AIM To study the chemical constituents from Polygonum hydropiper L..METHODS The petroleum ether,ethyl acetate and n-butanol fractions of 95％ ethanol extract from P.hydropiper were isolated and purified by silica,Sephadex LH-20 and recrystallization,then the structures of obtained compounds were identified by spectral data.RESULTS Thirteen compounds were isolated and identified as β-sitosterol (1),aniba dimer A (2),succinic acid (3),quercetin (4),gallic acid (5),daucosterol (6),quercetin-3-O-β-D-glucoside (7),kaempferol-3-O-β-D-glucoside (8),quercetin-3-O-β-galactoside (9),kaempferol-3-O-β-galactoside (10),stigmast-4-ene-3β,6a-diol (11),fumaric acid (12),ellagic acid (13).CONCLUSION Compounds 11 and 12 are isolated from genus Polygonum for the first time,compounds 2,8,10 and 13 are first obtained from this plant.

Objective To investigate the effect of diabetes mellitus (DM) on adenosine postcondi-tioning-induced reduction of myocardial ischemia-reperfusion (I∕R) injury in rats. Methods Adult male Sprague-Dawley rats, weighing 230-260 g, were used in the study. Type 2 DM was induced by high-fat diet and intraperitoneal l％ streptozocin 35 mg∕kg and confirmed by fasting blood glucose concentration>16. 7 mmol∕L 72 h later. Eighteen rats with type 2 DM were divided into 3 groups (n= 6 each) using a ran-dom number table: sham operation group (DS group), I∕R group (DI∕R group) and adenosine postcondi-tioning group (DAP group). Eighteen healthy nondiabetic rats were selected and randomly divided into 3 groups (n= 6 each): sham operation group (NS group), I∕R group (NI∕R group) and adenosine postcon-ditioning group (NAP group). Myocardial I∕R was induced by 30 min occlusion of the left anterior descend-ing branch of coronary artery followed by 2 h of reperfusion. Venous blood samples were collected from the femoral vein at 2 h of reperfusion for measurement of plasma cardiac troponin I (cTnI) and creatine kinase-MB (CK-MB) concentrations (by enzyme-linked immunosorbent assay). The rats were then sacrificed im-mediately after blood sampling for determination of the myocardial ischemic area and infarct size. Results The plasma cTnI and CK-MB concentrations were significantly increased, and the percentage of myocardial infarct size was increased after myocardial I∕R in nondiabetic and diabetic rats. Adenosine postconditioning significantly decreased plasma cTnI and CK-MB concentrations and percentage of myocardial infarct size in nondiabetic and diabetic rats (P<0. 05). Compared with group NAP, the plasma concentrations of cTnI and CK-MB were significantly increased, and the percentage of myocardial infarct size was increased in group DAP (P<0. 05). Conclusion DM can weaken cardioprotection induced by adenosine postcondition-ing in rats.

Objective:To summarize the precision fluid management of patients with severe blast injury in the emergency intensive care unit, so as to help patients smoothly pass through the dangerous period and recover smoothly.Methods:Based on the experience of fluid management in 6 patients admitted to the Second Affiliated Hospital Zhejiang University School of Medicine in the tanker truck explosion on 14 June, 2020. The main measures included: fluid volume management and dynamic adjustment; assessment of intake, output and urine volume, and dynamic adjustment of infusion volume and speed; monitoring of pulmonary oxygenation and timely adjustment of fluid resuscitation strategies; monitoring indexes and providing nursing care strategies for fluid management.Results:Finally, among 6 patients with severe blast injury, 5 patients were discharged from the hospital with follow-up treatment after they suffered from the shock and infection phases and refined fluid management, 1 patient died due to severe injury and ineffective rescue.Conclusions:Adopting individualized, phased, and refined liquid management strategy has clinical significance for patients with severe blast injury to smoothly pass the risk period.

Objective To investigate the effects of high intensity electric field on cell growth,apoptosis and microstructure of human pancreatic cancer cell line PANC-1.Methods The PANC-1 cells in the logarithmic growth period were selected,and cells in the high voltage electrical treatment group were treated with high voltage electric field 250,500,750,1000 V/cm,respectively.The effects of different high voltage electric fields on cell growth and microstructure of PANC-1 cells were determined by cell viability,cell death staining,apoptosis detection,transmission electron microscopy and scanning electron microscopy.Results Compared with control group,the high voltage electric pulse significantly inhibited the growth of PANC-1 cells in the field dependent manner.Moreover,when the field was more than 500 V/cm,the cell viability was significantly decreased (P＜0.05).High voltage electric pulse could induce cell apoptosis.When the field was higher than 750 V/cm,serious necrosis was noticed.In the 1000 V/cm group,the integrity of cell membrane and the structure of organelles was seriously damaged.Conclusion High voltage electric pulse could significantly inhibit the growth of PANC-1 cells and would be a promising method in cancer treatment.

Objective:To investigate the mechanism by which Melittin-K1 reverses multidrug resistance of BEL-7402/5-FU cells.Methods:CCK-8 assay was used to evaluate the effect of Melittin-K1 on the growth of BEL-7402/5-FU cells and to explore whether Melittin-K1 could reverse the drug resistance of BEL-7402/5-FU cells. The expression of MDR1 mRNA level was detected by real-time fluorescence quantitative PCR assay. The flow cytometry was used to measure the expression of P-glycoprotein (P-gp) on the cell membrane surface and the accumulation of rhodamine-123 in cells.Results:Melittin-K1 significantly inhibited the growth of BEL-7402/5-FU cells in vitro in a time and dose-dependent manner. Melittin-K1 suppressed the level of MDR1 mRNA and inhibited the surface expression and function of P-gp in BEL-7402/5-FU cells. Conclusions:Melittin-K1, a novel peptide, exhibited the activity of reversing multidrug resistance of liver cancer cells.