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.

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.

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.

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 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 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

AIM:To study alterations of cardiac sarcoplasmic reticulum (SR) function in vitamin D 3-induced calcium overload rats. METHODS: The Ca-overload rat models were prepared by vitamin D 3 plus nicotine. Cardiac SR was seperated by centrifuging. The measurement of SR Ca 2+ uptake and Ca 2+ release activities were preformed by the Millimore filtration technique. Specific SR [ 3H]-ryanodine binding capacity was measured by radioligand method. RESULTS: Compared with control,myocardial calcium content in calcium overload rats increased by 78%( P

AIM: To explore the effects of angiotensin II on aortic calcification in the rat. METHODS: Arterial calcification of Sprague-Dawley rats was induced by vitamin D_3 plus nicotine. Calcification was confirmed by Von Kossa staining, measurement of calcium content, [~(45)Ca~(2+)] accumulation and alkaline phosphatase (ALP) activity of vascular tissue. RESULTS: The results showed that calcium content, [~(45)Ca~(2+)] accumulation and ALP activity in calcified arteries increased significantly compared with those of control. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in calcified aorta were also increased as compared with control. Captopril (inhibitor of ACE) and losartan (Ang Ⅱ receptor inhibitor) decreased significantly the content of calcium, [~(45)Ca~(2+)] uptake and ALP activity in calcified aorta. Ang Ⅱ levels in plasma and aortic tissues and the amount of angiotensinogen mRNA in aortic tissue were down-regulated by captopril. The amount of angiotensinogen mRNA and the content of Ang Ⅱ in the calcified aorta were also decreased by losartan. CONCLUSION: The captopril and losartan significantly alleviate the vascular calcification. [

Objective To examine whether the two vascular paracrine/autocrine factors, angiotensin Ⅱ (Ang Ⅱ) and endothelin, participate in the pathogenesis of arterial calcification. Methods Nicotine and vitamin D3 treated rats were studied. Vascular calcification was confirmed by using Von Kossa staining, measurement of calcium content,45Ca2+ uptake assay and alkaline phosphatase (ALP) activity. The plasma and vascular Ang Ⅱ and endothelin levels were measured by using radioimmunoassay. Angiotensinogen and endothelin mRNA levels were determined by RTPCR. Results The arterial calcium content, 45Ca2+ uptake and ALP activity were increased in calcification groups compared with control ( P ＜ 0.01 ). Administration of the angiotensin receptor antagonist losartan, the endothelin receptor antagonist bosentan, and the angiotensin-converting enzyme inhibitor captopril reduced significantly the arterial calcium content, 45Ca2+ uptake and ALP activity. In addition, the plasma and aortic Ang Ⅱ and endothelin contents, and vascular angiotensinogen and endothelin mRNA expression were significantly up-regulated ( P ＜0.05).Conclusions These findings suggest that functional renin-angiotensin system and endothelin pathway are involved in vascular calcification, and that activation of these systems could potentiate pathogenesis of arterial calcification. ( J Geriatr Cardiol 2004;1(2) :108-113. )