Objective The inhaled sevoflurane has been demonstrated to protect against myocardial ischemia/reperfusion (I/R) injury. However, the relative mechanisms of sevoflurane‐mediated cardioprotection remain largely unknown. This study intends to explore the effect of miR‐155 on the sevoflurane‐mediated cardioprotection by regulating Sirtuin 1 (SIRT1) in mouse models of myocardial I/R. Methods Left anterior descending coronary artery ligation was used to induce models of myocardial I/R in mice. The I/R mice were treated with sevoflurane, sevoflurane + mimics negative control (NC) or sevoflurane + miR‐155 mimics. The expression of microRNA‐155 (miR‐155) and SIRT1 was examined by quantitative real‐time polymerase chain reaction and Western blot assay. Then cardiac functions and hemodynamic alterations were evaluated. Evans blue‐2,3,5‐triphenyltetrazolium chloride and terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling assay staining methods were adopted to evaluate infarct size and cardiomyocyte apoptosis, respectively. Results In the I/R mice, miR‐155 was expressed at a high level and SIRT1 at a low level. SIRT1 was confirmed to be a target gene of miR‐155. The treatment of sevoflurane could reduce miR‐155 expression and increased SIRT1 expression in the myocardial tissues, under which conditions, cardiac functions were promoted, accompanied by reduced infarct size and inhibited cardiomyocyte apoptosis. In response to miR‐155 upregulation, the sevoflurane‐treated I/R mice showed reduced cardiac functions, and increased infarct size and cardiomyocyte apoptosis. Conclusion The findings obtained in this study provide evidence suggesting that miR‐155 targets and negatively regulates SIRT1 expression, a mechanism by which the protection of sevoflurane is inhibited against myocardial I/R in mice.

Objective The purpose of this study is to uncover the effects of long chain noncoding RNA (lncRNA) metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) on sevoflurane‐induced neurotoxicity in developing rats. Methods Sevoflurane neurotoxicity model was established by sevoflurane treatment in 7‐day‐old Sprague‐Dawley rats. The rats were treated with Sevo or MALAT1 small interfering RNA to detect the MALAT1 expression, pathological change, ultrastructure, neuronal apoptosis, expression of apoptosis‐related proteins, expression of neurotrophic factors BDNF and NGF, spatial learning and memory function change, as well as neuron cell density of hippocampal tissues. Results MALAT1 was highly expressed in hippocampus tissues of rats. Downregulation of MALAT1 alleviated the pathological change, improved the ultrastructure, inhibited apoptosis of neuronal cells, declined caspase 3 and Bax while elevated Bcl‐2, BDNF and NGF, improved capability of spatial learning and memory, and increased density of hippocampal neurons in hippocampal tissues of sevoflurane‐induced rats. Conclusion Suppression of MALAT1 can reduce the apoptosis of hippocampal neurons induced by sevoflurane anesthesia, improve the capability of spatial learning, and memory function and alleviate the loss of hippocampal nerve cells in developing rats. To a certain extent, it plays the role of protecting brain nerve cells.

Litchi (Litchi chinensis Sonn.) is a famous fruit in south China, and it is also effective for chest tightness or chest pain, irritability, flatulence, epigastric pain and neuralgic pain, hernia pain and testicular swelling, cough, etc. It is valued because a great amount of polyphenol was found in litchi pericarp. In this paper, we got litchi pericarp pure extract by a simple purification method, then evaluated its activity to clear oxygen free radicals in vitro, and evaluated its myocardial protection effect in vivo through acute myocardial ischemia rat model. The results showed that the pure extract had protective effect on myocardial ischemia injury in a certain dose-effect relationship, which reflected in the electrocardiogram, myocardial pathological morphology and other indicators such as cardiac function enzymes, serum and myocardial antioxidant capacity, and eNOS, Bcl-2 and Bax gene expression. Furthermore, we analyzed the components of pure extract by UPLC-MS, ESI-MS and NMR. The main components of PLPE were procyanidin which were identified as procyanidin B2(1), (-)-epicatechin(2), epicatechin-(4β → 8,2β → O → 7)-epicatechin-(4β → 8)-epicatechin(3), A-type procyanidin trimer(4), B-type procyanidin dimer(5) and procyanidin A2(6).This study proved that litchi pericarp extract may have antioxidant activity and cardioprotection effect. It suggested that litchi pericarp may be good for cardiovascular disease. Copyright © 2017 John Wiley & Sons, Ltd.