Abstract
The aim of this study was to investigate the effects of thymosin β4 on myocardial apoptosis following burns. Fifty healthy Sprague Dawley (SD) rats were randomly divided into the normal control group, resuscitation group the low-dose Tβ4 (thymosin β4) group (2g), the medium-dose Tβ4 group (6g), and the high-dose Tβ4 group (18g). The rats were immersed in 95°C hot water for 18 seconds, and then the model of 30% body surface area (TBSA) III° scald was established. The resuscated rats were injected with lactate Ringer's solution for antishock rehydration, while the Tβ4 treatment group was injected with lactate Ringer's solution for antishock rehydration, and the animals were sacrificed 6 h after scald. The degree of histopathological damage was observed by HE (hematoxylin and eosin) staining. Western blot was used to detect STAT1 and STAT3 protein expression levels. Real-time PCR was used to detect mRNA expressions of STAT1 and STAT3. The results showed that the apoptosis rate of the resuscitation group was significantly higher than that of the control group (P < 0.01). Compared with the resuscitation group, the apoptosis rate of thymosin β4 in the treatment group was significantly reduced (P < 0.01). Compared with the normal control group, the expression of STAT1 protein was increased and the expression of STAT3 protein was decreased in model group rats after ischemia and reperfusion. Compared with the model group, the expression of STAT1 protein decreased and the expression of STAT3 protein increased after ischemia-reperfusion in the thymosin β4 treatment group. Thymosin β4 may protect the myocardium by downregulating STAT1 and upregulating STAT3 expression and inhibiting myocardial apoptosis induced by ischemia and reperfusion after severe scald injury.
Highlights
Ischemia-reperfusion injury after a severe burn is one of the pathological bases of myocardial cell damage after burn, which can lead to cardiac dysfunction, induce or promote the aggravation of burn shock, and is often accompanied by myocardial cell apoptosis and tissue necrosis
Compared with the resuscitation group, the ratio of STAT1 to its corresponding β-actin bands was 0.932 ± 0.005, 0.923 ± 0.004, and 0.596 ± 0.008, respectively. e expression of STAT1 protein in cardiomyocytes of rats treated with adenomycin β4 was significantly decreased (P < 0.05; P < 0.01). e ratio of STAT3 to β-actin bands in the normal control group was 0.751 ± 0.006
In the pathogenesis of ischemia-reperfusion injury, apoptosis of myocardial tissue cells plays an important role in the pathological process of ischemia-reperfusion injury, that is to say, ischemia-reperfusion injury is realized by regulating the apoptotic process of myocardial tissue cells [6]. e decrease of cardiac function in the early burn is closely related to myocardial cell apoptosis. erefore, inhibiting myocardial cell apoptosis can improve cardiac insufficiency [7, 8]. e results of this study indicated that apoptosis of cardiomyocytes occurred in rats after severe scalding, and adenothymidin β4 could inhibit the apoptosis of cardiomyocytes after severe scalding
Summary
Ischemia-reperfusion injury after a severe burn is one of the pathological bases of myocardial cell damage after burn, which can lead to cardiac dysfunction, induce or promote the aggravation of burn shock, and is often accompanied by myocardial cell apoptosis and tissue necrosis. Excessive myocardial cell apoptosis plays an important role in myocardial ischemia-reperfusion injury. Recent studies have suggested that Tβ4 has a neuroprotective effect and can reduce astrosporin-induced motor neuron death [2] It can reduce the damage of excitatory amino acids to cortical neurons and the whole rat model [3] and improve the neurological injury symptoms of cerebral ischemia rats [4]. We established a rat model of severe scald to investigate the effects of thymosin β4 with different doses in the treatment of severe scalding and inhibited apoptosis after ischemia-reperfusion by downregulating STAT1 and upregulating STAT3 expression in myocardial cells. We established a rat model of severe scald to investigate the effects of thymosin β4 with different doses in the treatment of severe scalding and inhibited apoptosis after ischemia-reperfusion by downregulating STAT1 and upregulating STAT3 expression in myocardial cells. e study aims to provide an experimental basis for the early protection of clinical cardiomyocytes
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