BACKGROUND:Previous studies by the research team have shown that the neuroprotective effect of ginsenoside Rb1 on improving cerebral ischemia-reperfusion injury may be related to the Wnt/β-catenin signaling pathway,but the specific mechanism of action remains unclear.OBJECTIVE:To explore the molecular mechanism of ginsenoside Rb1 in alleviating cerebral ischemia-reperfusion injury in mice.METHODS:100 C57BL/6 mice were randomly divided into four groups.The sham operation group(n=25)did not undergo model establishment.In the cerebral ischemia-reperfusion injury group(n=25),the middle cerebral artery occlusion model was established by thread embolism.In the ginsenoside Rb1 group(n=25),the middle cerebral artery occlusion model was established by thread embolism and ginsenoside Rb1 was intraperitoneally injected every day for 3 days before the establishment.In ginsenoside Rb1+inhibitor group(n=25),the middle cerebral artery occlusion model was established by thread embolism and ginsenoside Rb1 and Wnt/β-catenin signaling pathway inhibitor XAV939 were intraperitoneally injected every day for 3 days before the establishment.Three days after modeling,Zea Longa score and balance beam test were used to evaluate the neurological deficits of mice.TTC staining was used to observe the volume of cerebral infarction.The dry-wet mass method was used to detect the degree of brain edema in mice.The activities of superoxide dismutase and glutathione peroxidase and the concentration of malondialdehyde in the parietal lobe of the ischemic side were detected by colorimetry.The co-expression of microglial marker Iba1 and inducible nitric oxide synthase(or arginase 1)was detected by immunofluorescence.The levels of aquaporin AQP4,inflammatory-related factors,and phosphorylation of Wnt/β-catenin pathway proteins glycogen synthase kinase 3β and β-catenin were detected by western blot assay.The mRNA expression of inflammatory factors was detected by q-PCR.RESULTS AND CONCLUSION:(1)Compared with cerebral ischemia-reperfusion injury group,the neurological deficit symptoms,cerebral infarction foci and brain tissue edema,oxidative stress and inflammatory response of the mice were alleviated;the number of M1 microglia(Iba1 and inducible nitric oxide synthase co-expressed)decreased;the number of M2 microglia(Iba1 and arginase 1 co-expressed)increased;the expression of phosphorylated glycogen synthase kinase 3β and phosphorylated β-catenin protein decreased in ginsenoside Rb1 group.Compared with ginsenoside Rb1 group,the neurological deficit symptoms,cerebral infarction foci and brain tissue edema,oxidative stress and inflammatory response of the mice were aggravated;the number of M1 microglia increased;the number of M2 microglia decreased;the expression of phosphorylated glycogen synthase kinase 3β and phosphorylated β-catenin protein increased in ginsenoside Rb1+inhibitor group.(2)The results indicate that ginsenoside Rb1 can regulate the polarization of microglia to M2 type and alleviate oxidative stress damage and inflammatory response after cerebral ischemia-reperfusion injury.Its mechanism may be related to the nuclear translocation of β-catenin mediated by the Wnt/β-catenin signaling pathway.

Objective To investigate the clinical efficacy of the"dynamic and static combination"approach in the treatment of Hepple Ⅰ-Ⅲ type osteochondral lesions of the talus(OLT),utilizing external ankle shaking,pulling,and poking manipulations in conjunction with ankle brace fixation.Methods A total of 82 patients diagnosed with OLT,who sought treatment at four hospitals between June 2022 and December 2023,were included in the study.Both the experimental and control groups received ankle immobilization using braces through-out the treatment period.The control group was administered Voltaren Emulgel topically twice daily(morning and evening),with each treatment course lasting 30 days,for a total of one course.The experimental group received additional therapeutic intervention involving shaking,pulling,and poking manipulations,conducted twice weekly,with the same duration and number of treatment courses as the control group.Follow-up assessments were scheduled at 2 weeks,4 weeks,and 2 months post-treatment.Outcome measures included the pain rating index(PRI),visual analogue scale(VAS)for pain intensity,current pain intensity(PPI),American Orthopaedic Foot & Ankle Society(AOFAS)ankle and hindfoot scores,proprioceptive function,and the size of OLT.Results During the longitudinal assessment conducted at 2-week,4-week,and follow-up intervals,the experimental group exhibited superior clinical outcomes compared to the control group,with statistically significant decreases in PRI,PPI,and AOFAS scores(all P＜0.05).VAS scores showed progressive improvement over time,with significant intergroup differences observed at both the 4-week and follow-up assessments(P＜0.05).Biomechanical analysis performed post-intervention indicated improved kinematic repositioning accuracy in the experimental group,as reflected by significantly reduced active-passive error angles(P＜0.05).Importantly,measurements of OLT area revealed notable therapeutic effects in the experimental group(P＜0.05),whereas no statistically significant changes were observed in the control group throughout the study period(all P＞0.05).Conclusions Under the guidance of the"dynamic and static combination"concept,the integration of shaking,pulling,and poking manipu-lation with conventional Western medicine-based conservative treatment for OLT demonstrates more pronounced advantages in alleviating pain,improving ankle joint function,restoring proprioception,facilitating lesion recovery,and enhancing overall quality of life.

Objective To investigate the clinical efficacy of the"dynamic and static combination"approach in the treatment of Hepple Ⅰ-Ⅲ type osteochondral lesions of the talus(OLT),utilizing external ankle shaking,pulling,and poking manipulations in conjunction with ankle brace fixation.Methods A total of 82 patients diagnosed with OLT,who sought treatment at four hospitals between June 2022 and December 2023,were included in the study.Both the experimental and control groups received ankle immobilization using braces through-out the treatment period.The control group was administered Voltaren Emulgel topically twice daily(morning and evening),with each treatment course lasting 30 days,for a total of one course.The experimental group received additional therapeutic intervention involving shaking,pulling,and poking manipulations,conducted twice weekly,with the same duration and number of treatment courses as the control group.Follow-up assessments were scheduled at 2 weeks,4 weeks,and 2 months post-treatment.Outcome measures included the pain rating index(PRI),visual analogue scale(VAS)for pain intensity,current pain intensity(PPI),American Orthopaedic Foot & Ankle Society(AOFAS)ankle and hindfoot scores,proprioceptive function,and the size of OLT.Results During the longitudinal assessment conducted at 2-week,4-week,and follow-up intervals,the experimental group exhibited superior clinical outcomes compared to the control group,with statistically significant decreases in PRI,PPI,and AOFAS scores(all P＜0.05).VAS scores showed progressive improvement over time,with significant intergroup differences observed at both the 4-week and follow-up assessments(P＜0.05).Biomechanical analysis performed post-intervention indicated improved kinematic repositioning accuracy in the experimental group,as reflected by significantly reduced active-passive error angles(P＜0.05).Importantly,measurements of OLT area revealed notable therapeutic effects in the experimental group(P＜0.05),whereas no statistically significant changes were observed in the control group throughout the study period(all P＞0.05).Conclusions Under the guidance of the"dynamic and static combination"concept,the integration of shaking,pulling,and poking manipu-lation with conventional Western medicine-based conservative treatment for OLT demonstrates more pronounced advantages in alleviating pain,improving ankle joint function,restoring proprioception,facilitating lesion recovery,and enhancing overall quality of life.

BACKGROUND:Previous studies by the research team have shown that the neuroprotective effect of ginsenoside Rb1 on improving cerebral ischemia-reperfusion injury may be related to the Wnt/β-catenin signaling pathway,but the specific mechanism of action remains unclear.OBJECTIVE:To explore the molecular mechanism of ginsenoside Rb1 in alleviating cerebral ischemia-reperfusion injury in mice.METHODS:100 C57BL/6 mice were randomly divided into four groups.The sham operation group(n=25)did not undergo model establishment.In the cerebral ischemia-reperfusion injury group(n=25),the middle cerebral artery occlusion model was established by thread embolism.In the ginsenoside Rb1 group(n=25),the middle cerebral artery occlusion model was established by thread embolism and ginsenoside Rb1 was intraperitoneally injected every day for 3 days before the establishment.In ginsenoside Rb1+inhibitor group(n=25),the middle cerebral artery occlusion model was established by thread embolism and ginsenoside Rb1 and Wnt/β-catenin signaling pathway inhibitor XAV939 were intraperitoneally injected every day for 3 days before the establishment.Three days after modeling,Zea Longa score and balance beam test were used to evaluate the neurological deficits of mice.TTC staining was used to observe the volume of cerebral infarction.The dry-wet mass method was used to detect the degree of brain edema in mice.The activities of superoxide dismutase and glutathione peroxidase and the concentration of malondialdehyde in the parietal lobe of the ischemic side were detected by colorimetry.The co-expression of microglial marker Iba1 and inducible nitric oxide synthase(or arginase 1)was detected by immunofluorescence.The levels of aquaporin AQP4,inflammatory-related factors,and phosphorylation of Wnt/β-catenin pathway proteins glycogen synthase kinase 3β and β-catenin were detected by western blot assay.The mRNA expression of inflammatory factors was detected by q-PCR.RESULTS AND CONCLUSION:(1)Compared with cerebral ischemia-reperfusion injury group,the neurological deficit symptoms,cerebral infarction foci and brain tissue edema,oxidative stress and inflammatory response of the mice were alleviated;the number of M1 microglia(Iba1 and inducible nitric oxide synthase co-expressed)decreased;the number of M2 microglia(Iba1 and arginase 1 co-expressed)increased;the expression of phosphorylated glycogen synthase kinase 3β and phosphorylated β-catenin protein decreased in ginsenoside Rb1 group.Compared with ginsenoside Rb1 group,the neurological deficit symptoms,cerebral infarction foci and brain tissue edema,oxidative stress and inflammatory response of the mice were aggravated;the number of M1 microglia increased;the number of M2 microglia decreased;the expression of phosphorylated glycogen synthase kinase 3β and phosphorylated β-catenin protein increased in ginsenoside Rb1+inhibitor group.(2)The results indicate that ginsenoside Rb1 can regulate the polarization of microglia to M2 type and alleviate oxidative stress damage and inflammatory response after cerebral ischemia-reperfusion injury.Its mechanism may be related to the nuclear translocation of β-catenin mediated by the Wnt/β-catenin signaling pathway.

Objective : To explore the regulatory mechanism of ginsenoside Rb1 on focal cerebral ischemia-reperfusion injury ( CIRI) ． Methods : A total of 60 C57 / BL mice were randomly divided into 6 groups (n = 10) : shamoperated group ，CIRI model group ，ginsenoside Rb1 low －，medium －，and high-dose group and nimodipine (positive control) group．The surgical method was used to construct the focal CIRI mouse model．The neurological function scores and behavioral tests were performed，and Nissl staining was utilized to detect the number of nissl bodies in the hippocampus．The effect of ginsenoside Rb1 on the molecule expression of the Wnt signaling pathway in the hippocampus was detected by qPCR , Western blot and immunohistochemistry assays．The regulatory mechanism of ginsenoside Rb1 was investigated through molecular docking and co-precipitation assays. Results : Compared with the CIRI model group，the addition of ginsenoside Rb1 reduced the neurological function scores of mice (P＜0. 05) ，shortened the time passing the balance beam (P＜0. 05) ，but increased the time entering the correct arm (P＜0. 05) and the swinging time and climbing time of mice (P ＜0. 05 ) ，indicating that ginsenoside Rb1 could effectively resume the function of the nervous system in mice and improve the behavioral ability of model mice．After ginsenoside Rb1 treatment，axis inhibition protein 2 (Axin2) and glycogen synthase kinase-3 β ( GSK- 3 β) in the hippocampus decreased，whereas the expression of Wnt3a，Wnt1 and β-catenin increased． Conclusion The ginsenoside Rb1 can improve neurological function of the CIRI mouse model and increase the number of Nissl bodies in the hippocampus，which is correlated with the activation of the Wnt signaling pathway，and it may be neuroprotective against focal CIRI during stroke treatment.

Objective To study the protective effect of basic fibroblast growth factor ( bFGF ) on endothelial function and structure of the basilar artery of atherosclerotic rats .Methods A total of forty-eight male adult Wister rats were randomly divided into the normal control , the atherosclerosis ( AS) model and the bFGF treatment groups .The AS model group and the bFGF treatment group were injected with a single dose of vitamin D 3 (6 ×105 IU/kg) and loaded with high fat diet for six consecutive weeks .The bFGF (9.5μg/kg, twice one day) was injection into the abdominal cavity after six weeks in the bFGF treatment group for two weeks , and an identical volume saline was given for the AS model group and the normal control group .After eight weeks , all the rats were sacrificed .The relaxation percentages of the isolated basilar artery in response to acetylcholine ( Ach) were detected and the pathological lesions of them were observed under a light microscope .ELISA and colorimetry assayed the content of serum VEGF and basilar arterial nitric oxide ( NO) .The basilar artery was used for primary culture of both vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs). The influence of bFGF on the proliferation vitality of VECs was measured in vitro with MTT assay.TRITC-phalloidin labeling the cytoskeleton microfilament of VSMCs was observed by laser confocal microscopy .Results The early AS plaques were presented after six weeks by hyper lipid foods .Compared with the AS model group , the relaxation percentage of the isolated basilar artery , the content of both serum VEGF and basilar arterial NO in the bFGF treatment group were obviously increased, but the pathologic injury of the basilar artery was significantly decreased (P<0.05).The proliferation vitality of VECs was obviously increased (P<0.05); the cytoskeleton microfilament of VSMCs was of obviously improvement .Conclusion AS may aggravate the basilar arterial injury , but bFGF may efficiently improve the arterial endothelial function and decrease the pathological lesion of the basilar artery in the AS model rats , which may promote the arterial protective effect .

Objective To observe the sequential ultrastroctural and electrophysiological changes in the sciatic nerve coagulated by a newly-designed microwave antenna. Methods A total of 75 Sprague-Dawley rats were randomly divided into groups A,B and C and irradiated with microwaves at 10,20 or 30 Watts,for 6 seconds to coagulate the left sciatic nerve.Electrophysiological effects and sequential uhrastructural changes were observed on the 0th,2nd,7th,30th and 60th days after coagulation.A static sciatic index was calculated based on measurements of the footprint on the 7th,30thand 60th days after coagulation.Results On the Oth,2nd,7th and 30th days after cpagulation,the static sciatic index,the nerve conduction velocity and the amplitude of the action potentials in groups B and C had decreased significantly compared with those before coagulation.On the 60th day after coagulation.significant recovery was observed in groups A and B,but not in group C.Only mild alteration in uhrastructure was found,and only in group A.The prominent changes in uhrastructure in group B included broken Schwann cell membranes and myelin disintegration.There were severe injuries in group C,including myelin disintegration,cell deformity,coagulative necrosis,axon necrosis,basement membrane necrosis and demyelination.The structure of the sciatic nerve in group B had partially recovered after 60 days,but group C showed no recovery at all. Conclusion Microwave coagulation of a nerve can block its conduction.and even destroy the nerve.Percutaneous microwave coagulation is clinically feasible and call be an alternative treatment for pain.

Objective To study the learning and memory abilities together with the morphological changes in astrocyte and neuron in the hippocampal CA3 area in mice induced by chronic cadmium exposure. Methods Twenty Kunming mice aged 4-5 months were selected by Y-maze and randomly divided into two groups. The cadmium exposed group treated with cadmium (CdCl2,2 mg/kg) by subcutaneous injection,twice a week for 3 consecutive months,and the normal control group were injected with the equal dose of saline. The learning and memory abilities were detected by Y-maze after 3 months of treatment. The structure of astrocytes and neurons in CA3 area of hippocampus were observed under light microscope,and the quantitatively analysis was performed by cell morphometric technique. Results Compared with the control group,learning and memory capacity determined by Y-maze test in the cadmium exposed group were lower (P