AIM: To observe the protective effects of shenmai injection on myocardial injury induced by 1,1-dipheyl-2-picryl hydrazyl (DPPH)free radic al in isolated rabbit hearts. METHODS: The isolated rabbit hear ts were perfused in a Langendorff model. Left ventricular pressure (LVP), the fi rst derivative of LVP (+dp/dt max ), left v entricular end-diastolic pressur e (LVEDP) and heart rate (HR) were recorded. Coronary flow (CF) and the activity of creatine kinase (CK) in coronary effluent were measured by timed collection of coronary effluent. RESULTS: Perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min caused a significant impairment of cardiac functi on, as shown by a decrease in LVP, +dp/dt ma x and HR and an increase in LV EDP as well as the increased release of CK. After perfusion with DPPH ( 0.25 ?mol?L -1 ) for 10 min, treatment with shenmai injection (1320 or 1 160) for 10 min produced a significant improvement of cardiac function and a d ecrease in the release of CK. CONCLUSION: Shenmai injection prot ects against myocardial injury induced by DDPH free radical in isolated rabbit h earts.

Objective To observe the delayed cardioprotective effect of the extract of Gingkgo biloba leaves(EGb761)and its possible mechanisms in rats.Methods Myocardial ischemia-reperfusion(I/R)injury was induced by 30 min of global ischemia and 30 min of reperfusion in isolated rat hearts.Heart rate(HR),coronary flow(CF),left ventricular pressure(LVP),and its first derivatives(+dp/dtmax)were recorded,and the releasing content of creatine kinase(CK),contents of malondialdehyde(MDA)and nitric oxide(NO)in myocardial tissues were measured.Results Single ig EGb761(50 or 100 mg/kg)at 24 h before I/R were done could significantly attenuate the damage of cardiac function(LVP and +dp/dtmax)and the lowering of NO level in myocardial tissues,and inhibit the increasing in CK release and MDA level induced by I/R in myocardial tissues.The delayed cardioprotective effects of EGb761 were markedly inhibited by pretreatment with L-NAME(5 mg/kg),an inhibitor of NO synthase,or HMR1883(3 mg/kg),an antagonist of sarcolemmal ATP-sensitive potassium channels(sarcKATP).Conclusion Pretreatment with EGb761 could protect against I/R-induced myocardial injury in rats,and the delayed cardioprotection of EGb761 may be related to increasing in NO production and opening of sarcKATP.

AIM To establish a new bioassay method for estimating the rat angiotensin Ⅰ converting engyme (ACE) activity in vivo by using ramipril (Ram), a ACE inhibitor. METHODS The change in mean arterial pressure induced by angioteuasin Ⅰ (AngⅠ) or bradykinin (BK) was measured before and 1, 24, 48 h after pretreatment with Ram (0 05,0 1 mg?kg -1 ,iv). The ACE activity was expressed by the pressor effect (%)of AngⅠ or the depressor effect (%) of BK. RESULTS The pressor effects of AngⅠ or the supernatant fraction of heart tissue homogenate containing AngⅠ were siginificantly reduced 1 h and 24 h after pretreatment with Ram, but not 48 h after pretreatment with Ram. In comparison of the depressor response of BK vs pressor response of AngⅠ 1 h after pretreatment with Ram,it was shown that the depressor effect of BK is more sensitive than the pressor effect of AngⅠ( P

OBJECTIVE:To study the protctive effect of ginkgo biloba extractEGBon the kindey in the case of is?chemia-reperfusion injury.METHODS:The model of renal ischemia-reperfusion injury in male rats was made by ligation of left renal artery for40min and3h of reperfusion.The rats with pretreatment were fed with EGB at different doses prior to operation.The content of malonadialdihydeMDA,the activity of superoxide dismutaseSODin renal cortex and the levels of blood urea nitrogenBUN,creatinineCrin plasma were measured.The pathological changes of renal tissues were observed by electron microscope.RESULTS:After ischemia-reperfusion,the activity of SOD in renal cortex was decreased,however,the content of MDA in renal cortex and the levels of BUN,Cr in plasma were increased.Pathological changes induced by ischemia-reperfusion in renal tissues were observed clearly.The pretreatment of rats with EGB significantly prevented reduction of SOD activity and increase of MDA content in renal cortex,decreased elevation of concentration of BUN and Cr in plas?ma.Pathological changes of proximal tubular cells in rat kidneys induced by ischemia-reperfusion were also prevented by the pretreatment with EGB.CONCLUSION:EGB can protect rats from renal injuries caused by ischemia-reperfusion.The mechanism of protective effects of EGB may be related to preserving the activity of SOD and alleviating lipid peroxidation.

OBJECTIVE:To provide reference for rational use of second class of psychotropic drugs in the clinic. METHODS:The second class of psychotropic drugs in outpatient department of our hospital during 2012-2015 were analyzed retrospectively in respects of the number of common drugs prescription,distribution of gender/age/disease diagnosis,DDDs and DUI,etc. RE-SULTS:During 2012-2015,second class of psychotropic drugs in outpatient department of our hospital accounted for 25.09%of to-tal prescription amout. The drugs with high use frequency were alprazolam,clonazepam,lorazepam and estazolam,accounting for 93.10% of total prescription amount of second class of psychotropic drugs. The proportion of male to female was 1∶1.50;the pa-tients aged 19-35 years old took up the biggest proportion,accounting for 34.62%. The proportion of schizophrenia prescription was the highest,accounting for 45.17%. DDDs of alprazolam was the highest,being 742 141.67;its DUI was 1.075;DUI of oth-er drugs was lower than 1.0. CONCLUSIONS:The use of second class of psychotropic drugs is basically reasonable in our hospi-tal. Guiding principles of Clinical Application of Psychotropic Drugs should be implemented strictly and continously to avoid abuse of second class of psychotropic drugs.

Objective To study the role of JAK-STAT singal transduction pathway in the interstitial fibrosis of unilateral ureter obstruction (UUO)mice. Methods Mice UUO model was established and the phosphorylation of JAK-STAT was examined at day 1,4,7 and 14 after ligation of the ureter.Mice in the treatment group were treated with daily injection of selective JAK2 inhibitor AG490 starting 2 h before ureter ligation until sacrifice while vehicle alone was given to mice in the model control group.Mice were sacrificed at day 14 after the establishment of model.Renal tubular lesion and interstitial fibrosis were assessed on paraffin section.Immunohistochemistry was used to detect renal macrophage infihration and α-SMA expression.The expression of collagen Ⅲ and MCP-1 mRNA was measured by RT-PCR.Phosphorylation of JAK2and STAT1 was examined by Western blotting. Results JAK2-STAT1 signaling transduction pathway was activated in UUO model.The activation of JAK2-STAT1 was closely correlated with the progression of renal injury,tubular histological lesions and interstitial fibrosis.AG490 treatment significantly inhibited the phosphorylation of JAK2 and STAT1 (P＜0.01).AG490 treatment also significantly reduced tubular lesions[(21.7 ±1.7)% vs (49.4±1.0)%]and interstitial fibrosis(1.0±0.1 vs 2.3±0.2),α-SMA expression(0.9±0.1 vs 2.1±0.2)and maerophage accumulation[(13.3±1.6)cells/HPF vs (34.4±1.0)cells/HPF](all P＜0.01).In addition,AG490 significantly inhibited the expression of collagen Ⅲ and MCP-1 mRNA. Conclusion JAK-STAT signaling plays an important role in renal tubulointerstitial inflammation and fibrosis.

AIM:To investigate the regulatory role of nuclear factor κB (NF-κB) in the expression of interleukin-6 in mesangial cells (MC) induced by interleukin-1β.METHODS:Activation of NF-κB was measured by electrophoresis mobility shift assay (EMSA). RT/PCR and ELISA were used to detect IL-6 mRNA expression and IL-6 production, respectively.RESULTS:rhIL-1β could rapidly stimulate the activation of NF-κB in MC, and increase the expression of IL-6 mRNA and protein. PDTC, one of the inhibitor of NF-κB， could inhibit the expression of IL-6 in mRNA and protein in MC stimulated by rhIL-1β.CONCLUSION:IL-6 expression induced by IL-1β may be regulated by NF-κB in MC, NF-κB may modulate the immune-inflammatory reaction in glomerular disease.

Objective To investigate the application technology and effect of Navien catheter in intracranial aneurysms embolization.Methods The clinical data of 15 patients with intracranial aneurysm treated with Navien catheter in Department of Neurosurgery of Yijishan Hospital Affiliated to Wannan Medical College from March to December 2016 were analyzed retrospectively. The extracranial segments of internal carotid arteries were seriously tortuous in all patients. The coaxial system was used during procedure. Whether the Navien catheter could be smoothly placed into the target artery or not was observed,and the coils or stent-assisted coils were used to embolize the intracranial aneurysms in the corresponding positions. The immediate embolization results were assessed by the Raymond grading. The intraoperative and postoperative complications were observed and the patients were followed up by imaging.Results All 15 patients had abnormal tortuosity of extracranial segments of internal carotid arteries. The Navien catheter was able to smoothly pass through the tortuous vessels and reach the desired position. The stent-assisted coil embolization was used in 9 patients,and the coil embolization was used in 6 patients. The success rate of the coil and stent placement technology was 100%. The stents were all accurately put in place without shift. According to the Raymond grading,the immediate embolization rate of aneurysms showed that 15 patients achieved Raymond gradeⅠ. One case developed internal carotid spasm during the procedure. The patient was improved after giving papaverine. Others did not have intraoperative complications,such as cerebral vasospasm,vascular dissection,in-stent thrombosis,and intraoperative aneurysm rupture. Five patients were followed up for 3 to 6 months with digital subtraction angiography (DSA). There was no recurrence of aneurysm and no in-stent stenosis and shift,No rebleeding or cerebral ischemia was observed.Conclusion Forpatients with severely tortuous in extracranial segments of internal carotid artery,using the Navien catheter may overcome artery tortuosity and other unfavorable factors of the patients and successfully reach the target vessel position,enable the embolization of intracranial aneurysms to be completed successfully.

AIM: To investigate the regulatory role of nuclear factor ?B (NF-?B) in the expression of interleukin-6 in mesangial cells (MC) induced by interleukin-1?.METHODS: Activation of NF-?B was measured by electrophoresis mobility shift assay (EMSA). RT/PCR and ELISA were used to detect IL-6 mRNA expression and IL-6 production, respectively.RESULTS: rhIL-1? could rapidly stimulate the activation of NF-?B in MC, and increase the expression of IL-6 mRNA and protein. PDTC, one of the inhibitor of NF-?B, could inhibit the expression of IL-6 in mRNA and protein in MC stimulated by rhIL-1?.CONCLUSION: IL-6 expression induced by IL-1? may be regulated by NF-?B in MC, NF-?B may modulate the immune-inflammatory reaction in glomerular disease.

AIM: To investigate the association of gene polymorphism at position 196 of tumor necrosis factor receptor Ⅱ (TNFRⅡ) with systemic lupus erythematosus (SLE) in Chinese, and establish recombinant retroviral vector to analyze the function of the TNFRⅡ 196M/R. METHODS: The genotype at position 196 of TNFRⅡ was determined by PCR-RFLP in 106 SLE patients and 119 healthy controls in china. Human TNFRⅡ196M cDNA were amplified by PCR and cloned into PMD18-T vector. Then, PMD18-TNFRⅡ196R was induced by site-directed mutagenesis. The recombinant T vector, PMD18-TNFRⅡ196M and PMD18-TNFRⅡ196R, were subcloned into retroviral vector PLXSN. Both normal and variant were transfected into rat mesangial cell. The effects of TNF? on production of sTNFRⅡ and IL-6 were study by ELISA. RESULTS: (1) The frequency of TNFRⅡ196R allele was significantly higher than those in controls (35.2% vs 14.3%, P