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The aim of this study was to investigate the influences of propofol on myocardial ischemia/reperfusion injury in rats through the Janus kinase/signal transducers and the activators of transcription (JAK/STAT) signaling pathway.A total of 48 Sprague-Dawley (SD) rats were randomly divided into four groups, including: the sham-operation group (n=12), the model group (n=12), the propofol group (n=12) and the inhibitor group (n=12). The rats in the sham-operation group only received thoracotomy, without the modeling of the ischemia/reperfusion injury. The model of myocardial ischemia/reperfusion injury was established in the rats of the model group, and the rats were given normal saline for intervention. The rats in the propofol group were utilized to prepare the model of myocardial ischemia/reperfusion injury and were intervened with propofol. Meanwhile, the rats in the inhibitor group received intervention with AG490 after the establishment of myocardial ischemia/reperfusion injury model. Immunohistochemistry was applied to detect the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax). Western blotting was utilized to measure the relative protein expressions of phosphorylated JAK2 (p-JAK2) and p-STAT3. The messenger ribonucleic acid (mRNA) expressions of Bax and Bcl-2 were determined via quantitative Polymerase Chain Reaction (qPCR). Furthermore, cell apoptosis was examined using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.Immunohistochemistry results showed that compared with the sham-operation group, the positive expression of Bax remarkably increased (p0.05), while Bcl-2 notably decreased (p0.05) in the model group, propofol group, and inhibitor group. The propofol group and inhibitor group showed a significant lower positive expression of Bax (p0.05) and evident higher positive expression of Bcl-2 (p0.05) when compared with the model group. However, there were no significant differences in the positive expressions of Bax and Bcl-2 between the propofol group and inhibitor group (p0.05). According to the results of Western blotting, the relative protein expression levels of p-JAK2 and p-STAT3 proteins were remarkably elevated in the model group, propofol group and inhibitor group in comparison with those in the sham-operation group (p0.05). Propofol group and inhibitor group exhibited remarkably lower protein expression levels of p-JAK2 and p-STAT3 compared with the model group (p0.05). However, no significant differences were observed in the protein expressions of p-JAK2 and p-STAT3 between propofol group and inhibitor group (p0.05). The results of qPCR manifested that the mRNA expression of Bax was notably higher (p0.05), whereas Bcl-2 was significantly lower (p0.05) in the model group, propofol group and inhibitor group than those of the sham-operation group. Compared with the model group, the mRNA expression of Bax was evidently declined (p0.05), while Bcl-2 was significantly elevated (p0.05) in the propofol group and inhibitor group. Meanwhile, there were no evident differences in the mRNA expressions of Bax and Bcl-2 between the propofol group and inhibitor group (p0.05). Subsequent TUNEL assay indicated that the model group, propofol group, and inhibitor group showed remarkably higher apoptosis rate than the sham-operation group (p0.05). Moreover, the apoptosis rate was remarkably reduced in the propofol group and inhibitor group in comparison with the model group (p0.05). However, no significant difference was observed in the apoptosis rate between propofol group and inhibitor group (p0.05).Propofol inhibits myocardial cell apoptosis after myocardial ischemia/reperfusion injury by repressing the JAK/STAT signaling pathway.

This study aims to assess the effect and mechanism of genetically modified adipose-derived mesenchymal stem cells (ASCs) with recombinant lentiviruses mediated knockdown of miR-140-5p in ASCs' osteogenesis in vitro and atrophic nonunion rat model.This study included 36 male adult Sprague-Dawley (SD) rats weighing 400 g to 450 g from the experimental animal facility of our university. Approval was obtained from the University Animal Care Committee before the study. Rats' ASCs were prepared and genetically modified with lentivirus (Lv)-empty (NC) or Lv-miR-140-5p-TuD (inhibitors). After that, the expressions of RUNX2 and osteocalcin (OCN) were detected in the ASCs. To confirm the mechanisms of miR-140-5p in ASCs, we predicted the target genes by bioinformatics analysis and then the target genes were verified by luciferase reporting assay. The artificial atrophic nonunion was created in the rat's femoral bone. Animals were randomly divided into three groups according to the material implanted into bone defects space: AT scaffolds (AT group, n=12), AT scaffold with Lv-NC modified (AT+ASCs+Lv-NC group, n=12), AT scaffold with the Lv-miR-140-5p-TuD modified ASCs (AT+ASCs+Lv-miR-140-5p-TuD group, n=12). After four weeks, the rats were euthanized for the following radiographic examination, histologic study and biomechanical testing.MiR-140-5p was down-regulated during osteogenic differentiation of ASCs, and inhibition of MiR-140-5p promoted osteogenesis of ASCs in vitro. Inhibition of MiR-140-5p promoted osteogenesis of ASCs and enhanced fracture in the atrophic nonunion rat model: AT+ASCs+Lv-NC group, AT+ASCs+Lv-miR-140-5p-TuD group resulted in a better bone formation and higher BMD and BMC than AT group, while excellent bone formation and the highest BMD and BMC were observed in AT+ASCs+Lv-miR-140-5p-TuD group. Both AT+ASCs+Lv-NC group and AT+ASCs+Lv-miR-140-5p-TuD group presented more mature characteristics in the micro-architecture than AT group, whereas AT+ASCs+Lv-miR-140-5p-TuD group presented the highest BV/TV, Tb.Th and Tb.N as well as the lowest Tb.Sp. The peak load of the operated femur increased by 94.43% AT+ASCs+Lv-miR-140-5p-TuD group, 50.68% in AT+ASCs+Lv-NC group compared to the control AT group, respectively. The result of luciferase reporting assay showed that miR-140-5p could directly target TLR4 and BMP2.This study demonstrates that lentiviruses-mediated knockdown of miR-140-5p can significantly promote osteogenesis of ACSs by directly regulating its' target genes, TLR4 and BMP2, and that combined adipose scaffold with genetically modified ASCs can significantly enhance fracture-healing and bone formation in the atrophic nonunion rat model.

The fabrication process, compressive strength and biocompatibility of porous beta-tricalcium phosphate (beta-TCP) ceramic scaffolds reinforced with 45P(2)O(5)-22CaO-25Na(2)O-8MgO bioglass (beta-TCP/BG) were investigated for their suitability as bone engineering materials. Porous beta-TCP/BG scaffolds with macropore sizes of 200-500 muicrom were prepared by coating porous polyurethane template with beta-TCP/BG slurry. The beta-TCP/BG scaffolds showed interconnected porous structures and exhibited enhanced mechanical properties to those pure beta-TCP scaffolds. In order to assess the effects of chemical composition of this bioglass on the behavior of osteoblasts cultured in vitro, porous scaffolds were immersed in simulated body fluid (SBF) for 2 weeks, and original specimens (without soaked in SBF) seeded with MC3T3-E1 were cultured for the same period. The ability of inducing apatite crystals in simulated body fluid and the attachment of osteoblasts were examined. Results suggest that apatite agglomerates are formed on the surface of the beta-TCP/BG scaffolds and its Ca/P molar ratio is approximately 1.42. Controlling the crystallization from the beta-TCP/BG matrix could influence the releasing speed of inorganic ions and further adjust the microenvironment of the solution around the beta-TCP/BG, which could improve the interaction between osteoblasts and the scaffolds.

The arrhythmias induced by chloroform-epinephine, BaCl2, and aconitine were prevented and antagonized by Ophiopogon total saponins (OTS) which were extracted from the root of Ophiopogon japonicus (Thunb) Ker-Gawl. The incidence of ventricular arrhythmia produced by ligation of the left anterior descending coronary artery was effectively decreased without any changes in the hemodynamic indices of dogs. The electrophysiological effects of OTS in vivo and in vitro were studied by means of contact electrode and intracellular microelectrode techniques. The results showed that OTS shortened APD10, APD50, APD90; decreased APA and Vmax of both monophasic and transmembrane action potentials. OTS also increased the ERP/APD ratio and prevented or abolished the arrhythmikinesis provoked by ouabain and aconitine. The anti-arrhythmic properties of OTS lead us to draw an inference that the anti-arrhythmic mechanism may be related to the blocking of sodium and calcium channels.

Five compounds were isolated from the seeds of Momordica charantia. This paper reports their structure determination by spectral (IR, UV, HNMR, CNMR, and MS) and chemical methods. The structures of I, II, III, IV and V were elucidated as vacine, mycose, 3-O-(beta-D-glucopyranosyl)-24 beta-ethyl-5 alpha-cholesta-7, trans-22E, 25 (27)-trien-3 beta-ol, momorcharaside A and momorcharaside B respectively. Mycose was the first time found in this plant and compound III was the first time found in the genus Momordica. IV and V were new compounds. IV exhibited obvious inhibition of DNA and RNA syntheses in S 180 tumor cells in preliminary pharmacological studies.