Objective To investigate the correlation between apathy and imaging markers in pa-tients with aCSVD.Methods A total of 143 patients diagnosed with aCSVD and hospitalized in the Department of Neurology of the First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology from August 2023 to August 2024 were continu-ously included as the study objects.According to MAES,they were divided into an apathetic group(MAES score＞14,68 cases)and a non-apathetic group(MAES score ≤14,75 cases).The clinical data and imaging markers were compared between the two groups.Results The apathetic group had significantly older age and larger ratio of hypertension,but shorter years of education and lower MAES score than the non-apathetic group(P＜0.05,P＜0.01).The apathetic group also had notably higher Fazekas score of white matter hyperintensity(WMH),larger recent small sub-cortical infarct(RSSI),lacunar infarct(LI),and perivascular space(PVS)in the basal ganglia and the centrum semiovale,more obvious cerebral atrophy and cerebral microbleed(CMB),and high-er total imaging burden score when compared with the non-apathetic group(P＜0.01).In the aCSVD patients,the MAES score was positively correlated with WMH Fazekas score,RSSI,LI,basal ganglia PVS,centrum semiovale PVS,cerebral atrophy,CMB,and total imaging burden score(P＜0.01).WMH Fazekas score was an independent risk factor for apathy in the aCSVD patients(OR=2.218,95％CI:1.343-3.664,P=0.002).Conclusion The higher the score of ima-ging markers in patients with aCSVD,the more severe the apathy.

Objective: To investigate the molecular mechanisms and pathways of action of total flavonoids of Dracocephalum moldavica L.(TFDM) in treating vascular cognitive impairment(VCI) based on network pharmacology and in vivo animal experiments. Methods : The swiss target prediction database, literature, and PubChem were used to screen the active components and action targets of TFDM. The online mendelian inheritance in man(OMIM) and GeneCards databases were utilized to screen for possible VCI targets. Venny software was used to obtain the intersection target of TFDM and VCI. The search tool for recurring instances of neighbouring genes(String) database and Cytoscape software was used to construct the PPI network. The database for annotation, visualization and integrated discovery(DAVID) database was utilized to screen for the kyoto encyclopedia of genes and genomes(KEGG) pathway and gene ontology(GO) enrichment analyses to explore the molecular mechanism and signaling pathway of TFDM for VCI. 24 rats were divided into Sham, Model, Donepezil, and TFDM groups. Except for the Sham group, the VCI model was created using modified bilateral common carotid artery ligation. After continuous gavage for 21 days, the Morris water maze test was used to evaluate the spatial learning and memory ability of rats. Hematoxy-lineosin(HE) staining was used to observe the pathological changes in the hippocampal CA1 and cortex region of the animals and immunohistochemistry detection of zonula occludens-1(ZO-1) content in the brains of the rats. Western blot was used to detect nuclear factor kappa-B p65(NF-κB p65) and tumor necrosis factor-α(TNF-α) in rat brains. Results : A total of 39 active ingredients of TFDM were screened, 209 corresponding targets, 10 417 gene targets of VCI, and 193 intersecting targets. According to the results of the GO enrichment of function analysis, TFDM could improve the response of reactive oxygen species and metabolic processes of reactive oxygen species, etc. KEGG pathway enrichment analysis suggested that TFDM might regulate TNF, IL-17 signing pathway, etc. The results of animal experiments showed that TFDM improved learning and memory while reduced pathological damage in the brains of VCI rats. In addition, TFDM upregulated the positive expression of ZO-1 and downregulated the protein levels of TNF-α and NF-κB p65(P<0.05). Conclusion TFDM can improve the cognitive function of VCI through multi-components and multi-targets, and its key mechanism may be related to inhibiting TNF-α/NF-κB p65 signaling pathway,reducing neuroinflammation,and improvement of blood-brain barrier permeability.

Objective To investigate the correlation between apathy and imaging markers in pa-tients with aCSVD.Methods A total of 143 patients diagnosed with aCSVD and hospitalized in the Department of Neurology of the First Affiliated Hospital of Baotou Medical College,Inner Mongolia University of Science and Technology from August 2023 to August 2024 were continu-ously included as the study objects.According to MAES,they were divided into an apathetic group(MAES score＞14,68 cases)and a non-apathetic group(MAES score ≤14,75 cases).The clinical data and imaging markers were compared between the two groups.Results The apathetic group had significantly older age and larger ratio of hypertension,but shorter years of education and lower MAES score than the non-apathetic group(P＜0.05,P＜0.01).The apathetic group also had notably higher Fazekas score of white matter hyperintensity(WMH),larger recent small sub-cortical infarct(RSSI),lacunar infarct(LI),and perivascular space(PVS)in the basal ganglia and the centrum semiovale,more obvious cerebral atrophy and cerebral microbleed(CMB),and high-er total imaging burden score when compared with the non-apathetic group(P＜0.01).In the aCSVD patients,the MAES score was positively correlated with WMH Fazekas score,RSSI,LI,basal ganglia PVS,centrum semiovale PVS,cerebral atrophy,CMB,and total imaging burden score(P＜0.01).WMH Fazekas score was an independent risk factor for apathy in the aCSVD patients(OR=2.218,95％CI:1.343-3.664,P=0.002).Conclusion The higher the score of ima-ging markers in patients with aCSVD,the more severe the apathy.

Objective To investigate the neuroprotective effect and mechanism of glycosides of Cistanche(GCs)on cerebral ischemia reperfusion injury(CIRI)in rats.Methods Forty-eight male Wistar rats were divided randomly into Sham,Model,GCs,and Nim groups.A rat model of focal CIRI was established by middle cerebral artery occlusion.Neurological function was scored using the Zea-Longa scoring method.The sensory and motor abilities of rats in each group were evaluated by sticker removal,balance beam,and open field tests.The area of cerebral infarction was detected by 2,3,5-triphenyltetrazolium chloride(TTC)staining,Nissl staining was used to observe the morphology of nerve cells,and terminal deoxynucleotidyl transferase dUTP nick end labeling was used to detect apoptosis of nerve cells.Expression levels of the apoptosis-related proteins B-cell lymphoma-2(Bcl-2),Bcl-2 associated X(Bax),and cysteine aspartic protease-3(Caspase-3)were detected by immunohistochemical staining and Western blot.Results Compared with the Sham group,the neurological deficit score was significantly increased(P＜0.05)and the times to remove stickers and passing the balance beam were significantly increased(P＜0.05),motor ability was decreased,infarct size was increased,the number of neurons was decreased,and the number of apoptotic cells was increased after CIRI.Bax and Caspase-3 expression were significantly increased(P＜0.05)and Bcl-2/Bax was significantly decreased(P＜0.05).Compared with the Model group,GCs improved the behavioral performance of CIRI model rats,reduced the infarct size,inhibited cell apoptosis,down-regulated the expression of Bax and Caspase-3(P＜0.05),and up-regulated the expression of Bcl-2/Bax(P＜0.05).Conclusions GCs have a neuroprotective effect on CIRI,and may play a role in inhibiting cell apoptosis by regulating the expression of the apoptosis-related factors Bax,Bcl-2,and Caspase-3.

Objective To investigate the neuroprotective effect and mechanism of glycosides of Cistanche(GCs)on cerebral ischemia reperfusion injury(CIRI)in rats.Methods Forty-eight male Wistar rats were divided randomly into Sham,Model,GCs,and Nim groups.A rat model of focal CIRI was established by middle cerebral artery occlusion.Neurological function was scored using the Zea-Longa scoring method.The sensory and motor abilities of rats in each group were evaluated by sticker removal,balance beam,and open field tests.The area of cerebral infarction was detected by 2,3,5-triphenyltetrazolium chloride(TTC)staining,Nissl staining was used to observe the morphology of nerve cells,and terminal deoxynucleotidyl transferase dUTP nick end labeling was used to detect apoptosis of nerve cells.Expression levels of the apoptosis-related proteins B-cell lymphoma-2(Bcl-2),Bcl-2 associated X(Bax),and cysteine aspartic protease-3(Caspase-3)were detected by immunohistochemical staining and Western blot.Results Compared with the Sham group,the neurological deficit score was significantly increased(P＜0.05)and the times to remove stickers and passing the balance beam were significantly increased(P＜0.05),motor ability was decreased,infarct size was increased,the number of neurons was decreased,and the number of apoptotic cells was increased after CIRI.Bax and Caspase-3 expression were significantly increased(P＜0.05)and Bcl-2/Bax was significantly decreased(P＜0.05).Compared with the Model group,GCs improved the behavioral performance of CIRI model rats,reduced the infarct size,inhibited cell apoptosis,down-regulated the expression of Bax and Caspase-3(P＜0.05),and up-regulated the expression of Bcl-2/Bax(P＜0.05).Conclusions GCs have a neuroprotective effect on CIRI,and may play a role in inhibiting cell apoptosis by regulating the expression of the apoptosis-related factors Bax,Bcl-2,and Caspase-3.