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Sphingosine Kinase Protects Heart Against Ischemia-Reperfusion Induced Injury and Attenuates Its Post-Ischemic Failure

Author: WangHong
Tutor: WangLiSheng；WangHanBin
School: PLA Military Academy of Medical Sciences
Course: Pathology and Pathophysiology
Keywords: Sphingosine Ischemia-reperfusion injury Myocardial ischemia model Myocardial cells Master's degree Gene transfection Thesis Experimental study Recombinant adenovirus Cell death
CLC: R541
Type: Master's thesis
Year: 2006
Downloads: 76
Quote: 0
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Abstract


1 - sphingosine phosphate (Sphingosinel-phosphate, S1P) by sphingosine kinase (sphingosine kinase 1 SPK1) catalyzes the production of a major product of the metabolism of sphingomyelin. The results show that, S1P can protect hypoxia-induced myocardial cell injury. Addition, SPK1 recently been shown to produce a key molecule mediated myocardial ischemic preconditioning. The SPK1 whether can protect ischemia and hypoxia caused by myocardial injury, as well as the adenovirus mediated SPK1 gene transfection whether as a treatment for ischemic heart disease, a new means is unclear, the subject this been systematically studied. We first observed SPK1/S1P active oxygen radicals H 2 O 2 protective effect induced myocardial cell death; followed by the use of hearts from ischemia reperfusion model study high the expressed gene SPK1 of cardiac ischemia-reperfusion resistance; Finally, myocardial ischemia caused by ligation of the left anterior descending artery model to explore the therapeutic effect of adenovirus mediated SPK1 local transfection of ischemic heart disease. The main results are as follows: H 2 O 2 can lead to the death of myocardial cells a dose-dependent; H 2 O2 significantly inhibit cardiac the SPK1 kinase activity and Edg-3 receptor expression, but to promote the Edg-1 receptor expression; heart multilocus 3 days after injection of Ad-SPK1 Cardiac the organization SPK1 kinase activity was significantly higher than the control group increased about 5 times; injection of Ad-SPK1 the heart ischemia-reperfusion injury obvious resistance, systolic and diastolic function of the heart there is no obvious damage in ischemia and reperfusion, reperfusion CK release was significantly reduce the frequency and duration of the arrhythmia was significantly lower than the GFP control group; the Ad-SPK1 local injection of the left anterior descending coronary myocardial ischemia caused significant therapeutic effect on performance in systolic and diastolic function of the heart has been significantly improvement in left ventricular systolic pressure (left ventricular systolic pressure, LVSP): Ad-SPK1 132.82 ± 13.03 Ad-GFP 76.96 ± 8.44 mmHg, p <0.01; left ventricular late diastolic blood pressure (left ventricular end-diastolic pressure, LVEDP): Ad-SPK1 4.34 ± 0.69 Ad-GFP 14.79 ± 1.08 mmHg, p <0.01; maximum dP / dt: a Ad-SPK1 5095.20 ± 384.79 Ad-GFP 2954.12 ± 195.05, p <0.01; left ventricular remodeling has been significantly improved performance in the ischemic area: Ad-SPK1 3.78 ± 0.96 38.86 ± 5.68 (% of Ad-GFP), p <0.01; left ventricular diameter: Ad-SPK14.63 ± 0.80 to 7.30 ± Ad-GFP 1.03mm p <0.01; left ventricular wall thickness: Ad-2.70 ± 0.29 SPK1, Ad-GFP 1.34 ± 0.36mm, p <0.01; HE staining and factor Ⅷ related antigen immunohistochemical analysis of the, SPK1 gene transfection significantly stimulate ischemia parts of angiogenesis; Sirius Red staining results showed that, SPK1 gene transfection significantly reduced collagen deposition in the ischemic partial. Through the above results, we can draw the adenovirus mediated SPK1 gene transfection to protect not only induced myocardial ischemia-reperfusion (cell) death, and can be protected by stimulating the growth of blood vessels and the inhibition of collagen deposition caused by ischemia heart dysfunction. Local the Ad-SPK1 injection may be a new approach for the treatment of ischemic heart disease.

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease
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