81?9.13)/ (53.40?6.32) mm Hg,1 mm Hg=0.133 kPa,all P

BACKGROUND: Vibrio vulnificus inside the body could activate the NF-κB signaling pathway and initiate the inflammatory cascade. The lung is one of the earliest organs affected by sepsis associated with acute lung injury. High mobility group protein B1 (HMGB1) is an important late-acting pro-inflammatory cytokine involving in the pathophysiology of sepsis. It is also involved in the injury process in the lung, liver and intestine. There has been no report on the involvement of HMGB1 in Vibrio vulnificus sepsis-induced lung injury. METHODS: Sixty rats were randomly divided into a normal control group (group A,n=10) and a Vibrio vulnificus sepsis group (group B,n=50). Sepsis was induced in the rats by subcutaneous injection of Vibrio vulnificus (concentration 6×108 cfu/mL, volume 0.1 mL/100g)) into the left lower limbs. The rats in group B were sacrificed separately 1, 6, 12, 24, and 48 hours after the infection. Their lungs were stored as specimens, lung water content was measured, and lung pathology was observed under a light microscope. The expressions of the HMGB1 gene and protein in the lungs were detected by RT-PCR and Western blot. Data were analyzed with one-way analysis of variance (ANOVA) and the LSD method for pair-wise comparison between the two groups.P<0.05 was considered statistically significant. RESULTS: Compared to group A (0.652±0.177), HMGB1 mRNA expression in the lungs of group B was significantly higher at 0 hour (1.161±0.358,P=0.013), 24 hours (1.679±0.235,P=0.000), and 48 hours (1.258±0.274,P=0.004) (P<0.05), and peaked at 24 hours. Compared to group A (0.594±0.190), HMGB1 protein expression at 6 hours (1.408±0.567,P=0.026) after infection was significantly increased (P<0. 05), and peaked at 24 hours (2.415±1.064,P=0.000) after infection. Compared to group A (0.699±0.054), lung water content was significantly increased at 6 hours (0.759±0.030,P=0.001),12 hours (0.767±0.023,P=0.000), 24 hours (0.771±0.043,P=0.000) and 48 hours (0.789±0.137,P=0.000) after infection (P<0.05). Compared to group A, pathological changes at 12 hours in group B indicate marked pulmonary vascular congestion, interstitial edema and inflammatory infiltration. Alveolar cavity collapse and boundaries of the alveolar septum could not be clearly identified. CONCLUSION:Vibrio vulnificus sepsis can lead to injury in rat lungs, and increased HMGB1 expression in lung tissue may be one of the mechanisms for injury from Vibrio vulnificus sepsis.

OBJECTIVEto investigate the changes of γ-aminobutyric acid (GABA) and glutamate (Glu) in the cerebral cortex following acute bromoxynil intoxication in mice and the protective effect of sodium dimercaptopropane sulfonate (Na-DMPS).

METHODS30 ICR mice were randomly divided into blank control group (10), exposure group (10) and Na-DMPS protection group (10). The levels of GABA and Glu in the cerebral cortex were measured by RP-HPLC. The glutamine (Gln) level and the glutamine synthetase (GS), glutamate decarboxylation enzyme (GAD), γ-aminobutyric acid transaminase (GABA-T) activity in the cerebral cortex were determined by UV colorimetric.

RESULTScompared with the control group [GABA: (3.41 ± 0.12) micromol/g, Glu (14.00 ± 0.16) micromol/g, Gln (1.25 ± 0.19) micromol/g, GAD (13.50 ± 0.25) micromol × g(-1) × h(-1), GABA-T (25.51 ± 0.21) micromol × g(-1) × h(-1), GS(142.19 ± 1.31) U/mg pro], the level of GABA [(3.14 ± 0.14) micromol/g] was decreased (P < 0.05), whereas the level of Glu [(17.54 ± 0.40) micromol/g] and Gln [(3.35 ± 0.27) micromol/g] were increased (P < 0.05), the activity of GAD [(11.93 ± 0.15 micromol × g(-1) × h(-1)], GABA-T [(24.15 ± 0.22) micromol × g(-1) × h(-1)], GS [(140.75 ± 1.01) U/mg pro] was decreased (P < 0.05) in acute intoxication group; Compared with the acute intoxication group, the level of GABA [(3.52 ± 0.30) micromol/g] was increased (P < 0.05), whereas the level of Glu [(14.20 ± 0.32) micromol/g] and Gln [(1.32 ± 0.17) micromol/g] were decreased (P < 0.05), the activity of GAD [(13.01 ± 0.45 micromol × g(-1) × h(-1)], GABA-T [(25.19 ± 0.26) micromol × g(-1) × h(-1), GS [(142.35 ± 1.20) U/mg pro] was increased (P < 0.05); In contrast, the levels of GABA, Glu, Gln and the activity of GAD, GABA-T, and GS in Na-DMPS protection group were not significantly different in comparison with control group (P > 0.05).

CONCLUSIONthe central toxic effects of mice with acute bromoxynil intoxication may be related to the changes of GABA and Glu content in the cerebral cortex;Na-DMPS can protect mice from bromoxynil-induced central toxic effects and GABA and Glu abnormal change in the cerebral cortex.

Animals ; Cerebral Cortex ; drug effects ; metabolism ; Female ; Glutamic Acid ; metabolism ; Male ; Mice ; Mice, Inbred ICR ; Nitriles ; poisoning ; Toxicity Tests, Acute ; Unithiol ; pharmacology ; gamma-Aminobutyric Acid ; metabolism

[Objective] To observe the effect of Xiangdan injection with the actions of activating blood and removing stasis for the treatment of acute tubular necrosis (ATN) after kidney transplantation. [Methods] Twenty-six patients with ATN after kidney transplantation were randomized into groups A and B. The two groups were treated with triple immuno-suppressive agents of cyclosporin A, prednisone and mycophenolic acid, with medicines for protecting liver function and gastric mucosa, and with preventive measures from infection. Additionally, group A (n = 16) was treated with Xiangdan injection, while group B ( n = 10) was not. After treatment, time for hemodialysis, renal function and renal flow resistance index of the transplanted kidney were compared between the two groups after the occurrence of ATN. [Results] Compared with group B, time for hemodialysis was shortened, the decrease of serum creatine (SCr) in the transplanted kidney quickened, and renal flow resistance index (RI) of the transplanted kidney decreased (P 0.05). [Conclusion] Xiangdan injection with the actions of activating blood and removing stasis can promote the early recovery of ATN after kidney transplantation.

Objective To observe whether appropriate intermittent exercise at the ischemic threshold can safely promote collateral circulation in an ischemic area of the myocardium through the increased expression of vascular endothelial growth factor(VEGF)and its receptor fetal liver kinase-1(Fik-1). Methods A balloon constrictor was surgically implanted in the first obtuse marginal coronary artery(OM1)of miniature pigs.The subjects were divided into 3 groups:a sham-operation group,a pure ischemia group,and an exercise training group.Subjects in the exercise training group performed individualized treadmill programs 30 min daily,5 d per week,for 8 weeks,including 2 two-minute episodes of exercise-induced ischemia.Two pre-exercise episodes of pure ischemia induced by brief OM1 occlusion were also conducted.Only pure ischemia was induced in the pure ischemia group,and the sham-operation group remained sedentary for the experimental period.Relative myocardial blood flow(RMBF)was measured using microspheres.VEGF and Flk-1 expression levels were measured by Western blotting and real time RT-PCR analyses.Cardiac troponin I(ctnI)levels were determined using an enzyme-linked immunosorbent assay(ELISA). Light and electron microscopy were employed to examine myocardia damage in the ischemic area.Results RMBFs in the exercise training group were significantly higher than those in the pure ischemia and sham-operation groups. RMBFs in the pure ischemia group were significantly higher than those in the sham-operation group.The expression of VEGF and Flk-1 proteins and mRNAs in the exercise training group were significantly higher than those in the pure ischemia and sham-operation groups,and the levels in the pure ischemia group were also significantly higher than those in the sham-operation group.After training,no myocardial damage and no ctnI increase was observed in the pure ischemia group.Microscopy revealed no obvious structural changes. Conclusion Intermittent exercise at the isehemia threshold intension can safely promote coronary collateral formation through upregulation of VEGF and Flk-1 expression in the ischemic myocardial area of a porcine model.

This study aims to explore the improvement and the mechanism of the Alisma plantago-aquatica Linn. (ApL) on chronic glomerulonephritis (CGN). All animal experiments were followed the regulation of the Experimental Animal Ethical Committee of Shanghai University of Traditional Chinese Medicine. CGN mouse model was established by a single tail-vein injection of doxorubicin (Dox) (20 mg·kg^-1). One week after Dox administration, the mice received water extract of ApL (85 and 255 mg·kg^-1) by gavage once a day for 14 days. At the end of experiment, the urine albumin-to-creatinine ratio (ACR), serum albumin (ALB), blood urea nitrogen (BUN) and serum creatinine (SCr) were detected, kidney histopathological H&E staining was analyzed. Active ingredients and action targets of ApL were collected from TCMSP database, and CGN-related targets were obtained from Genecards database. STRING platform was employed to perform protein-protein interaction (PPI), and Metascape platform was used for KEGG pathway and GO enrichment analysis. The results of experiments demonstrated that ApL (85 and 255 mg·kg^-1) could reduce the ACR and the content of SCr and BUN, and increase the content of ALB in mice. Network pharmacology results predicted that nuclear factor kappa-B (NF-κB)-related pathway and biological process of oxidoreductase activity regulation may be involved in the ApL-provided amelioration on CGN. The verification results showed that ApL could inhibit the activation of NF-κB and the expression of inflammatory factors in mice, and reduce the activity of renal myeloperoxidase (MPO). Meanwhile, ApL promoted the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) and increased the expression of its downstream gene mRNA, and reduced the level of renal malondialdehyde (MDA) and reactive oxygen species (ROS), and further elevated renal glutathione (GSH) level. Based on network pharmacology combined experiments, this study found that ApL may improve CGN in mice through multiple targets and multiple pathways, in which the inhibition of NF-κB signaling and the activation of Nrf2 signaling may be important mechanisms involved.