September 2020
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7 Reads
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1 Citation
Journal of the College of Physicians and Surgeons--Pakistan: JCPSP
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September 2020
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7 Reads
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1 Citation
Journal of the College of Physicians and Surgeons--Pakistan: JCPSP
January 2020
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21 Reads
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17 Citations
Acta Cirúrgica Brasileira
Purpose: To investigate the protective effect of L-carnitine on myocardial injury in rats with heatstroke. Methods: orty-eight rats were randomly divided into control, heatstroke and 25, 50 and 100 mg/kg L-carnitine groups. The last three groups were treated with 25, 50 and 100 mg/kg L-carnitine, respectively, for seven successive days. Then, except for the control group, the other four groups were transferred into the environment with ambient temperature of (39.5 ± 0.4 °C) and relative humidity of (13.5 ± 2.1%) for 2 h. The core temperature (Tc), mean arterial pressure (MAP), heart rate (HR) and serum and myocardial indexes were detected. Results: Compared with the heatstroke group, in the 100 mg/kg L-carnitine group, the Tc was significantly decreased, the MAP and HR were significantly increased, the serum creatine kinase, lactate dehydrogenase, alkaline phosphatase, aspartate aminotransferase, tumor necrosis factor α and interleukin 1β levels were significantly decreased, the myocardial superoxide dismutase and glutathione peroxidase levels were significantly increased, the myocardial malondialdehyde level was significantly decreased and the cardiomyocyte apoptosis index and myocardial caspase-3 protein expression level were remarkably decreased (p < 0.05). Conclusions: The L-carnitine pretreatment can alleviate the myocardial injury in heatstroke rats through reducing the inflammatory response, oxidative stress and cardiomyocyte apoptosis.
December 2018
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448 Reads
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53 Citations
Cellular & Molecular Biology Letters
Background Post-infarction cardiac injury is closely associated with cardiac remodeling and heart dysfunction. Mammalian STE20-like kinase 1 (Mst1), a regulator of cellular apoptosis, is involved in cardiac remodeling in post-infarction heart, but the mechanisms remain poorly defined. We aimed to explore the role of Mst1 in regulating chronic post-infarction cardiac injury, with a focus on mitochondrial homoeostasis. Methods Wild-type (WT) and Mst1-knockout mice were as the cardiac myocardial infarction model. Cardiac fibrosis, myocardial inflammation response, heart dysfunction and cardiomyocyte death were measured in vivo using immunohistochemistry, immunofluorescence, western blot, qPCR and TUNEL assays. Cardiomyocytes were isolated from WT and Mst1-knockout mice, and a chronic hypoxia model was used to induce damage. Mitochondrial function was determined via JC1 staining, ROS measurement, cyt-c leakage detection and mitochondrial apoptotic pathways analysis. Mitochondrial fission was observed using immunofluorescence. A pathway activator and inhibitor were applied to establish the signaling pathways involved in regulating mitochondrial homeostasis. Results Our study demonstrated that Mst1 expression was significantly upregulated in the heart post-infarction. Activated Mst1 induced cardiac fibrosis, an excessive inflammatory response, and cardiomyocyte death, whereas the genetic ablation of Mst1 protected the myocardium against chronic post-infarction injury. Function assays showed that upregulation of Mst1 activity contributed to JNK pathway activation, which led to Drp1 migration from the cytoplasm onto the surface of the mitochondria, indicative of mitochondrial fission activation. Excessive mitochondrial fission caused mitochondrial fragmentation, resulting in mitochondrial potential collapse, ROS overproduction, mitochondrial pro-apoptotic leakage into the cytoplasm, and the initiation of caspase-9-mediated mitochondrial apoptosis. By contrast, Mst1 deletion helped to maintain mitochondrial structure and function, sending pro-survival signals to the cardiomyocytes. Conclusions Our results identify Mst1 as a malefactor in the development of post-infarction cardiac injury and that it acts through the JNK-Drp1-mitochondrial fission pathway.
... Since there are so little studies on the effects of LC tendon recovery, we aimed to research the effects of LC on an Achilles tendon injury model. It has been reported that the most effective dose of LC is 100 mg/kg/day (19)(20)(21). For this reason, LC was preferred to administer once daily at dose of 100 mg/kg intraperitoneally in our study. ...
January 2020
Acta Cirúrgica Brasileira
... Particularly the decelerating capacity index (DC) or sympathovagal imbalance is a common underlying disorder in patients with type 2 diabetics (Wang et., 2018). Therefore, the promotion of DC detection will bring the far-reaching influence on prevention and treatment of sudden cardiac death for the patients with type 2 diabetics (Wang et al., 2020). Artificial intelligence, machine learning, health care robots, and algorithms for clinical decisionmaking are currently being sought after in diverse fields of clinical medicine and bioengineering in cardiology (Johnson et al., 2018). ...
September 2020
Journal of the College of Physicians and Surgeons--Pakistan: JCPSP
... Here, the protective effect of JNK inhibition is mediated via mitochondrial JNK, as the inhibition of the protein-protein interaction between JNK and SAB reduces oxidative stress and, finally, infarct size after 30 min ischemia and 24 h reperfusion [200]. Increased JNK phosphorylation is also observed upon the activation of mammalian STE20-like kinase 1, leading to the mitochondrial translocation of the fission protein dynamin-related protein (Drp)1, which, in turn, causes excessive mitochondrial fission, ROS formation, and apoptosis [217]. It is suggested that I/R injury decreases the protein amounts of dual-specificity protein phosphatase 1, which activates JNK. ...
December 2018
Cellular & Molecular Biology Letters