0.05) in vitamin D_3 plus nicotine (VDN) group. The values of +LV dp/dt_ max and-LV dp/dt_ max were significantly lower in VDN group (P

The endoplasmic reticulum (ER) serves several important functions, mainly post-translational modification, folding and assembly of newly synthesized secretary proteins, synthesizing lipids and cellular calcium storage. Various factors can disrupt ER homeostasis and disturb its functions, which leads to the accumulation of unfolded and misfolded proteins and to potential cellular dysfunction and pathological consequences, collectively termed ER stress. Recent progress suggests that ER stress plays a key role in the immune response, diabetes, tumor growth, and some neurodegenerative diseases. In particular, ER stress is involved in several processes of cardiovascular diseases, such as ischemia/reperfusion injury, cardiomyopathy, cardiac hypertrophy, heart failure, and atherosclerosis. Further research on the relation of ER stress to cardiovascular diseases will greatly enhance the understanding of these pathological processes and provide novel avenues to potential therapies.

Objective:To investigate the changes of pulmonary IMD and its receptor system - calcitonin receptor-like receptor (CL) and receptor activity modifying proteins (RAMPs) mRNA in acute lung injury(ALI) induced by oleic acid of rats. Methods: Contents of IMD in plasma and lung homogenates were measured by radioimmunoassay(RIA). The lung mRNA of IMD, CL and RAMPs was determined by semi-quantitative RT-PCR. Results: Compared with control group, in ALI group, the contents of IMD_ 1-53 in plasma and lung homogenates were decreased by 20.8% and 74.5% (all P

Objective To test the hypothesis that IL-10 may promoting left ventricular remodeling and cardiac function by modulating extracellular matrix after acute myocardial infarction. Methods Male adult rats were randomly divided into three groups:control group (n=6),MI/AAV2 group (n=16) and MI/AAV2-IL-10 group (n=16). Establishing animal modol of experimental myocardial infarction and recombinant adeno-associated virus type 2 (AAV)/IL-10 (AAV2-rhIL-10) and AAV2 were injected around the ischemic zone. Echocardiography parameters,hemodynamic parameters,left ventricular mass index (LVMI),collagen volume fraction (CVF),perivascular circumferential area (PVCA),collagen type Ⅰ&Ⅲ volume fraction and mRNA levels of collagen type Ⅰ&Ⅲ,matrix metalloproteinases-2 (MMP-2) and tissue inhibitor of metalloproteinase-1 (TIMP-1) were compared among the three groups. Results Improved cardiac function was observed in MI/AAV2-IL-10 group shown by echocardiography and hemodynamic examination. Four weeks after myocardial infarction,thickness of different parts of LV was not different in MI/AAV2-IL-10 group and MI/AAV2 group. Nevertheless CVF,PVCA and collagen type Ⅰ volume fraction was significantly descending in remote zone of MI/AAV2-IL-10 group compared with that of MI/AAV2 group. The mRNA expression of collagen type I and MMP-2 was lower in MI/AAV2-IL-10 group than that in MI/AAV2 group. Conclusion Recombinant IL-10 expression mediated by AAV2-rhIL-10 transfection of rats' myocardium promotes LV remodeling and cardiac function after acute myocardial infarction. The promotion was partially achieved by inhibition myocardium collagen deposition.

Aim To determine the protective effects of IMD on ischemia/reperfusion(I/R) injury and its possible mechanism.Method Isolated rat hearts were perfused by Langendorff mode,and after 45 min global ischemia and 30 min reperfusion ventricular function was measured on a Power Lab,and adequate amount of ventricular tissues and perfusate were collected for biochemical measurement.Results Treatment with IMD during the reperfusion period significantly attenuated the effects of I/R on cardiac function inhibition and tissue injury.Compared with I/R group,IMD induced increase in △LVP,LV(dp/dtmax,HR and CF,whereas induced decrease in LVDP.Reperfusion with IMD exerted decrease in LDH,total protein,Mb and MDA content compared with I/R group,but increased myocardial cAMP content.All these values were similar to the effects of ADM.Furthermore,I/R induced significant increase in Bmax and Kd value.Conclusion IMD exerted beneficial effects on cardiac injury induced by I/R which might be mediated by cAMP pathway.And the cardioprotective effects of IMD were equal to ADM,a potent cytoprotective factor.

Aim To observe the influence of hydrogen sulfide on L-arginine/nitric oxide synthase(NOS)/NO pathway,explore the interaction between H_2S and NO as cardiovascular regulatory gasotransmitters.Methods Aortic thin slices in vitro were administrated with NaHS(10~(-7) mol?L~(-1)～10~(-4) mol?L~(-1)),a donor of H_2S,and incubated for 4 hours,or 50 ?mol?L~(-1) NaHS and incubated for 2 h,4 h and 6 h,respectively.The nitrite production Was measured with greiss assay;NOS activity and L-arginine transportation,with isotope tracer method;the eNOS and CAT1-A gene expression,with RT-PCR.Results After being given with NaHS(50 ?mol?L~(-1)) one time,and incubating for 2 h,the nitrite production decreased by 62%,NOS activity reduced by 48% and L-arginine transport decreased by 50%.After incubation for 6 h,the nitrite production further was inhibited by 19%(P0.05).NaHS(10~(-7) mol?L~(-1)～10~(-4) mol?L~(-1)) inhibited the L-arginine/NOS/NO pathway in a dose-dependent manner,and IC_(50) was 0.499,3.198 and 3.927 ?mol?L~(-1)(P

Objective To test the hypothesis that IL-10 may promoting left ventricular remodeling and cardiac function by modulating extracellular matrix after acute myocardial infarction. Methods Male adult rats were randomly divided into three groups: control group (n=6) , MI/AAV2 group (n=16) and MI/AAV2-IL-10 group (n=16). Establishing animal modol of experimental myocardial infarction and recombinant adeno-associated virus type 2 (AAV)/IL-10 (AAV2-rhIL-10) and AAV2 were injected around the ischemic zone. Echocardiography parameters, hemodynamic parameters, left ventricular mass index (LVMI) , collagen volume fraction (CVF) , perivascu-lar circumferential area (PVCA) , collagen type Ⅰ & Ⅲ volume fraction and mRNA levels of collagen type Ⅰ & Ⅲ , matrix metalloproteinases-2 ( MMP-2 ) and tissue inhibitor of metalloproteinase-1 ( TIMP-1) were compared among the three groups. Results Improved cardiac function was observed in MI/AAV2-IL-10 group shown by echocardiography and hemodynamic examination. Four weeks after myocardial infarction, thickness of different parts of LV was not different in MI/AAV2-IL-10 group and MI/AAV2 group. Nevertheless CVF, PVCA and collagen type Ⅰ volume fraction was significantly descending in remote zone of MI/AAV2-IL-10 group compared with that of MI/ AAV2 group. The mRNA expression of collagen type I and MMP-2 was lower in MI/AAV2-IL-10 group than that in MI/AAV2 group. Conclusion Recombinant IL-10 expression mediated by AAV2-rhIL-10 transfection of rats' myocardium promotes LV remodeling and cardiac function after acute myocardial infarction. The promotion was partially achieved by inhibition myocardium collagen deposition.

AIM: To investigate the effect of endothelin (ET), angiotensin II (AngII) and homocysteine (Hcy) on C-type natriuretic peptide (CNP) synthesis and release. METHODS: Human endothelial cell was cultured; CNP was measured by radioimmunoassay method. RESULTS: ET and AngII could augment CNP synthesis in human endothelial cells. Compared with control group, 10-9,10-8,10-7 mol/L ET and Ang II increased CNP content of endothelial cells by 1%(P＞0.05), 49%(P＜0.05),117%(P＜0.01) and 137% (P＜0.01),165%(P＜0.01),201%(P＜0.01),respectively. A great dose of ET and Ang II also stimulated CNP release from cultured human endothelial cells. Hcy had no effect on CNP synthesis, but 10-9，10-8,10-7 mol/L Hcy enhanced CNP release from cultured human endothelial cells by 17%(P＞0.05),84%(P＜0.01) and 555%(P＜0.01), respectively. CONCLUSION: ET, AngII and Hcy might be involved in the synthesis and release of human endothelial cell CNP.

Objective: To study the effect of urotensin(U Ⅱ) on nitric oxide synthase(NOS)/nitric oxide(NO) system in rat aorta. Methods: The aortic slices were incubated in vitro. The medium nitrite content, vascular NOS activities and cGMP content were measured. Results: After incubation of aorta for 1.5－3.0 h, UⅡ(10－9－10－7　mol*L－1) increased nitrite production ( 14.8%－80.9%, P<0.01) in dose-dependent manner. U Ⅱ significantly stimulated the total NOS activities, mainly activated constitutive NOS (P<0.05 or P<0.01), however, the inducible NOS activities were not altered (P>0.05). Incubation of aortic slices with U Ⅱ (10－9－10－7 mol*L－1) increased vascular cGMP content in dose-dependent manner. Co-incubation vascular tissue with U Ⅱ and　GN-L-nitro-arginine, an inhibitor of NOS, obviously inhibited the U Ⅱ-induced NOS activation, NO production and cGMP formation. Conclusion: The results suggest that U Ⅱ can activate the vascular NOS/NO pathway, increasing tissue NO production and cGMP content.

Objective To investigate the role of endogenous Hydrogen Sulfide (H2S) in airway inflammation and responsiveness in a rat model of chronic passive-smoking.Methods Male SD rats were randomly divided into a control group (breathing fresh air) and a passive smoking group [cigarette smoking (CS) passively] ,with 18 rats in each group.Six rats in each group were randomly intraporitoneally injected with normal saline, sodium hydrosulfide (NailS) or propargylglycine (PPG, an irreversible inhibitor of cystathionine-γ-lyase).The animals were divided into six subgroups,ie.Con group, Naris group, and PPG group, CS group, CS + Naris group, and CS + PPG group.After 4 months,lung histological change and airway tension were measured.The H2 S levels of plasma and lung tissue were analyzed by the sensitive sulphur electrode assay.The expression of cystathionine-γ-lyase (CSE) was measured by western blot.Results Compared with the Con group, CSE protein expression in lung tissues was increased in CS group(P < 0.05) ; the H2S levels of plasma were significantly higher in GS group,NariS group and CS + Naris group,and much lower in PPG group (P < 0.05, respectively).Compared with CS group, the H2 S levels of plasma were significantly higher in CS + Naris group, and much lower in CS + PPG group (P < 0.05, respectively).The H2S level of lung tissue in each group had no significant difference (P > 0.05).Compared with Con group, score of lung pathology was significant elevated, and the responsiveness of airway smooth muscles to Ach and KCI was significant augmented in CS group.Compared with CS group, the score of lung pathology was decreased, and the responsiveness of airway smooth muscles was decreased in CS + NariS group(P < 0.05), and vise versa in CS + PPG group (P < 0.01).Conclusion H2 S can alleviate airway inflammation and hyperresponsiveness induced by CS, and administration of H2S might be of clinical benefit in airway inflammation and airway responsiveness.