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rp105对大鼠心肌缺血再灌注损伤的保护作用及其对tlr4pi3k-akt信号通路的影响word论文
减少对大鼠心肌缺血再灌注的损伤,从而发挥保护作用。关键词:RP105基因转染缺血再灌注损伤 TLR4/PI3K-AKTIIIAbstractObjective: in this article, we used a replication defect type recombinant adenovirus carrying RP105 gene (Ad - RP105) as the carrier to transfect myocardial tissue of rat in vivo, making RP105 in myocardial tissue of rats with high expression. Then we built cardiac ischemia reperfusion model of rats in vivo, through a TLR-4-PI3K-AKT signaling pathway as the breakthrough point, and research on the protection of RP105 gene on myocardial ischemia reperfusion (I/R) injury from expression of gene and protein.Methods: 48, SPF male SD rats were randomly divided into four groups (n = 12): (1) The Sham group: physiological saline + control (only thread ligation); (2) I/R group: normal saline + ischemia reperfusion group; (3) The Ad-R group: Ad-RP105 + ischemia reperfusion group (Ad-RP105, a replication defect type recombinant adenovirus carrying RP105 gene); (4) The Ad-G group: Ad-GFP + ischemia reperfusion group (Ad-GFP, a recombinant adenovirus with green fluorescent protein). The myocardial transfection was through by multi-point injection virus into rat myocardium; Pull pressure tube method is adopted to establish the myocardial ischemia reperfusion (I/R) injury rat model in vivo; Automatic biochemical analyzer was used to test the activity of LDH, CK, CK-MB in serum of rats; the pathological morphological changes of myocardial tissue were observed by optical microscope; Evans blue staining and triphenyl four azole nitrogen chloride (TTC) staining and computer image analysis system were used to detect myocardial ischemia and infarction area; Real-time PCR was adopted to detect the level of expression of RP105, TLR - 4, PI3K, and AKT mRNA in myocardial tissue; Western blot was employed to detect the expression of RP105, TLR-4, PI3K, and AKT protein in myocardial tissue.Results: (1) Rats carrying recombinant adenovirus in myocardial tissue in vivo were living in good condition, and the transfection effic
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