Objective To study the effects of Wortmannin, inhibitor of PI3K and SB202190, inhibitor of P38 MAPK and PD98059, inhibitor of ERK1/2 on the migration of epidermal growth factor (EGF)-induced vascular smooth muscle cells (VSMCs). Methods There were fives groups in this experiment, including control group, EGF group, PD98059 (PD) group, SB202190(SB) group and Wortnannin (WT) group. The migration rate of the VSMCs was measured by wound healing assay. Results At the 24th hours after wounding, there was obvious migration in EGF group compared to control group. The migration of VSMCs was significantly inhibited in PD group, SB group and WT group compared to the EGF group, but there were no significant difference among three inhibitor groups. At the 30th hours after woun-ding, there was still obvious migration in EGF group compared to control group. The migration of VSMCs was significantly inhibited in the three iuhibitors group compared to the EGF group, and there were significant difference among three inhibitor groups. Furthermore, inhibiting effect on VSMCs in SB group was more obvious compared to PD group and WT group. Conclusion These results suggested that the migra-tion of EGF-induced VSMCs may play a role through PI3K, P38 MAPK and ERKI/2 signal pathways, and the effect of P38 MAPK signal pathway is very important.

Objective To explore the main risk factorrelated to the incidence of chroniobstructive pulmonary disease (COPD) among Chinese people in mainland so ato provide the basifothe decision making on COPD prevention .MethodEighpublished literatureof case-control studieon the risk factoof COPD were collected and analyzed quantitatively and synthetically by the metanalysi;the RevMan 5 .2 software waadopted to perform the consistency tesand calculate the pooled oddradio (OR) value and 95% CI .The risk factorwith the Ovalue＞1 were performed the calculation of population attributable risk pro-portion(PARP) .ResultThe pooled oddradio value,95% CI and PARP were smoking OR= 2 .12(1 .58 -2 .86) ,PARP=28 .16% ;occupational exposure OR=1 .82(1 .04-3 .18) ,PARP=11 .60% ;family history of respiratory disease OR=1 .82(1 .36-2 .44) ,PARP=14 .25% ;coal and biomasfuel focooking and heating OR=3 .29(1 .01-10 .67) ,PARP=41 .29% ;low body masindex OR=2 .58(1 .78-3 .74) ,PARP=5 .71% ;low educational degree OR=1 .24(1 .02 -1 .50) ,PARP=12 .93% ;history of re-currenrespiratory tracinfection during childhood OR= 2 .10 (0 .99 -4 .47 ) ,PARP= 13 .39% ;passitive smoking OR= 1 .00 (0 .89-1 .11) .Conclusion Smoking ,occupational exposure ,family history of respiratory disease ,coal and biomasfuel focooking and heating ,low body masindex ,low educational degree and history of recurrenrespiratory tracinfection during childhood are the risk factorinfluencing the incidence of COPD among Chinese people in mainland .

AIM:The study aimed to explore the effect of curcumin(Cur)on lipopolysaccharide(LPS)-in-duced RAW264.7 cell-derived osteoclasts,together with its underlying mechanism.METHODS:An osteoclast model was established by treating RAW264.7 cells with LPS.The viability of the cells was assessed by CCK-8 assays and osteo-clast formation was evaluated by tartrate-resistant acid phosphatase(TRAP)activity.The levels of reactive oxygen species(ROS),Fe2+,glutathione(GSH),and malondialdehyde(MDA)were examined by biochemical assays.Mitochondrial morphology was assessed by transmission electron microscopy.The mRNA and protein levels of p53,glutathione peroxi-dase 4(GPX4),and solute carrier family 7 member 11(SLC7A11)were determined by RT-qPCR and Western blot,re-spectively.RESULTS:Treatment with LPS successfully induced osteoclasts formation in RAW264.7 cells.The TRAP results showed that compared with the LPS-treated group,the number of osteoclasts and TRAP activity in the curcumin-treated group decreased dose-dependently(P<0.01).Compared with the control group,the LPS+Erastin group showed significantly increased TRAP activity(P<0.01),while after curcumin treatment,the TRAP activity declined in a dose-de-pendent manner(P<0.01).The results of the biochemical tests showed that compared with the control group,the LPS+Erastin group had significantly elevated levels of ROS,Fe2+,and MDA,while the GSH level was significantly reduced(P<0.01),and compared with the LPS+Erastin group,the ROS,Fe2+,and MDA levels in the curcumin group decreased(P<0.01)and GSH levels increased(P<0.01).These effects were all dose-dependent.Transmission electron microscopy showed that compared with the LPS group,the LPS+Erastin group had reduced mitochondrial cristae and increased mem-brane density,while after treatment with curcumin,both these effects were reversed.The RT-qPCR and Western blot re-sults showed that compared with the control group,the mRNA and protein levels of p53 in the LPS+Erastin group were sig-nificantly increased,while those of of SLC7A11 and GPX4 were significantly reduced(P<0.01).After curcumin treat-ment,the p53 mRNA and protein levels were reduced while the levels of SLC7A11 and GPX4 were increased(P<0.01).CONCLUSION:Curcumin can inhibit lipopolysaccharide-induced differentiation of RAW264.7 cells into osteoclasts,and its mechanism may be related to the inhibition of the p53/SLC7A11/GPX4 signaling pathway.