Aim To investigate the protective effects of echinacoside ( ECH ) on oxidative stress injury in vascular dementia rats. Methods Vascular dementia model was duplicated by means of permanent ligation of bilateral common carotid artery at two times intervals for three days. Biochemical methods was used to detect the GSH, NO, GSH-Px, NOS in each group rat’ s cor-tex and hippocampus. The change of the tissue struc-ture in CA1 area of hippocampus in each group was ob-served and analyzed by microscope after HE staining. Results Compared with sham group, the content of GSH and activity of GSH-Px in the rats of the model group were decreased significantly ( P<0. 01 ) , while the content of NO and activity of NOS were increased obviously (P<0. 05, P <0. 01). Meanwhile, in tis-sue structure of rat’ s hippocampal CA1 area, the num-bers of cells were reduced, cell arrangement was sparse and in disorder, cell form was not intact and cell struc-ture was not normal, cytoplasm, nucleus and cyto-plasm were blurry, nuclei were hyperchromatic and in contraction, and were changed to triangular or irregular shape, lacking nucleoli, and proliferation of glial cells appeared. Compared with the model group, the content of GSH and activity of GSH-Px in the rats of the treat-ment groups were increased significantly ( P<0. 05 , P<0 . 01 ) , while the activity of NOS was decreased ob-viously (P<0. 05, P<0. 01). Meanwhile, in rat tis-sue structure of hippocampal CA1 area, the rat cells in each treatment group were arranged in order, the form of structure was normal, the nuclei were less hyper-chromatic and contracted. Compared with Gal group and sham group, the rats of ECH high dosage group were not different in every part of experiment ( P >0. 05 ) . Conclusion ECH exerts protection on oxida-tive stress injury in vascular dementia rats.

Objective:To design Keap1-tat peptide and explore its neuroprotective role on hipocampal CA1 neuron,as well as the effect on spacial learning and memory function following global cerebral ische-mia.Methods:Adult male Sprague Dawley (SD)rats were subjected to global cerebral ischemia (GCI) by four-vessel occlusion for 1 5 min and randomly divided into five groups:sham,sham+Keap1-tat,is-chemia/reperfusion (I/R),Keap1-tat peptide-and vehicle-administrated groups.For Keap1-tat or vehi-cle groups,the rats were treated with Keap1-tat (30,50,1 00 μg in 5 μL 0.9%saline)or the same vo-lume vehicle by intracerebroventricular injection (icv)30 min prior to ischemia.Cresyl violet staining was used to observe the surviving neurons and 4-hydroxy-2-noneal (4-HNE ) and 8-hydroxy-2′-deox-yguanosine (8-OHdG)immunostaining were used to detect the change of markers response to oxidative stress in hippocampal CA1 region.The spatial learning and memory function of the rats was evaluated using Morris water maze.Results:Compared with sham group,the number of surviving neurons in ische-mia-reperfusion and vehicle groups significantly decreased in the hippocampal CA1 region (P<0.05 ), while administration of Keap1-tat significantly decreased the damage following GCI (P<0.05),and the dose of 50 μg existed the most effective neuroprotective role.Furthermore,immunostaining intensity of 4-HNE and 8-OHdG,markers of oxidative stress damage attenuated by Keap1-tat peptide as compared with vehicle group in CA1 region.Of significant interest,the time of finding underwater platform in Keap1-tat group animals was significantly short,and after removing the platform,the probe time of Keap1-tat group animals in the original quadrant where the platform was significantly increased compared with that of vehi-cle and I/R group animals (P<0.05).Conclusion:Keap1-tat peptide can effectively attenuate neuro-nal damage in hippocampal CA1 region and improve learning and memory function,which might bedue to the attenuation of oxidative stress caused by GCI.

Aim Tostudytheeffectsofechinacoside on striatal and hippocampus extracellular fluid of mono-amine neurotransmitter in Parkinsonˊs disease rat, and discuss the possible mechanism of the ECH effect on brainprotection.Methods Doublepointinjectionof 6-hydroxy dopamine damaged was adopted to make PD model, the corresponding drugs or normal saline were intraperitoneally injected for 4 consecutive weeks, mi-cro-dialysis program in double targets was taken after treatment, the dialysate was injected into HPLC-EDC, and striatal and hippocampus extracellular fluid of DA, DOPAC, HVA, NA, 5-HT levels of each group were measured. Results Compared with control group, striatal and hippocampus extracellular fluid of DA, DOPAC, HVA, NE, 5-HT levels were significantly re-duced in model group ( P <0. 01 ); compared with model group, striatal and hippocampus extracellular fluid of DA, DOPAC, HVA, NE, 5-HT levels were significantly increased in treatment group ( P <0 . 05 , P<0. 01 ) , and the content of five kinds of substances in ECH high dose group was similar to that in MD group.Conclusion ECHcouldincreaseextracellular monoamine neurotransmitters in striatum and hippo-campus, ECH has a therapeutic effect on PD, and echinacoside is possible mechanisms of the brain pro-tective effect of PD rats.

Objective To explore the neuroprotective role of Genistein (GEN) on hippocampal CA1 neurons and the possible mechanism following global cerebral ischemia ( GCI) in rats.Methods Seventy five rats were subjected to global cerebral ischemia ( GCI ) by four-vessel occlusion and randomly divided into five groups , sham, ischemia/reperfusion (I/R), GEN, ICI 182,780 and vehicle groups.Fluoro-Jade B and neuron-specific nuclear-binding protein ( NeuN) staining was used to observe CA 1 neuronal survival .TUNEL was used to detect apoptotic neurons .Spatial learning and memory function of the rats were evaluated by Morris water maze .Results The best dose of neuroprotective role of GEN was 1.0mg/kg body weight.Compared with sham, TUNEL-positive neurons in the hippocampal CA1 region increased significantly in I/R and vehicle groups (P<0.01), while post-treatment with GEN (1.0mg/kg) at 5min after ischemia by tail vein injection decreased markedly (P<0.01).Treatment of 1.0mg/kg GEN markedly attenuated spatial learning and memory deficits of the rats after ischemic insult compared to I /R group.Furthermore, ICI 182,780 significantly abolished the neuroprotective role of GEN (P <0.01).Conclusion The low-dose (1.0mg/kg) GEN significantly attenuates neuronal damage and cognitive deficits following GCI in rats , and the mechanism may be involved in estrogen receptor activity.

Aim To investigate the effects of echina-coside ( ECH ) on the learning and memory capacities and brain level of oxygen free radicals of rats with de-mentia induced by amyloid β-peptide. Methods Six-ty Sprague Dawley rats, weighing (300±10) g, were randomly divided with 10 rats pergroup into 6 groups:sham operated group, model, ECH high dose (40 mg ·kg-1·d-1), ECH middle dose (20 mg· kg-1· d-1), ECH low dose (10 mg·kg-1·d-1) and Hup A (Huperzine A, 0. 02 mg·kg-1·d-1) group. Mor-ris maze tests were conducted for evaluating the learn-ing and memory ability. Content of malondialdehyde (MDA), nitric oxide (NO) and activities of superox-ide dismutase ( SOD) and NO synthase ( NOS) in the hippocampus and cortex were detected. ResultsAβ25-35 induced significant learning and memory im-pairment in the rats. Compared with the rats in model group, those treated with ECH at different doses all manifested alleviation of learning and memory impair-ment ( P<0 . 01 , P<0 . 05 ) . Cotents of MDA of ECH treatment group were obviously decreased, while SOD activities were obviously increased, and significantly reduced the release of NO and NOS in the hippocam-pus and cortex brain tissue ( P <0 . 01 , P <0.05 ) . Conclusion ECH can enhance the learning and mem-ory ability in rats with AD, which is presumably relat-ed to accelerating the cleaning of oxygen free radicals and reducing oxidative stress in brain of AD rats.

Aim To investigate the influence of echi-nacoside ( ECH ) on monoaminergic neurotransmitter extracellular of the hippocampus and cerebral cortex in rat model of Alzheimer′s disease ( AD) , and ultimately to provide a theoretical basis for ECH′s improving the ability of learning and memory. Methods 60 male SD rats were randomly divided into 6 groups with 10 rats in each group : sham operation group, model, ECH groups of low, medium and high doses (10, 20, 40μg ·g-1 ·d-1 ) , and Hup A ( Huperzine A, 0. 02 μg· g-1·d-1) group. The AD rat model was established by abdominal cavity injection with D-galactose and uni-laterally injected with amyloid beta-protein fragment 25-35 ( Aβ25-35 ) into the right hippocampus. Morris wa-ter maze test was used to study the animals′ ability of spatial learning and memory. The synchronous dual-probe dual-channel brain microdialysis sampling tech-nology was applied to collect dialysates from different encephalic areas continuously, and combined with HPLC electrochemical detection were used to measure the extracellular levels of norepinephrine ( NE) , dopa-mine (DA), 5-serotonin (5-HT). Results 1. Com-pared with the sham operation group, the mean escape latency of the model group was significantly prolonged ( P<0. 05 ) , and the time that rats were in the plat-form quadrant was significantly shortened ( P<0. 05 );on the contrary, compared with the model group, the mean escape latency of ECH groups were significantly shortened ( P<0. 05 ) , and the time that rats were in the platform quadrant was significantly extended ( P<0. 05). 2. Compared with the sham operation group, the contents of NE,DA and 5-HT were significantly de-creased in the model group ( P <0. 05 ) . However, compared with the model group , ECH could improve the concentrations of NE, DA, 5-HT in the hippocam-pus and cerebral cortex, and these monoamine levels of the brain regions were restored to near control. Con-clusion ECH can effectively improve the ability of learning and memory of rats with AD, giving a rise to the monoamine neurotransmitter both in hippocampus and cortex, exerting a positive effect on treatment of cognitive dysfunction . The ECH low dose group is sig-nificantly lower than the ECH groups of medium and high doses and Hup A group in improving the ability of learning and memory.

The aim of this study is to investigate the effect of echinacoside (ECH) on cholinergic neurotransmitter extracellular of hippocampus and striatum and its possible mechanisms of neuro-protective effect against vascular dementia rats. In this study brain microdialysis technique combined with HPLC-IMER-ECD (high-performance liquid chromatography-immobilized enzyme reactor-electrochemical detector) was used. The bilateral common carotid arteries occluded in two times operation at 72 h interval for vascular dementia model rats were used and the successful vascular dementia model rats were examined by Morris water maze. The content of acetylcholine (ACh) and choline (Ch) of microdialysate extracellular of hippocampus and striatum was determined by HPLC-IMER-ECD and the AChE activity in the hippocampus was measured. The results showed that the success rate of vascular dementia model was 83.08% after six weeks; the results also showed that echinacoside and galantamine could increase the content of ACh and reduce the content of Ch extracellular of hippocampus and striatum significantly and the AChE activity increased significantly compared with that of the model group. The results suggested that echinacoside could promote the recovery of cholinergic neurotransmitter levels in vascular dementia rats' brain, which may be one of the mechanisms of neuro-protection.

Objective:To investigate the effect of ionizing radiation on the ferroptosis of skin cells and the potential therapeutic strategy of ferroptosis inhibitor Ferrostatin-1 (Fer-1) on irradiated skin cells.Methods:HaCaT cells were pre-treated with Fer-1 before X-ray irradiation. After irradiation, CCK-8 assay and LDH release assay were used to detect cell viability and cell death, flow cytometry was used to detect the lipid peroxidation levels, crystal violet staining assay was used to detect colony forming ability, and the expressions of ferroptosis related proteins ACSL4 and GPX4 were detected by Western blot.Results:The cell viability of HaCaT cells was significantly decreased ( t=5.63, 8.74, P<0.05) and the release of LDH was significantly increased ( t=3.98, 5.08, 9.27, P<0.05) after different doses of X-ray irradiation. The cell viability was improved ( t=5.79, P<0.05) and the release of LDH was reduced ( t=12.36, 11.96, 18.13, 9.96, P<0.05) after the pre-treatment with Fer-1. The lipid peroxidation levels of HaCaT cells were significantly increased ( t=9.59, P<0.05) and the clonogenic survival ability were reduced ( t=4.26, P<0.05) after 10 Gy X-ray irradiation, while Fer-1 pre-treatment reduced ( t=6.48, 17.04, P<0.05) the increase of lipid peroxidation level induced by X-ray irradiation and also effectively restore ( t=3.96, P<0.05) the clonogenic survival ability. The expressions of ACSL4 and GPX4 were decreased after 10 Gy X-ray irradiation, while they recovered to normal level ( t=5.23, 7.16, 4.78, 8.29, 6.43, P<0.05) after the pre-treatment with Fer-1. Conclusions:Ferroptosis inhibitor Fer-1 alleviates the progress of radiation-induced skin injury by inhibiting ferroptosis after ionizing radiation at the cellular level, which provides a potential strategy for the protection of radiation injury.

Objective: To analyze the epidemiological characteristics and genetic characteristics of sapovirus (SaV) in a cluster of schools in Changzhou, so as to provide a reference for the treatment of clustered vomiting and diarrhea events in schools. Methods: The epidemiological data and laboratory test data of sapovirus clusters in Changzhou from 2019 to 2022 were collected and analyzed. Partial VP1 genes of SaV positive samples were amplified and sequenced for phylogenetic analysis. Results: A total of 8 cases of clusters of SaV epidemics were reported in Changzhou City from 2019 to 2022, with 118 reported cases. The total attack rate was 1.47%, and the median of the attack number was 15. There were 6 outbreaks in kindergartens and 2 outbreaks in primary schools, which were reported in the epidemic period from September to December. The main clinical manifestations were vomiting (113 cases, 95.76 %), abdominal pain (39 cases, 33.05%), and diarrhea (16 cases, 13.56%). Among the 8 outbreaks, 17 sample strains were successfully sequenced. 5 outbreaks were GII.3 , and the other 3 outbreaks were GI.1, GI .3 and GII.2. GI and GII were the main genotypes in this area, and GII .3 was the predominant strain. Conclusion SaV is an important pathogen in the clusters of vomiting and diarrhea in schools after the transmission of norovirus. Continuous surveillance of SaV should be carried out to further understand its epidemiological characteristics and genotype distribution, so as to provide scientific basis for the prevention and control of the epidemic in schools.