AIM:To explore the impact of chronic stress on postoperative cognitive dysfunction in rats and to elucidate the mechanistic link to histone deacetylase 2(HDAC2).METHODS:A repeated social defeat stress model and a prolonged isoflurane anesthesia model were established in mice.The rats were randomly assigned to four groups:control(Ctrl)group,isoflurane anesthesia(Iso)group,chronic social defeat stress(RSDS)group,and chronic social de-feat stress combined with isoflurane anesthesia(RSDS+Iso)group.Anxiety-like behaviors were evaluated using the social avoidance test and the novelty-suppressed feeding test.Cognitive function was assessed through the novel object recogni-tion test and the Morris water maze.Plasma corticosterone levels were measured via enzyme-linked immunosorbent assay(ELISA).Primary hippocampal neurons were isolated from fetal mouse hippocampi and classified into four groups:con-trol group,chronic stress combined with prolonged isoflurane anesthesia(Cort+Iso)group,CAY-10683 intervention(CAY),and CAY-10683 treatment(CAY+Cort+Iso)group.Cell viability was determined using CCK-8 assay,and pro-tein expression levels of brain-derived neurotrophic factor(BDNF)and HDAC2 were analyzed by Western blot.RE-SULTS:The RSDS mouse model was successfully established,with ELISA results indicating a significant increase in plasma corticosterone levels in mice subjected to chronic stress combined with prolonged isoflurane anesthesia.Behavioral assessments and Western blot analyses revealed that mice exposed to prolonged isoflurane anesthesia following chronic stress showed marked declines in cognitive function and hippocampal BDNF protein expression levels.Additionally,chronic stress significantly elevated HDAC2 protein expression in the hippocampi of mice undergoing prolonged isoflurane anesthesia.Treatment with an HDAC2 inhibitor reduced HDAC2 protein expression in primary hippocampal neurons sub-jected to chronic stress combined with prolonged isoflurane anesthesia,concurrently increasing BDNF protein expression levels.CONCLUSION:Chronic stress significantly worsens postoperative cognitive dysfunction induced by prolonged isoflurane anesthesia,associated with increased HDAC2 protein expression in the hippocampus.Inhibition of HDAC2 ef-fectively counteracts the reduction in BDNF,a protein crucial for cognitive function,caused by the combination of chronic stress and prolonged isoflurane anesthesia.

AIM:To explore the impact of chronic stress on postoperative cognitive dysfunction in rats and to elucidate the mechanistic link to histone deacetylase 2(HDAC2).METHODS:A repeated social defeat stress model and a prolonged isoflurane anesthesia model were established in mice.The rats were randomly assigned to four groups:control(Ctrl)group,isoflurane anesthesia(Iso)group,chronic social defeat stress(RSDS)group,and chronic social de-feat stress combined with isoflurane anesthesia(RSDS+Iso)group.Anxiety-like behaviors were evaluated using the social avoidance test and the novelty-suppressed feeding test.Cognitive function was assessed through the novel object recogni-tion test and the Morris water maze.Plasma corticosterone levels were measured via enzyme-linked immunosorbent assay(ELISA).Primary hippocampal neurons were isolated from fetal mouse hippocampi and classified into four groups:con-trol group,chronic stress combined with prolonged isoflurane anesthesia(Cort+Iso)group,CAY-10683 intervention(CAY),and CAY-10683 treatment(CAY+Cort+Iso)group.Cell viability was determined using CCK-8 assay,and pro-tein expression levels of brain-derived neurotrophic factor(BDNF)and HDAC2 were analyzed by Western blot.RE-SULTS:The RSDS mouse model was successfully established,with ELISA results indicating a significant increase in plasma corticosterone levels in mice subjected to chronic stress combined with prolonged isoflurane anesthesia.Behavioral assessments and Western blot analyses revealed that mice exposed to prolonged isoflurane anesthesia following chronic stress showed marked declines in cognitive function and hippocampal BDNF protein expression levels.Additionally,chronic stress significantly elevated HDAC2 protein expression in the hippocampi of mice undergoing prolonged isoflurane anesthesia.Treatment with an HDAC2 inhibitor reduced HDAC2 protein expression in primary hippocampal neurons sub-jected to chronic stress combined with prolonged isoflurane anesthesia,concurrently increasing BDNF protein expression levels.CONCLUSION:Chronic stress significantly worsens postoperative cognitive dysfunction induced by prolonged isoflurane anesthesia,associated with increased HDAC2 protein expression in the hippocampus.Inhibition of HDAC2 ef-fectively counteracts the reduction in BDNF,a protein crucial for cognitive function,caused by the combination of chronic stress and prolonged isoflurane anesthesia.

Objective　To investigate the effect of fatty acid binding protein 7 （FABP7） on blood-brain barrier （BBB） permeability in cerebral ischemia/reperfusion （I/R） rats and the mechanisms involved. Methods　BBB cell model was established by co-culture of rat brain microvascular endothelial cells and astrocytes. The BBB model of I/R injury was established by using oxygen-glucose deprivation and reoxygenation （OGD/R） method. This model was treated with the FABP7 recombinant protein （rh-FABP7） alone or together with S7155.ENDOHM instrument，Western blotting and flow cytometry were used to determine the transendothelial electrical resistance （TEER），FABP7，TJ and matrix metalloproteinase （MMP） protein levels，and apoptosis. The rat brain I/R model was established，and rh-FABP7 was injected intraperitoneally. The neurological function score，wet and dry weight method，and Evans blue staining were used to determine the neurological function，brain water content，and BBB permeability of rats. Results　FABP7 overexpression reversed the OGD/R-induced down-regulation of TEER，and FABP7 and TJ protein expression，as well as the up-regulation of MMP2/9 expression and apoptosis （P<0.05）. S7155 treatment promoted the effect of FABP7 on MMP2/9 and TJ protein levels，TEER，and apoptosis （P<0.05）. Moreover，FABP7 overexpression reversed the I/R-induced increase of neural function score，brain water content，and BBB permeability and decrease of FABP7 protein level in rats（P<0.05）. Conclusion　FABP7 alleviated the damage of brain I/R to BBB integrity by inhibiting MMP2/9.

Objective To clarify the distribution of etiological factors in elderly versus non-elderly outpatients with vertigo/dizziness for optimizing the diagnosis and therapy. Methods We retrospectively analyzed data of outpatients with vertigo/dizziness in Shaanxi Provincial People's Hospital from April 2015 to April 2017 and conducted diagnoses in accordance with the currently wide-accepted diagnostic criteria. Results A total of 3 356 patients with chief complains of vertigo/dizziness were recruited ,and their top seven etiological factors were benign paroxysmal positional vertigo (n＝ 1 320 ,39.3%) ,chronic subjective dizziness(n＝680 ,20.3%) ,vestibular migraine(n＝386 ,11.5%) ,posterior circulation ischemia (n＝213 ,6.4%) ,Meniere's disease (n ＝ 138 ,4.1%) ,vestibular neuritis (n＝ 121 ,3.6%) ,and vestibular paroxysmia(n＝76 ,2.3%). The top four etiological factors for the elderly patients (n＝1 255)were benign paroxysmal positional vertigo (n＝ 498 ,39.7%) ,chronic subjective dizziness (n＝ 279 ,22.2%) ,posterior circulation ischemia(n＝161 ,12.8%) ,and vestibular migraine(n＝73 ,5.8%) ;while the top four etiological factors for non-elderly patients (n＝ 2 101)were benign paroxysmal positional vertigo (n＝ 822 ,39.1%) , chronic subjective dizziness(n＝401 ,19.1%) ,vestibular migraine(n＝313 ,14.9%) ,and vestibular neuritis(n＝105 ,5.0%). The detection rate in elderly patients versus non-elderly patients was significantly higher in chronic subjective dizziness (22.2% vs.19.1%,P＝ 0.032 )and in posterior circulation ischemia (12.8%vs.2.5%,P＝0.000) ,and was significantly lower in vestibular neuritis (1.3% vs.5.0%,P＝ 0.000 ) ,in vestibular migraine(5.8% vs.19.4%,P ＝ 0.000)and in other causes (1.0% vs.2.7%,P ＝ 0.002) . Conclusions The ratio of posterior circulation ischemia is markedly higher in elderly outpatients than in non-elderly outpatients ,whereas the ratios of vestibular migraine and vestibular neuritis in elderly patients are lower than in non-elderly outpatients.