The aim of this study was to investigate the effects of propofol on myocardial ischemia-reperfusion injury (MIRI) and its mechanism by establishing in vivo rat models. Sprague-Dawley rats were selected for the construction of MIRI models in vivo. All rats were divided into three groups, including sham operation group (Sham operation), MIRI group and MIRI + propofol group. At 2 h after reperfusion, myocardial tissues and blood samples were collected from rats. The expression levels of serum lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB), as well as serum interleukin-6 (IL-6), IL-10 and tumor necrosis factor-α (TNF-α), were measured in each group of rats, respectively. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) assay was employed to detect the apoptosis of myocardial cells. Additionally, the messenger ribonucleic acid (mRNA) and protein expressions of Ras homolog gene family, member A (RhoA) and Rho-associated coiled-coil-containing pess and represses I/R-induced myocardial cell apoptosis in MIRI rats by inhibiting the activity of the Rho/Rock signaling pathway. The aim of this study was to explore the effects of sevoflurane (SEV) pretreatment on Adriamycin (ADR)-induced myocardial injury through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) pathway. A total of 24 rats weighing 200-250 g were divided into four groups, including control group (C group), ADR injection group (ADR group), SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group). Afimoxifene progestogen Receptor modulator H9c2 cells were cultured in vitro and were divided into control group (C group), ADR treatment group (ADR group), and SEV pretreatment group (ADR + SEV group) and inhibitor group (ADR + SEV + LY group) as well. Next, the content of aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK) in the serum was detected via Enzyme-Linked Immunosorbent Assay (ELISA). Hematoxylin-eosin (HE) staining assay was performed to determine the severity of myocardial injury. Meanwhile, the apoptosis rate of cells was detected throughhosphorylation level of the PI3K/Akt/GSK-3β signaling pathway.Compared with C group, ADR significantly increased the content of AST, LDH and CK in the serum (p less then 0.01), reduced protein expression levels of p-GSK-3β, p-PI3K and p-Akt (p less then 0.01), increased apoptosis rate (p less then 0.01), and induced myocardial injury. SEV pretreatment significantly alleviated the effect of ADR, manifested as significantly lowered content of AST, LDH and CK in the serum (p less then 0.01), distinctly elevated protein expression levels of p-GSK-3β, p-PI3K and p-Akt (p less then 0.01), notably reduced apoptosis rate (p less then 0.01), and relieved myocardial injury. LY294002 remarkably inhibited the protective effect of SEV against myocardial injury (p less then 0.01) CONCLUSIONS SEV is able to prominently ameliorate ADR-induced myocardial injury by regulating the phosphorylation level of the PI3K/Akt/GSK-3β signaling pathway. To investigate the changes of CaM-CaMK-CREB signaling pathway and related neuron factors in hippocampus of rats after sevoflurane and propofol administration. A total of 90 SD rats, half male and half female, were selected. They were randomized into anesthesia group (AG) and control group (CG), in which 30 rats under propofol anesthesia in the AG were included in group A, 30 rats under sevoflurane anesthesia were included in group B, and 30 rats under mixed ventilation of air and oxygen were included in the CG. Before (10 rats were killed in each group) and at the end of anesthesia (2 weeks of anesthesia and 7 days of Morris water maze test), rats were respectively killed and then an appropriate amount of hippocampus was separated. Human tumor necrosis factor-alpha (TNF-α), vascular endothelial growth factor (VEGF), calmodulin (CaM), calmodulin-dependent kinase Ⅱ a (CaMK II a), NMDA receptor 2B (NR2B), cysteine aspartate specific protease-3 mRNA (Caspase-3mRNA) and protein contents were detected. The la Simultaneously, the expression levels of NR2BmRNA, Caspase-3mRNA and protein in hippocampus of group A and group B were substantially higher than those of the CG, and those in group B were substantially lower than those in group A (p<0.001). What's more, the TNF-a and VEGF expression levels in hippocampus of group A and B were markedly higher than those of the CG, and those in group B were dramatically lower than those of group A (p<0.001). Sevoflurane anesthesia on the CaM-CaMK-CREB signaling pathway and learning and memory function of rats is less volatile, which does better in safeguarding stability.Sevoflurane anesthesia on the CaM-CaMK-CREB signaling pathway and learning and memory function of rats is less volatile, which does better in safeguarding stability. The aim of this study was to investigate the effects of dexmedetomidine (DEX) on proliferation and apoptosis of esophageal cancer (EC) cells, and to explore the possible underlying mechanism. EC cells (Eca109) were randomly divided into two groups, namely, Control group and DEX group. The viability, proliferation, and apoptosis of Eca109 cells were detected using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, 5-Ethynyl-2'-deoxyuridine (EdU) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. Meanwhile, the messenger ribonucleic acid (mRNA) and protein expression levels of extracellular signal-regulated kinase (ERK) 1/2 and c-Myc in Eca109 cells were measured by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) and Western blotting, respectively. The viability of Eca109 cells was remarkably weakened in DEX group when compared with Control group (p<0.05). DEX could significantly inhibit the proliferation and promote the apoptosis of Eca109 cells (p<0.05). Moreover, the mRNA and protein levels of ERK1/2 and c-Myc in Eca109 cells declined notably (p<0.05). DEX represses the proliferation and facilitates the apoptosis of Eca109 cells prominently. The possible underlying mechanism may be associated with the inhibition of c-Myc gene expression through the ERK signaling pathway.DEX represses the proliferation and facilitates the apoptosis of Eca109 cells prominently. The possible underlying mechanism may be associated with the inhibition of c-Myc gene expression through the ERK signaling pathway.