To explore the effects and processes of various hesperidin(HP)dosages on atherosclero-sis(AS)in rabbits caused by high-fat diet in conjunction with anhydrous ethanol arterial damage.A total of twenty-five healthy male rabbits,six months of age,were chosen,given a week to accli-mate and feed,and then randomly assigned to five groups:the model group,the control group,and the groups receiving low,middle,and high doses of HP.The control group received normal feed during the experiment;the model group received high-fat feed for 30 days,after which the common carotid artery was perfused with anhydrous ethanol to create a pathological model of AS;the HP low,middle,and high dose groups received high-fat feed continuously for 30 days based on the model group,with 100,150,and 200 mg/kg of HP added to the diets,respectively.The blood cell counts,including white blood cells(WBC),lymphocytes(lym),monocytes(Mon),red blood cells(RBC),hemoglobin concentration(HGB),platelet count(PLT),and granulocytes were measured using hematology analyzer.The serum total cholesterol(TC),triglycerides(TG),low density lipo-protein cholesterol(LDL-C),and high-density lipoprotein cholesterol(HDL-C)were analyzed u-sing biochemical analyzer.An ELISA kit was used to measure the expression of inflammatory factors and the level of oxidative factors,while a blood cell analyzer was used to measure the quan-tity of blood cells and a biochemical analyzer was used to measure the level of four kinds of blood lipids.At the end of the test,the test rabbits were sacrificed to take carotid arteries for pathological tissue sections HE,Oil Red O and Masson staining to observe the structure of the wall with lipid infiltration and other conditions.The results indicated a significant increase in body weight in the model group compared to the HP dose group(P＜0.01).In comparison to the model group,HP in-tervention significantly reduced the levels of WBC,Mon,PLT,and the percentage of Gran(P＜0.01).Additionally,HP intervention significantly decreased serum inflammatory cytokines,inclu-ding TG,TC,and LDL-C,while increasing HDL-C levels(P＜0.01).The plasma levels of TNF-αand IL-1 decreased significantly following HP intervention(P＜0.01),whereas the level of IL-10 increased significantly(P＜0.01).Furthermore,SOD activity was significantly higher(P＜0.01)and MDA content was significantly lower(P＜0.01)after HP intervention.Histological examina-tion revealed that HP intervention significantly reduced lipid deposition in tubular walls,inflamma-tory cell infiltration,and the extent of elastic fiber damage.These results suggest that HP may at-tenuate atherosclerosis in rabbits by modulating lipid levels,inflammatory factors,and oxidative stress.

To explore the effects and processes of various hesperidin(HP)dosages on atherosclero-sis(AS)in rabbits caused by high-fat diet in conjunction with anhydrous ethanol arterial damage.A total of twenty-five healthy male rabbits,six months of age,were chosen,given a week to accli-mate and feed,and then randomly assigned to five groups:the model group,the control group,and the groups receiving low,middle,and high doses of HP.The control group received normal feed during the experiment;the model group received high-fat feed for 30 days,after which the common carotid artery was perfused with anhydrous ethanol to create a pathological model of AS;the HP low,middle,and high dose groups received high-fat feed continuously for 30 days based on the model group,with 100,150,and 200 mg/kg of HP added to the diets,respectively.The blood cell counts,including white blood cells(WBC),lymphocytes(lym),monocytes(Mon),red blood cells(RBC),hemoglobin concentration(HGB),platelet count(PLT),and granulocytes were measured using hematology analyzer.The serum total cholesterol(TC),triglycerides(TG),low density lipo-protein cholesterol(LDL-C),and high-density lipoprotein cholesterol(HDL-C)were analyzed u-sing biochemical analyzer.An ELISA kit was used to measure the expression of inflammatory factors and the level of oxidative factors,while a blood cell analyzer was used to measure the quan-tity of blood cells and a biochemical analyzer was used to measure the level of four kinds of blood lipids.At the end of the test,the test rabbits were sacrificed to take carotid arteries for pathological tissue sections HE,Oil Red O and Masson staining to observe the structure of the wall with lipid infiltration and other conditions.The results indicated a significant increase in body weight in the model group compared to the HP dose group(P＜0.01).In comparison to the model group,HP in-tervention significantly reduced the levels of WBC,Mon,PLT,and the percentage of Gran(P＜0.01).Additionally,HP intervention significantly decreased serum inflammatory cytokines,inclu-ding TG,TC,and LDL-C,while increasing HDL-C levels(P＜0.01).The plasma levels of TNF-αand IL-1 decreased significantly following HP intervention(P＜0.01),whereas the level of IL-10 increased significantly(P＜0.01).Furthermore,SOD activity was significantly higher(P＜0.01)and MDA content was significantly lower(P＜0.01)after HP intervention.Histological examina-tion revealed that HP intervention significantly reduced lipid deposition in tubular walls,inflamma-tory cell infiltration,and the extent of elastic fiber damage.These results suggest that HP may at-tenuate atherosclerosis in rabbits by modulating lipid levels,inflammatory factors,and oxidative stress.

BACKGROUND:Alzheimer's disease is a degenerative neurological disorder characterized primarily by cognitive impairment.Acupuncture is a kind of traditional Chinese medicine therapy for treating Alzheimer's disease,but its mechanism is not yet clear. OBJECTIVE:To observe the effects of electroacupuncture with"Zhi San Zhen"on the Notch signaling pathway,β-amyloid protein(Aβ)and synaptic plasticity in 5xFAD mice. METHODS:Sixteen male,6-month-old 5xFAD mice,SPF-grade,were randomly divided into the electroacupuncture with"Zhi San Zhen"group(electroacupuncture group)and the model group,with eight mice in each group.Eight SPF-grade,male,6-month-old C57BL/6 mice were used as the wild control(wild)group.The electroacupuncture group received electroacupuncture with"Zhi San Zhen"intervention,5 times a week for 4 consecutive weeks.The model group and the wild group did not receive electroacupuncture intervention.The Morris water maze was used to preliminarily assess their learning and memory abilities.Thioflavin S staining was performed to detect Aβ plaque deposition.Western blot and real-time quantitative polymerase chain reaction(RT-qPCR)were used to measure the expression levels of transmembrane receptor protein Notch-1,Notch 1 intracellular domain(NICD),hairy and enhancer of split 1(Hes 1),hairy and enhancer of split 5(Hes 5),synaptophysin(SYN),postsynaptic density protein-95(PSD-95),and Aβ. RESULTS AND CONCLUSION:Compared with the model group,the wild group and the electroacupuncture group showed shortened escape latency,increased platform crossing times,and longer target quadrant dwell time(P<0.05).Compared with the wild group,the model group had significantly increased deposition of Aβ plaques,while electroacupuncture with"Zhi San Zhen"inhibited the deposition of Aβ plaques in the hippocampus of 5xFAD mice(P<0.05).Compared with the wild group,the model group had decreased mRNA levels of SYN,PSD-95,Notch 1,NICD,Hes 1,and Hes 5 in the hippocampal tissue of mice,and increased mRNA levels of Aβ(P<0.05).Electroacupuncture with"Zhi San Zhen"increased the mRNA levels of SYN,PSD-95,Notch 1,NICD,Hes 1,and Hes 5 in the hippocampal tissue,and decreased the mRNA level of Aβ(P<0.05).Compared with the Wild group,the model group had decreased protein expression levels of SYN,PSD-95,Notch 1,NICD,Hes 1,and Hes 5 in the hippocampal tissue of mice,and increased protein expression levels of Aβ(P<0.05).Electroacupuncture with"Zhi San Zhen"upregulated the protein expression levels of SYN,PSD-95,Notch 1,NICD,Hes 1,and Hes 5,and inhibited the protein expression of Aβ(P<0.05).To conclude,electroacupuncture with"Zhi San Zhen"can improve the learning and memory abilities of 5xFAD mice,possibly by inhibiting the deposition of Aβ protein and activating the Notch signaling pathway in the hippocampus to enhance synaptic plasticity.

Objective To analyze the effects of mild traumatic brain injury ( mTBI) on functional brain network parameters and to study the properties of small world of patients. Methods Ten patients with mild traumatic brain injury and 13 healthy controls matched by age and sex were collected from the Ninth People's Hospital Affiliated to Medical College of Shanghai Jiao Tong University. Resting functional magnetic resonance images of all subjects were collected. Functional networks were constructed and brain network properties were analyzed. Results The brain injury group and the healthy control group had small world at-tributes in the selected sparseness range. The global efficiency of patients with mTBI patients was significantly reduced compared to healthy control group (0. 174±0. 141 vs 0. 184±0. 062),t=2. 417,P=0. 025),and the shortest path length was increased compared to healthy control group (0. 797±0. 930 vs 0. 734±0. 488),t=-2. 083,P=0. 048). Conclusion The functional brain network of patients with mTBI patients has small world attributes,and the parameters of functional brain network of patients have changed.

Aim To study the effect of Macrophage colony-stimulating factor(M-CSF) on MMP-9 in RAW 264.7 cell and explore the relationship between atherosclerosis caused by M-CSF and the activity of MMP-9. Methods Gelatin zymography analysis was used to investigate the effect of M-CSF and PD98059 on the activity of MMP-9 in cultured RAW 264.7 cell.Western blot was used to study the effect of M-CSF and PD98059 on the express of p-ERK1/2 in cultured RAW 264.7 cell. Results The enzyme activity of MMP-9 was significantly increased after 24-hour M-CSF treatment.Meanwhile, M-CSF upregulated the expression of p-ERK1/2. Pre-treatment with PD98059 blocked partly the increased expression of p-ERK1/2 and the activity of MMP-9 induced by M-CSF. Conclusion M-CSF can induce the secretion of MMP9 in RAW 264.7 cell, which may be mediated by the phosphorylation of ERK1/2.