Migraine is a recurrent chronic nervous system disease, the pathogenesis of which has not yet been fully clear. The disease has high incidence, recurrence and disability, seriously affecting the quality of life of patients, and bringing serious economic burden to society. At present, domestic specific therapeutic drugs are scarce and have serious side effects, which make the clinical treatment effect very limited. In recent years, with the further research on migraine, specific drugs for migraine treatment have been found, which bring more choices for the treatment of acute attack of migraine. At the same time, it also brings more hope to the preventive treatment of migraine. This article summarizes a large number of clinical trials on the treatment of migraine drugs by reviewing relevant literatures at home and abroad, systematically evaluates the safety, effectiveness and tolerance of these drugs in migraine treatment, and provides more help for migraine drug treatment research.

Objective:To investigate the effect of P2X4R silencing on 6-hydroxydopamine (6-OHDA) induced Parkinson's disease (PD) cell model and its mechanism. Methods:(1) According to the 6-OHDA concentrations, the SH-SY5Y cells were divided into 0 μmol/L 6-OHDA group, 50 μmol/L 6-OHDA group, 100 μmol/L 6-OHDA group, and 150 μmol/L 6-OHDA group. CCK-8 was used to detect the cell survival rate, Western blotting was used to detect the P2X4R protein expression, and real time quantitative RT-PCR was used to detect the P2X4R mRNA expression. The optimal concentration of 6-OHDA was selected to induce PD cell model. (2) SH-SY5Y cells at logarithmic phase were transfected with P2X4R siRNA lentiviral plasmids of different sequences (P2X4R-siRNA540, P2X4R-siRNA792, and P2X4R-siRNA1401) and nonsense sequence normal control plasmid (NC-siRNA), respectively (P2X4R-siRNA540 group, P2X4R-siRNA792 group, P2X4R-siRNA1401 group, and NC-siRNA group); the P2X4R mRNA and protein expressions were detected by real time quantitative RT-PCR and Western blotting, and the P2X4R siRNA sequence with the best silencing effect was screened to establish P2X4R silencing cell line. (3) The PD cells induced by the optimal concentration of 6-OHDA were transfected by P2X4R-siRNA enjoying the best silencing effect, NC-siRNA, and P2X4R antagonist CORM-2 (PD+P2X4R-siRNA group, PD+NC-siRNA group, and PD+CORM-2 group); CCK-8 and flow cytometry were used to detect the survival rate and apoptosis rate of cells in each group, and Western blotting was used to detect the protein expressions of connexin (PANX1), toll-like receptor (TLR)-2, Caspase-3 and cleaved Caspase-3. (4) The PANX1 or TLR-2 over-expression plasmids (pCMV3-PANX1 and pCMV3-TLR2), and negative control plasmid (pCMV3-NCV) were transfected into cells from the PD+P2X4R-siRNA group (PD+P2X4R-siRNA+pCMV3-PANX1 group, PD+P2X4R-siRNA+pCMV3-TLR2 group, and PD+P2X4R-siRNA+pCMV3-NCV group); CCK-8 and flow cytometry were used to detect the survival rate and apoptosis rate of cells in each group; Western blotting was used to detect the TLR-2, Caspase-3 and cleaved Caspase-3 protein expressions. Results:(1) As compared with that in the 0 μmol/L 6-OHDA group, the cell survival rate in 50, 100, and 150 μmol/L 6-OHDA groups was significantly decreased in a dose-dependent manner, and the P2X4R protein and mRNA expression levels were significantly increased in a dose-dependent manner ( P<0.05); among them, 100 mol/L 6-OHDA was the most suitable concentration to induce PD cell model. (2) As compared with those in the NC-siRNA group, the P2X4R mRNA and protein expressions in P2X4R-siRNA540 group, P2X4R-siRNA792 group, and P2X4R-siRNA1401 group were significantly decreased ( P<0.05); P2X4R mRNA and protein expressions were the lowest in the P2X4R-siRNA540 group. (3) As compared with PD+NC-siRNA group, the PD+P2X4R-siRNA group and PD+CORM-2 group had significantly increased survival rate, significantly decreased apoptosis rate, and statistically decreased Caspase-3, cleaved Caspase-3, PANX1 and TLR-2 protein expression levels ( P<0.05). (4) As compared with PD+P2X4R-siRNA+pCMV3-NCV group, the TLR2 protein expression in PD+P2X4R-siRNA+pCMV3-PANX1 group was significantly lower ( P<0.05); as compared with PD+P2X4R-siRNA+pCMV3-NCV group, PD+P2X4R-siRNA+pCMV3-TLR2 group had significantly increased cell survival rate, significantly decreased apoptosis rate, and significantly decreased Caspase-3 and cleaved Caspase-3 protein expressions ( P<0.05). Conclusion:P2X4R silencing can significantly improve the survival rate of PD cell model induced by 6-OHDA, reduce apoptosis and expressions of apoptosis related proteins (Caspase-3 and cleaved Caspase-3), and play a neuroprotective role, whose mechanism may be related to PANX1/TLR-2 signal pathway.

OBJECTIVE： To systematically evaluate the effects of Shenqi fuzheng injection combined with conventional chemotherapy on the immune function of patients with advanced non-small cell lung cancer （NSCLC）， and provide evidence-based reference for clinical medication. METHODS： Retrieved from Cochrane Library， PubMed， Medline， Embase， CNKI， Wanfang database， VIP and CBM， Shenqi fuzheng injection combined with conventional chemotherapy （trial group） versus conventional therapy （control group） for advanced NSCLC were collected. After literature screening， data extraction and quality evaluation with Cochrane system evaluator manual 5.1.0 risk evaluation tool， Meta-analysis was performed by using Rev Man 5.3 statistical software. RESULTS： A total of 16 literatures were included， involving 1 324 cases. Results of Meta-analysis showed that there were no statistical significance in the difference of objective remission rate （ORR） [RR＝1.14， 95％CI（0.91，1.43）， P＝0.25] and the level of  CD8+ [MD＝－1.26，95％CI（－4.10， 1.59），P＝0.39] between 2 groups. The levels of CD3+ [MD＝17.48， 95％CI（13.40， 21.56）， P＜0.000 01 ]， CD4+[MD＝12.26， 95％CI（8.39 16.13）， P＜0.000 01]， CD4+/CD8+ [MD＝0.33，95％CI（0.27， 0.39），P＜0.000 01] and the percentage of NK cells [MD＝9.33， 95％CI（5.72， 12.94）， P＜0.000 01] in trial group were significantly higher than control group. Results of subgroup analysis for medication duration of Shenqi fuzheng injection showed that after 1-14 d treatment of Shenqi fuzheng injection， the levels of CD3+ [MD＝17.11， 95％CI（12.37 ，23.17），P＜0.000 01]， CD4+[MD＝13.28，95％CI（8.33， 18.23），P＜0.000 01]， CD4+/CD8+[MD＝0.36，95％CI（0.28，0.43），P＜0.000 01] and the percentage of NK cells [MD＝12.06，95％CI（7.52，16.61），P＜0.000 1] in trial group were significantly higher than control group. After 21 d treatment of Shenqi fuzheng injection， the levels of CD3+[MD＝14.88， 95％CI（7.51，22.26），P＜0.000 01]， CD4+[MD＝10.56，95％CI（5.57，15.56），P＜0.000 01]， CD8+[MD＝3.02， 95％CI（1.80， 4.23），P＜0.000 01]， CD4+/CD8+[MD＝0.29，95％CI（0.23， 0.35），P＜0.000 01] and the percentage of NK cells [MD＝5.58，95％CI（2.49， 8.67），P＝0.000 4] in trial group were significantly higher than control group. There was no statistical significance in the level of CD8+ between 2 groups after 7-14 d treatment of Shenqi fuzheng injection [MD＝－4.26，95％CI（－12.60， 4.09），P＝0.32]. The incidence of leukopenia， nausea and vomiting， and renal dysfunction in trial group were significantly lower than control group. There was no statistical significance in the incidence of hemoglobin decreased and thrombocytopenia between 2 groups. The results of publication bias showed that there was a greater possibility of publication bias in this study. CONCLUSIONS： Shenqi fuzheng injection combined with conventional chemotherapy may improve the immune function of patients with advanced NSCLC and improve the safety after chemotherapy. But more large-scale， milltiple-center and high-quality RCT are needed to validate this conclusion.

AIM: To study the protective effect and mechanism of rosuvastatin on cerebral ischemia-reperfusion injury. METHODS: (1) Cerebral infarction and OGD/R cell models were established to detect the effects of different concentrations of rosuvastatin on cell proliferation and apoptosis; (2) Different concentrations of rosuvastatin were used to treat OGD/R cell models and to observe rosuvastatin effects on cell morphology and expression and localization of UCP2-SIRT3 in cells; (3) UCP2 silent cell line was constructed to observe cell mitochondrial morphology and expression and localization of TOMM20 and SIRT3 molecules in cells, and to study the channels and mechanisms that play a protective role of rosuvastatin in OGD/R cell model; (4) The mitochondrial membrane potential, mitochondrial gene PGC1, Drp1 and Opa1 expression were detected to study the protective effect of rosuvastatin on mitochondria. RESULTS: (1) Rosuvastatin of different concentrations could significantly reduce OGD/R cell apoptosis and increase cell survival rate; (2) Rosuvastatin exerted cell protection by affecting the expression of UCP2 and SIRT3 in cells, thereby protecting cells from OGD/R injury; (3) Rosuvastatin affected the expression of TOMM20 by regulating UCP2, increased mitochondrial transmembrane transport and energy metabolism, enhanced mitochondrial function, and improved cell state and reduced apoptosis. CONCLUSION: Rosuvastatin inhibits mitochondrial damage of OGD/R cells by regulating UCP2/SIRT pathway, thereby exerting neuron protection.