AIM:To investigate the role of lipocalin 2(LCN2)in lipopolysaccharide(LPS)-induced microg-lia polarization in mice and to elucidate the potential mechanisms involving the P38 mitogen-activated protein kinase(MAPK)pathway.METHODS:BV2 microglia were treated with LPS to induce M1 polarization,and short hairpin RNA(shRNA)and exogenous LCN2 protein were used to silence or overexpress LCN2 in BV2 cells.BV2 microglia were cul-tured in vitro and divided into the following groups:control,LPS(100 μg/L),LPS+sh-NC,LPS+sh-LCN2,and LPS+LCN2(1 mg/L).Flow cytometry was used to detect the number of CD16/32+and CD206+T cells.Western blot and RT-qP-CR were employed to measure the protein and mRNA levels of P38 MAPK,PGC-1α,and PPARγ to assess the effects of LCN2 on LPS-induced BV2 cell polarization and the P38 MAPK pathway.Additionally,the P38 MAPK pathway inhibitor SB203580 was used to treat LPS or LCN2-induced cells.The cells were categorized into control,LPS,LPS+LCN2(1 mg/L),LPS+SB203580(50 nmol/L),and LPS+LCN2+SB203580 groups.ELISA was used to measure inflammatory factor levels,Western blot was used to detect M1/M2 marker proteins,and Western blot and RT-qPCR were used to analyze pro-tein and mRNA expressions in the P38 MAPK pathway.RESULTS:LPS significantly increased LCN2 expression in BV2 cells(P＜0.05)and induced M1 polarization(P＜0.01).Silencing LCN2 reduced LCN2 expression and M2 polarization in LPS-induced BV2 cells(P＜0.01),increased M1 polarization(P＜0.01),and inhibited activation of the P38 MAPK-PGC-1α-PPARγ pathway(P＜0.05).Conversely,exogenous addition of LCN2 promoted M2 polarization in LPS-induced BV2 cells and activated the P38 MAPK pathway(P＜0.05).The use of a P38 MAPK pathway inhibitor further confirmed that LCN2 modulates LPS-induced microglia polarization through the P38 MAPK pathway.CONCLUSION:LCN2 inhibits LPS-mediated M1 polarization of BV2 microglia by activating the P38 MAPK pathway,thereby playing a protective role in neuroinflammatory responses.

AIM:To investigate the role of lipocalin 2(LCN2)in lipopolysaccharide(LPS)-induced microg-lia polarization in mice and to elucidate the potential mechanisms involving the P38 mitogen-activated protein kinase(MAPK)pathway.METHODS:BV2 microglia were treated with LPS to induce M1 polarization,and short hairpin RNA(shRNA)and exogenous LCN2 protein were used to silence or overexpress LCN2 in BV2 cells.BV2 microglia were cul-tured in vitro and divided into the following groups:control,LPS(100 μg/L),LPS+sh-NC,LPS+sh-LCN2,and LPS+LCN2(1 mg/L).Flow cytometry was used to detect the number of CD16/32+and CD206+T cells.Western blot and RT-qP-CR were employed to measure the protein and mRNA levels of P38 MAPK,PGC-1α,and PPARγ to assess the effects of LCN2 on LPS-induced BV2 cell polarization and the P38 MAPK pathway.Additionally,the P38 MAPK pathway inhibitor SB203580 was used to treat LPS or LCN2-induced cells.The cells were categorized into control,LPS,LPS+LCN2(1 mg/L),LPS+SB203580(50 nmol/L),and LPS+LCN2+SB203580 groups.ELISA was used to measure inflammatory factor levels,Western blot was used to detect M1/M2 marker proteins,and Western blot and RT-qPCR were used to analyze pro-tein and mRNA expressions in the P38 MAPK pathway.RESULTS:LPS significantly increased LCN2 expression in BV2 cells(P＜0.05)and induced M1 polarization(P＜0.01).Silencing LCN2 reduced LCN2 expression and M2 polarization in LPS-induced BV2 cells(P＜0.01),increased M1 polarization(P＜0.01),and inhibited activation of the P38 MAPK-PGC-1α-PPARγ pathway(P＜0.05).Conversely,exogenous addition of LCN2 promoted M2 polarization in LPS-induced BV2 cells and activated the P38 MAPK pathway(P＜0.05).The use of a P38 MAPK pathway inhibitor further confirmed that LCN2 modulates LPS-induced microglia polarization through the P38 MAPK pathway.CONCLUSION:LCN2 inhibits LPS-mediated M1 polarization of BV2 microglia by activating the P38 MAPK pathway,thereby playing a protective role in neuroinflammatory responses.

Objective To investigate the standard hemicraniectomy and temporal muscleresection therapeutic in the treatment effect of massive cerebral infarction patients .Methods Looking back at my hospital from February 2006 to October 2012 massive cerebral infarction patients ,30 cases were divided into two groups ,namely simple drug treatment(group A) ,the standard hemicrani-ectomy combined temporal muscleresection treatment (group B) .Followed up two groups of patients and deaths neurological deficit situation after treatment ,compared two groups of patients in hospital mortality and one month after treatment ,neurological impair-ment score .Results After treatment ,the patient midline reply ,mortality ,cure rates three aspects ,group B than the group A .Con-clusion Standard hemicraniectomy combined temporal muscle resection in the treatment can reduce the mortality rate of patients w ith active .