Objective To observe the effects of Ganlu Xiaodu Dan and its incomplete prescription on expressions of MiR-146a and TLR4 mRNA in RD cells infected by EV71. Methods With technique of cell culturing, Ganlu Xiaodu Dan therapy group, incomplete Qing prescription therapy group, incomplete Li prescription therapy group, normal cells control group, model control group and ribavirin control group were set, and tests for virus toxicity and medicine toxicity in cells were taken, then expressions of miRNA-146a and TLR4 mRNA in these RD cells 24 hours after intervention with medicine were detected. Results Compared with normal cells control group, miR-146a in mRNA model control group decreased and TLR4 mRNA increased. Compared with model control group, miR-146a mRNA in Ganlu Xiaodu Dan therapy group, incomplete Qing prescription therapy group and incomplete Li prescription therapy group all increased while TLR4 mRNA decreased, and differences between ribavirin control group and model control group were not significant. Compared with Ganlu Xiaodu Dan therapy group, both expressions of miR-146a and TLR4 mRNA in incomplete Qing prescription therapy group were lower; miR-146a increased and TLR4 mRNA decreased in incomplete Li prescription therapy group. Compared with incomplete Qing prescription therapy group, miR-146a mRNA in incomplete Li prescription therapy group increased, but expression of TLR4mRNA between them was not significant. Conclusion Ganlu Xiaodu Dan can regulate the immune reactions caused by infection of EV71 by increasing expression of miR-146a mRNA and reducing expression of TLR4 mRNA. There may be antagonism effect between incomplete Qing prescription and incomplete Li prescription.

Objective To explore anti-EV71 effects of Ganlu Xiaodudan in vitro. Methods Ribavirin was taken as control drug, with the help of cell culture to observe anti-EV71 inhibition rate of Ganlu Xiaodudan in inhibiting-virus-directly experiment, therapeutic-inhibiting-virus experiment, preventive-inhibiting-virus experiment and preventive-therapeutic-inhibiting-virus experiment. Results In inhibiting-virus-directly experiment, therapeutic-inhibiting-virus experiment and preventive-therapeutic-inhibiting-virus experiment, virus inhibition rate of Ganlu Xiaodudan was higher than ribavirin. In preventive-inhibiting-virus experiment, virus inhibition rates of Ganlu Xiaodudan and ribavirin both were almost zero. Conclusion Ganlu Xiaodudan has better antiviral effects on EV71 than ribavirin, and it can affect more than one link of multiplication of EV71.

OBJECTIVE: To explore the nature of pathology of sluggishness of lung-defensive qi and to offer objective experimental indexes for weifen syndrome (defensive phase syndrome). METHODS: According to the completely random design, the plasma levels of vasoactive intestinal peptide (VIP) and thromboxane B2 (TX2) of 19 patients with weifen syndrome and 13 patients with qifen syndrome (qi phase syndrome) were detected by radioimmunoassay. The plasma levels of VIP and TX2 at different stages of weifen syndrome and qifen syndrome were observed. RESULTS: The plasma levels of VIP in weifen syndrome and in the late stage of weifen syndrome increased greatly at different stages as compared to qifen syndrome and the blank group (P < 0.01), while the plasma level of TX2 of weifen syndrome was higher only at the late stage than the blank group and qifen syndrome (P < 0.01). As for the levels of VIP and TX2 in weifen syndrome with different internal organs infected, there was no significant difference (P > 0.05). CONCLUSION: VIP may be an index reflecting the pathology of weifen syndrome, and it is one of the material foundations of sluggishness of lung-defensive qi, but it has nothing to do with the infected internal organs. The level of TX2 increases only after the fever of patients with weifen syndrome subsided, so it can not be the basis for diagnosis of the early stage of weifen syndrome. It doesn't increase in qifen syndrome either, the mechanism remains to be further studied.

Objective:To compare the effects of propofol, fospropofol disodium and sevoflurane on pulmonary metastasis after radical mastectomy for breast cancer in mice.Methods:SPF-grade healthy female C57 mice, aged 4-6 weeks, weighing 14-18 g, were used in this study. Eighteen mouse breast cancer models were successfully prepared by luciferase-labeled mouse 4T1 breast cancer cells, and the mice were divided into 3 groups ( n=6 each) by the random number table method: sevoflurane group (S group), propofol group (P group) and fospropofol disodium group (PD group). Group S inhaled 3% sevoflurane, propofol 200 mg/kg was intraperitoneally infused in group P, and fospropofol disodium 182 mg/kg was injected via the tail vein in group PD, and anesthesia was maintained for 3 h to perform radical mastectomy in three groups. The lung metastasis of mouse breast cancer cells was evaluated by in vivo imaging at 2 weeks after surgery, and then the mice were sacrificed, and lung tissues were obtained for determination of the expression of extracellular regulatory protein kinase 1/2 (ERK1/2), phosphorylated ERK1/2 (p-ERK1/2), P38 and phosphorylated P38 (p-P38) by Western blot. Results:Compared with S group, the number of lung metastases and total number of cell metastases in breast cancer cells were significantly decreased, and the expression of p-ERK1/2 and p-P38 in lung metastases was down-regulated in P group and PD group ( P<0.05). There was no significant difference in the parameters mentioned above between P group and PD group ( P>0.05). Conclusions:Propofol and fospropofol disodium have better efficacy than sevoflurane in reducing lung metastasis after radical mastectomy, which may be related to down-regulation of p-ERK1/2 and p-P38 expression in mice.

Objective:To investigate the relationship between the mechanism of mental dependence of propofol and adenosine A2A receptor-neurotransmitter-extracellular signal-regulated kinase (ERK) pathway in rats.Methods:Forty-eight healthy male Sprague-Dawley rats, aged about 7 weeks, weighing 200-300 g, were used in this study.The model of propofol dependence was established by intraperitoneal injection of propofol 40 mg/kg for 14 consecutive days.The rats were divided into 6 groups ( n=8 each) using a random number table method: central control group (group c-C), central agonist group (group c-CGS), central antagonist group (group c-DMPX), peripheral control group (group p-C), peripheral agonist group (group p-CGS) and peripheral antagonist group (group p-DMPX). Adenosine A2A agonist CGS-21680 2.5 ng/0.5 μl was intracranially injected immediately after establishing the model in group c-CGS, while the equal volume of normal saline was given instead in c-C group.CGS-21680 0.1 mg/kg was intraperitoneally injected in group p-CGS, while the equal volume of normal saline was given instead in group p-C.Adenosine A2A receptor antagonist DMPX 50 ng/0.5 μl was intracranially injected at 20 min before each propofol injection in group c-DMPX, and DMPX 0.25 mg/kg was intraperitoneally injected in group p-DMPX.The position preference value (CPP value) was determined before establishing the model, immediately after establishing the model, and after administration of agonist or normal saline (after intervention). The animals were sacrificed at 1 day after establishing the model, and blood samples and brain tissues were obtained for determination of the levels of dopamine (DA) and glutamate (Glu) in plasma and hippocampus and content of serotonin (5-HT) in cerebral cortex (by enzyme-linked immunosorbent assay) and expression of phosphorylated ERK1/2 (p-ERK1/2) in cerebral cortex (by Western blot). Results:Compared with the baseline before establishing the model, CPP value was increased immediately after establishing the model in c-C, c-CGS, p-C and p-CGS groups ( P<0.05), and no significant change was found in CPP value immediately after establishing the model in c-DMPX and p-DMPX groups ( P>0.05). Compared with the value immediately after establishing the model, no significant change was found in CPP value after intervention in c-C and p-C groups ( P>0.05), and CPP value was increased after intervention in c-CGS and p-CGS groups ( P<0.05). Compared with group c-C, the contents of hippocampal DA and Glu were significantly increased in group c-CGS, and the contents of hippocampal Glu were decreased, the content of 5-HT in cerebral cortex was increased, and the expression of p-ERK1/2 was down-regulated in group c-DMPX ( P<0.05). Compared with group p-C, no significant change was found in levels of DA and glutamate (Glu) in plasma and hippocampus and 5-HT and p-ERK1/2 in cerebral cortex in group p-CGS ( P>0.05), and the contents of hippocampal DA and Glu were significantly decreased, the content of 5-HT in cerebral cortex was increased, and the expression of p-ERK1/2 was down-regulated in group p-DMPX ( P<0.05). Conclusion:The mechanism underlying the development of propofol mental dependence may be related to activating adenosine A2A receptors, increasing excitatory neurotransmitters in brain, and thus up-regulating ERK activity in rats.