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 evaluate the value of fMRI guided brain surgery for the lesions in or around Broca's area.Methods Forty-three patients with lesions in or adjacent to the Broca's area were studied.fMRI imaging was obtained by BOLD technique with the tasks of reciting.Fiber tract imaging of white matter was obtained by DTI technique.All functional imaging and anatomic imaging were transferred to neuronavigation system.The technique of direct cortical stimulation was used to validate the language cortex in fMRI.The lesions were resected in microscope.Results Broca's area activation was detected in 38 cases..The distance between the fMRI peak and direct cortical stimulation was rated as overlapping (<1 cm diatance) in 25 cases and neighbouring (<2 cm diatance) in 11 cases.Total lesion resection was achieved in 17 cases, subtotal resection in 14 cases, and partial resection in 12 cases.Postoperative neurological functions were improved in 8 cases, unchanged in 31 cases, and temporary worsen in 4 cases.Conclusions The identification of the Broca's area by reciting task in fMRI is sensitive and precise.The fMRI is helpful to decrease the side effect injury in the brain surgery for the lesions in or around the Broca's area.

Objective To investigate the cortex gray matter configuration in amnestic mild cognitive impairment(aMCI)patients using MRI technology, FMRIB software library(FSL)and Freesurfer software.Methods Twenty aMCI patients and 20 normal control subjects were recruited and studied. They were matched by age, sex and education. All the patients and healthy volunteers underwent MRI scan using SEMENTS trio 3.0 T MRI. The subtile three-dimensional brain images were obtained using high resolution scanning technique. The imaging data was processed and analyzed with FSL and Freesurfer software. The cortex gray matter density and thickness in different brain areas of aMCI patients and normal control subjects were calculated and compared using statistic analysis. Results Compared to that in the controls, cortex gray matter density in the aMCI patients showed remarkable decreases in left frontal lobe, temporal lobe,parietal lobe, and slight decrease in right thalamus, temporal lobe and island lobe; For cortex thickness,aMCI patients showed significant decreases in left anterior cingulate gyrus((2. 19 ±0. 24)mm), inferior parietal lobe((2. 27 ± 0. 15)mm), bilateral parahippocampal gyrus((2. 03 ± 0. 15),(2. 04 ±0. 17)mm), precentral gyrus((2. 20 ± 0. 11),(2. 31 ± 0. 19)mm), postcentral gyrus((1.88 ± 0. 11),(1.82 ± 0. 09)mm), superior frontal gyrus((2. 42 ± 0. 34),(2. 40 ± 0. 28)mm), middle frontal gyrus ((2.31±0.31),(2.33 ±0.29)mm), supramarginal gyrus((2.53 ±0.33),(2.55 ±0.23)mm),temporal pole((3.41 ±0.68),(3.30 ±0.56)mm)and transverse temporal gyrus((2.04 ±0. 12),(2. 01 ± 0. 11)mm; t = 2. 13-3.75, P ＜ 0. 05), no significant changes in the other areas(t = 0. 09-1.88, P ＞ 0. 05). Conclusions Our results suggest that there are significant changes in gray matter configuration in cortex of aMCl patients. The changes of cortical thickness is earlier than the changes of gray matter density.

Objective To study cortical thickness of the occipital lobe in children with ametropic amblyopia by using MRI technique and the FreeSurfer software.MethOds Nine children with ametropic amblyopia were included in the amblyopic group and 8 normal children were included in the control group.All the children underwent brain MRI on the Siemens Avanto 1.5 T scanner.For the cortical thickness analysis,3-demensional MPRAGE images were collected and analyzed with FreeSurfer software package.Cortical thickness of related regions in the occipital lobe (including the cuneus,later occipital,lingual,and pericalcarine gyri) were recorded and compared. Results The cortical thickness of the lingual,pericalcarine gyri on the left hemisphere and the cuneus,lateraloccipital,lingual gyri on the right hemisphere in amblyopic group were lower than the control group (P＜0.05). Conclusion Morphological changes existed in the occipital lobe in ametropic amblyopic children.The analysis technique with the FreeSurfer package has a potential value in the clinical application.