ABSTRACT
To observe whether HMGB1could enhance the paracrine effect of MSCs when the Mesenchymal stem cells [Mesenchymal stem cells, MSCs] are pre-proccessed by High Mobility Group Box-1 [High Mobility Group Box-1, HMGB1]. And to observe whether it can further increase the quantity of local angiogenesis in myocardial infarcts on the rat model with acute myocardial infarction, HMGB1 was combined with MSCs transplantation. MSCs in rats were cultivated with adherence and centrifugation method. Receptors of TLR4and RAGE in HMGB1 were tested. The MSCs were interfered by HMGB1 with different concentration gradient respectively, then the expression of VEGF was tested with ELISA method. SD male rats were divided into four groups: the model group, the MSCs transplantation group, the HMGB1 injection group, the HMGB1 injection plus MSCs transplantation group [n = 24], preparing rat model with acute myocardial infarction. The serum VEGF concentration levels were detected on the 3[rd] day, 7th and 28th day with ELISA method. On the 28th day after post operation the density of angiogenesis in infarction area was detected by immunohistochemal. [1] MSCs owned the expression of TLR4 and RAGE. [2] the secretion of VEGF increased significantly after the intervention of HMGB1 with concentration of 12.5 ng/mL, 25 ng/mL, 50 ng/mL, 100 ng/mL and 200ng/ml on MSCs compared with the control group. While the concentration was 400ng/ml or 800ng/ml, the secretion of VEGF decreased compared with the control group [P < 0.05]. [3] detection of the serum VEGF on the 3[rd] or7th day after post operation was arranged: The results showed that: HMGB1 injection plus MSCs transplantation group > MSCs transplantation group >HMGB1 injection group >model group [P < 0.05]. [4] the quantity of CD31 stained angiogenesis in HMGB1 injection plus MSCs transplantation group increased obviously. Combining MSCs transplantation, contributed to new angiogenesis of rats with acute myocardial infarction in myocardial infarction area and its near area in rats with acute myocardial infarction
ABSTRACT
Objective To observe the effect of pravastatin on the expression of heat shock protein B7 (HSPB7) in acute myocardial infarction (AMI) rats. Methods A total of 80 AMI rats were randomly divided into AMI group and pravas-tatin (P) group. Forty SD rats were used as sham operation (SH) group. Rats were then subdivided into 1 h, 3 h, 6 h and 12 h subgroups (10 for each group). Rats were not ligated after thoracotomy in SH group. The 1eft anterior descending coronary ar-tery was ligated in rats of AMI group. The 1eft anterior descending coronary artery was ligated in P group and given intragas-tric administration of 0.5 mg/(kg · d) pravastatin. The other groups were given the same amount of normal saline via gavage. The left ventricle infarcted myocardial tissues were taken at each time intervals. The corresponding myocardial tissues were harvested in sham-operated rats. The HSPB7 mRNA and protein expressions were measured by RT-PCR and immunohisto-chemistry respectively.Results The expression levels of HSPB7 mRNA and protein were significantly higher in the AMI group and P group than those of SH group(P<0.01). The expression levels of HSPB7 mRNA and protein were significantly increased 1 h after AMI and reached the peak value at 3 h after AMI. The expression levels of HSPB7 mRNA and protein were still higher in 6-h group and 12-h group than those of SH group. The expression levels of HSPB7 were higher in differ-ent time points of P group than those of AMI group. Conclusion HSPB7 could express in the early stage of acute myocardi-al infarction in rats. Pravastatin could promote the upregulation of HSPB7 in myocardial infarcted border zone after AMI, which may play a protective role in early myocardial infarction.