AIM:To investigate the effect of quercetin on the biological functions of rat bone marrow-derived endothelial progenitor cells (EPCs) and its potential mechanisms.METHODS:The bone marrow-derived mononuclear cells of Sprague-Dawley rats were isolated by density gradient centrifugation.The differentiated EPCs were cultured specially and stained with DiI-Ac-LDL and FITC-UEA-1.CD133+ and FLK-1+ were detected on the cell surfaces.After 14 d, the EPCs were incubated with a PI3K inhibitor BYL719 (3 μmol/L) and an ERK inhibitor FR180204 (15 μmol/L).After incubation of the inhibitors for 2 h, the cells were treated with quercetin at different concentrations (0, 10, 20, 40, 80 and 100 μmol/L).MTT assay and Transwell assay were used to detect cell viability and the number of migratory cells.The protein levels of AKT, eNOS, ERK and their phosphorylated status were determined by Western blot.RESULTS:Quercetin enhanced the viability and migration of the EPCs at a dose-dependent manner.However, the PI3K inhibitor BYL719 suppressed the QUE-induced cell viability and migration.Moreover, ERK inhibitor FR180204 exerted the similar inhibitory effect on the cell viability but had no effect on cell migration.Quercetin activated the phosphorylation of AKT, eNOS and ERK.On the other hand, BYL719 was observed to inhibit the phosphorylation of AKT and ERK.FR180204, however, was showed to inhibit the phosphorylation of ERK only.On the contrast, the stimulatory effects that quercetin exerted on the expression of eNOS and its phosphorylation were suppressed by BYL719 and FR180204.CONCLUSION:Quercetin stimulates the viability and migration of EPCs via PI3K/AKT/eNOS and ERK/eNOS signaling pathway, which would be beneficial for cardiovascular health.

ObjectiveTo observe the expression of spinal G protein-gated inwardly-rectifying potassium （GIRK） channel subunits 1 and 2 in spinal dorsal horn of morphine-tolerant rats and investigate the regulatory mechanism. MethodsTwenty four rats were equally and randomly divided into 4 groups： saline， morphine， morphine + saline and morphine + εV1-2. The morphine-tolerant rat model was established by intrathecal administration of morphine （15 μg/d） for 7 days. Thirty minutes before daily morphine administration， rats received protein kinase C-ε（PKCε） selective inhibitor εV1-2 to test its effect on morphine tolerance and GIRK1-2 expression. All rats received behavioral tests on days 1， 3， 5 and 7 and thereafter immunofluorescence. ResultsDouble fluorescence staining showed that GIRK1 and GIRK2 were expressed primarily in the spinal laminae I-Ⅱ and co-immunostained with μ-opioid receptor （MOR）. Seven-day intrathecal administration of morphine induced antinociceptive tolerance and a significant reduction of the spinal GIRK1 （22.45±10.58 vs. 62.83±20.80， P<0.001） and GIRK2 （23.67±8.78 vs. 50.17±11.05， P=0.001） fluorescence intensity， as compared with saline control rats. In addition， pretreatment with εV1-2 significantly delayed the reduction of morphine antinociception （P<0.001） and prevented the decrease of GIRK1 （54.50±10.37 vs. 19.33±9.48， P<0.001） and GIRK2 （39.83±6.24 vs. 15.83±9.58， P=0.001） expression induced by morphine treatment. ConclusionsMorphine tolerance is closely related to down-regulation of GIRK1-2 expression and PKCε plays a crucial regulatory role herein.

Objective     To explore the effect of 16F gastric tube on pain relief in postoperative lung cancer patients. Methods     A total of 118 lung cancer patients were treated with radical resection of lung cancer in our hospital between January 2015 and May 2016. The patients were assigned into two groups: a 16F gastric tube group (16F group, 60 patients, 30 males and 30 females at age of 41-73 (52.13±7.83) years and a 28F drainage tube group (28F group, 58 patients, 25 males and 33 females at age of 45-75 (55.62±4.27) years. Clinical effects were compared between the two groups. Results     There was no statistical difference in drainage time (4.47±1.03 d vs. 4.24±1.16 d, P=0.473), drainage amount (560.37±125.00 ml vs. 656.03±132.45 ml, P=0.478), incidences of pneumothorax (5/60 vs. 2/58, P=0.439), pleural effusion (6/60 vs. 3/58, P=0.522), and subcutaneous emphysema (3/60 vs. 1/58, P=0.635) between the two groups (P>0.05). The pain caused by the drainage tube in the16F group was less than that in the 28F drainage tube group with a statistical difference (F=4 242.996, P<0.001). The frequency of taking analgesics in the 16F group was significantly less than that in the 28F group (12/60 vs. 26/58, P<0.001). Conclusion     The effects of draining pleural effusions and promoting lung recruitment are similar between the 16F group and the 28F group. However, the wound pain caused by 16F gastric tube is significantly less than that by 28F drainage tube.