The Effect of Different Hyperbaric Oxygen Treatment Time Windows on Neurological Function and Prognosis in Acute Cerebral Infarction

Objective:To observe the effects of different hyperbaric oxygen treatment time windows on the prognosis and neurological function of acute cerebral infarction.Method:160 patients with acute cerebral infarction admitted to Xiangyang Central Hospital in Hubei Province were randomly divided into four groups,each with 40 cases,using a random number table method.According to the 2017 guidelines for the treatment of cerebral infarction,the control group received routine treatment for acute cerebral infarction;On the basis of the control group,patients in Group A received hyperbaric oxygen therapy within 48 hours of onset;Group B patients receive hyperbaric oxygen therapy within 3-6 days of onset;Group C patients receive hyperbaric oxygen therapy within 7-12 days of onset.Observe the efficacy,recurrence,and neurological function recovery of four groups of patients after treatment.Result:There was no statistically significant difference in the National Institutes of Health Stroke Scale(NIHSS)and Barthel Index(BI)scores among the four groups before treatment(P>0.05).There were statistically significant differences in NIHSS and BI scores between 14 and 30 days after treatment and before treatment(F=16.352,27.261,11.899,28.326,P<0.05).At 14 and 30 days after treatment,the NIHSS score in Group A decreased compared to the control group,Group B,and Group C,while the BI score increased compared to the control group,Group B,and Group C,with statistical significance(P<0.05).There was no statistically significant difference in NIHSS and BI scores between Group C and the control group after treatment(P>0.05).After 30 days of treatment,the total effective rate of Group A was higher than that of the control group and Group C,and the difference was statistically significant(X2=6.135,P<0.05).The one-year recurrence rate of Group A and Group B is lower than that of Group C and the control group,and the difference is statistically significant(X2=8.331,P<0.05).There was no statistically significant difference in adverse reactions among the four groups(P>0.05).Conclusion:Patients with acute cerebral infarction who receive hyperbaric oxygen therapy within 48 hours can improve neurological function and reduce the recurrence rate.The efficacy of receiving hyperbaric oxygen therapy within 7-12 days of onset is equivalent to that of not receiving hyperbaric oxygen therapy.

Erythropoietin inhibits ferroptosis and ameliorates neurological function after spinal cord injury

Ferroptosis is one of the critical pathological events in spinal cord injury.Erythropoietin has been reported to improve the recovery of spinal cord injury.However,whether ferroptosis is involved in the neuroprotective effects of erythropoietin on spinal cord injury has not been examined.In this study,we established rat models of spinal cord injury by modified Allen’s method and intraperitoneally administered 1000 and 5000 IU/kg erythropoietin once a week for 2 successive weeks.Both low and high doses of erythropoietin promoted recovery of hindlimb function,and the high dose of erythropoietin led to better outcome.High dose of erythropoietin exhibited a stronger suppressive effect on ferroptosis relative to the low dose of erythropoietin.The effects of erythropoietin on inhibiting ferroptosis-related protein expression and restoring mitochondrial morphology were similar to those of Fer-1(a ferroptosis suppressor),and the effects of erythropoietin were largely diminished by RSL3(ferroptosis activator).In vitro experiments showed that erythropoietin inhibited RSL3-induced ferroptosis in PC12 cells and increased the expression of xCT and Gpx4.This suggests that xCT and Gpx4 are involved in the neuroprotective effects of erythropoietin on spinal cord injury.Our findings reveal the underlying anti-ferroptosis role of erythropoietin and provide a potential therapeutic strategy for treating spinal cord injury.

miR-181b promotes angiogenesis and neurological function recovery after ischemic stroke

Promotion of new blood vessel formation is a new strategy for treating ischemic stroke.Non-coding miRNAs have been recently considered potential therapeutic targets for ischemic stroke.miR-181b has been shown to promote angiogenesis in hypoxia and traumatic brain injury model,while its effect on ischemic stroke remains elusive.In this study,we found that overexpression of miR-181b in brain microvascular endothelial cells subjected to oxygen-glucose deprivation in vitro restored cell prolife ration and enhanced angiogenesis.In rat models of focal cerebral ischemia,ove rexpression of miR-181b reduced infarction volume,promoted angiogenesis in ischemic penumbra,and improved neurological function.We further investigated the molecular mechanism by which miR-181b participates in angiogenesis after ischemic stroke and found that miR-181b directly bound to the 3’-UTR of phosphatase and tensin homolog(PTEN) mRNA to induce PTEN downregulation,leading to activation of the protein kinase B(Akt) pathway,upregulated expression of vascular endothelial growth facto rs,down-regulated expression of endostatin,and promoted angiogenesis.Taken togethe r,these results indicate that exogenous miR-181b exhibits neuroprotective effects on ischemic stro ke through activating the PTEN/Akt signal pathway and promoting angiogenesis.

Influence of ganglioside combined with methylprednisolone sodium succinate on efficacy and neurological function in patients with acute myelitis

BACKGROUND Acute myelitis(AM)can lead to sudden sensory,motor and autonomic nervous dysfunction,which negatively affects their daily activities and quality of life,so it is necessary to explore optimization from a therapeutic perspective to curb the progression of the disease.AIM To investigate the effect of ganglioside(GM)combined with methylprednisolone sodium succinate(MPSS)on the curative effect and neurological function of patients with AM.METHODS First,we selected 108 AM patients visited between September 2019 and September 2022 and grouped them based on treatment modality,with 52 patients receiving gamma globulin(GG)+MPSS and 56 patients receiving GM+MPSS,assigned to the control group(Con)and observation group(Obs),respectively.The therapeutic effect,neurological function(sensory and motor function scores),adverse events(AEs),recovery(time to sphincter function recovery,time to limb muscle strength recovery above grade 2,and time to ambulation),inflammatory factors(IFs)[interleukin(IL)-6,C-reactive protein(CRP),and tumor necrosis factor(TNF)-α]and other data of the two groups were collected for evaluation and comparison.RESULTS The Obs had:(1)A significantly higher response rate of treatment than the Con;(2)Higher scores of sensory and motor functions after treatment that were higher than the baseline(before treatment)and higher than the Con levels;(3)Lower incidence rates of skin rash,gastrointestinal discomfort,dyslipidemia,osteoporosis and other AEs;(4)Faster posttreatment recovery of sphincter function,limb muscle strength and ambulation;and(5)Markedly lower posttreatment IL-6,CRP and TNF-αlevels than the baseline and the Con levels.CONCLUSION From the above,it can be seen that GM+MPSS is highly effective in treating AM,with a favorable safety profile comparable to that of GG+MPSS.It can significantly improve patients’neurological function,speed up their recovery and inhibit serum IFs.

Na^(+)/K^(+)-ATPase:ion pump,signal transducer,or cytoprotective protein,and novel biological functions

Na^(+)/K^(+)-ATPase is a transmembrane protein that has important roles in the maintenance of electrochemical gradients across cell membranes by transporting three Na^(+)out of and two K^(+)into cells.Additionally,Na^(+)/K^(+)-ATPase participates in Ca^(2+)-signaling transduction and neurotransmitter release by coordinating the ion concentration gradient across the cell membrane.Na^(+)/K^(+)-ATPase works synergistically with multiple ion channels in the cell membrane to form a dynamic network of ion homeostatic regulation and affects cellular communication by regulating chemical signals and the ion balance among different types of cells.Therefo re,it is not surprising that Na^(+)/K^(+)-ATPase dysfunction has emerged as a risk factor for a variety of neurological diseases.However,published studies have so far only elucidated the important roles of Na^(+)/K^(+)-ATPase dysfunction in disease development,and we are lacking detailed mechanisms to clarify how Na^(+)/K^(+)-ATPase affects cell function.Our recent studies revealed that membrane loss of Na^(+)/K^(+)-ATPase is a key mechanism in many neurological disorders,particularly stroke and Parkinson's disease.Stabilization of plasma membrane Na^(+)/K^(+)-ATPase with an antibody is a novel strategy to treat these diseases.For this reason,Na^(+)/K^(+)-ATPase acts not only as a simple ion pump but also as a sensor/regulator or cytoprotective protein,participating in signal transduction such as neuronal autophagy and apoptosis,and glial cell migration.Thus,the present review attempts to summarize the novel biological functions of Na^(+)/K^(+)-ATPase and Na^(+)/K^(+)-ATPase-related pathogenesis.The potential for novel strategies to treat Na^(+)/K^(+)-ATPase-related brain diseases will also be discussed.

The ferroptosis activity is associated with neurological recovery following chronic compressive spinal cord injury

Chronic compressive spinal cord injury in compressive cervical myelopathy conditions can lead to rapid neurological deterioration in the early phase,followed by partial self-recovery,and ultimately an equilibrium state of neurological dysfunction.Ferroptosis is a crucial pathological process in many neurodegenerative diseases;however,its role in chro nic compressive spinal cord injury remains unclear.In this study,we established a chronic compressive spinal cord injury rat model,which displayed its most severe behavioral and electrophysiological dysfunction at 4 wee ks and partial recovery at 8 weeks after compression.Bulk RNA sequencing data identified enriched functional pathways,including ferroptosis,presynapse,and postsynaptic membrane activity at both 4 and 8 wee ks following chro nic compressive spinal co rd injury.Tra nsmission electron microscopy and malondialdehyde quantification assay confirmed that ferroptosis activity peaked at 4 weeks and was attenuated at 8 weeks after chronic compression.Ferro ptosis activity was negatively correlated with behavioral score.Immunofluorescence,quantitative polymerase chain reaction,and western blotting showed that expression of the anti-ferroptosis molecules,glutathione peroxidase 4(GPX4) and MAF BZIP transcription factor G(MafG),in neuro ns was suppressed at 4 weeks and upregulated at 8 weeks following spinal co rd compression.There was a positive correlation between the expression of these two molecules,suggesting that they may work together to contribute to functional recovery following chronic compressive spinal cord injury.In conclusion,our study determined the genome-wide expression profile and fe rroptosis activity of a consistently compressed spinal cord at different time points.The results showed that anti-fe rroptosis genes,specifically GPX4 and MafG,may be involved in spontaneous neurological recovery at 8 weeks of chronic compressive spinal cord injury.These findings contribute to a better understanding of the mechanisms underlying chronic compressive spinal cord injury and may help identify new therapeutic targets for compressive cervical myelopathy.

Effects of professional rehabilitation training on the recovery of neurological function in young stroke patients

Young stroke patients have a strong desire to return to the society, but few studies have been conducted on their rehabilitation training items, intensity, and prognosis. We analyzed clinical data of young and middle-aged/older stroke patients hospitalized in the Department of Neurological Rehabilitation, China Rehabilitation Research Center, Capital Medical University, China from February 2014 to May 2015. Results demonstrated that hemorrhagic stroke （59.6%） was the primary stroke type found in the young group, while ischemic stroke （60.0%） was the main type detected in the middle-aged/older group. Compared with older stroke patients, education level and incidence of hyperhomocysteinemia were higher in younger stroke patients, whereas, incidences of hypertension, diabetes, and heart disease were lower. The average length of hospital stay was longer in the young group than in the middle-aged/older group. The main risk factors observed in the young stroke patients were hypertension, drinking, smoking, hyperlipidemia, hyperhomocysteinemia, diabetes, previous history of stroke, and heart disease. The most accepted rehabilitation program consisted of physiotherapy, occupational therapy, speech therapy, acupuncture and moxibustion. Average rehabilitation training time was 2.5 hours/day. Barthel Index and modified Rankin Scale scores were increased at discharge. Six months after discharge, the degree of occupational and economic satisfaction declined, and there were no changes in family life satisfaction. The degrees of other life satisfaction （such as friendship） improved. The degree of disability and functional status improved significantly in young stroke patients after professional rehabilitation, but the number of patients who returned to society within 6 months after stroke was still small.

How does the motor relearning program improve neurological function of brain ischemia monkeys?

The motor relearning program can significantly improve various functional disturbance induced by ischemic cerebrovascular diseases. However, its mechanism of action remains poorly understood. In injured brain tissues, glial fibrillary acidic protein and neurofilament protein changes can reflect the condition of injured neurons and astrocytes, while vascular endothelial growth factor and basic fibroblast growth factor changes can indicate angiogenesis. In the present study, we induced ischemic brain injury in the rhesus macaque by electrocoagulation of the M1 segment of the right middle cerebral artery. The motor relearning program was conducted for 60 days from the third day after model establishment. Immunohistochemistry and single-photon emission CT showed that the numbers of glial fibrillary acidic protein-, neurofilament protein-, vascular endothelial growth factor- and basic fibroblast growth factor-positive cells were significantly increased in the infarcted side compared with the contralateral hemisphere following the motor relearning program. Moreover, cerebral blood flow in the infarcted side was significantly improved. The clinical rating scale for stroke was used to assess neurological function changes in the rhesus macaque following the motor relearning program. Results showed that motor function was improved, and problems with consciousness, self-care ability and balance function were significantly ameliorated. These findings indicate that the motor relearning program significantly promoted neuronal regeneration, repair and angiogenesis in the surroundings of the infarcted hemisphere, and improve neurological function in the rhesus macaque following brain ischemia.

Neural differentiation of human Wharton＇s jelly-derived mesenchymal stem cells improves the recovery of neurological function after transplantation in ischemic stroke rats

Human Wharton＇s jelly-derived mesenchymal stem cells（h WJ-MSCs）have excellent proliferative ability,differentiation ability,low immunogenicity,and can be easily obtained.However,there are few studies on their application in the treatment of ischemic stroke,therefore their therapeutic effect requires further verification.In this study,h WJ-MSCs were transplanted into an ischemic stroke rat model via the tail vein 48 hours after transient middle cerebral artery occlusion.After 4 weeks,neurological functions of the rats implanted with h WJ-MSCs were significantly recovered.Furthermore,many h WJ-MSCs homed to the ischemic frontal cortex whereby they differentiated into neuron-like cells at this region.These results confirm that h WJ-MSCs transplanted into the ischemic stroke rat can differentiate into neuron-like cells to improve rat neurological function and behavior.

Inhibition of inflammatory cytokines after early decompression may mediate recovery of neurological function in rats with spinal cord injury

A variety of inlfammatory cytokines are involved in spinal cord injury and inlfuence the recov-ery of neuronal function. In the present study, we established a rat model of acute spinal cord injury by cerclage. The cerclage suture was released 8 or 72 hours later, to simulate decompres-sion surgery. Neurological function was evaluated behaviorally for 3 weeks after surgery, and tumor necrosis factorα immunoreactivity and apoptosis were quantiifed in the region of injury. Rats that underwent decompression surgery had significantly weaker immunoreactivity of tumor necrosis factorα and signiifcantly fewer apoptotic cells, and showed faster improvement of locomotor function than animals in which decompression surgery was not performed. De-compression at 8 hours resulted in signiifcantly faster recovery than that at 72 hours. These data indicate that early decompression may improve neurological function after spinal cord injury by inhibiting the expression of tumor necrosis factorα.

Neurological function following intra-neural injection of fluorescent neuronal tracers in rats

Fluorescent neuronal tracers should not be toxic to the nervous system when used in long-term labeling. Previous studies have addressed tracer toxicity, but whether tracers injected into an intact nerve result in functional impairment remains to be elucidated. In the present study, we examined the functions of motor, sensory and autonomic nerves following the application of 5% Fluoro-Gold, 4% True Blue and 10% Fluoro-Ruby （5 pL） to rat tibial nerves via pressure injection. A set of evaluation methods including walking track analysis, plantar test and laser Doppler perfusion imaging was used to determine the action of the fluorescent neuronal tracers. Additionally, nerve pathology and ratio of muscle wet weight were also observed. Results showed that injection of Fluoro-Gold significantly resulted in loss of motor nerve function, lower plantar sensibility, increasing blood flow volume and higher neurogenic vasodilatation. Myelinated nerve fiber degeneration, unclear boundaries in nerve fibers and high retrograde labeling efficacy were observed in the Fluoro-Gold group. The True Blue group also showed obvious neurogenic vasodilatation, but less severe loss of motor function and degeneration, and fewer labeled motor neurons were found compared with the Fluoro-Gold group. No anomalies of motor and sensory nerve function and no myelinated nerve fiber degeneration were observed in the Fluoro-Ruby group. Experimental findings indicate that Fluoro-Gold tracing could lead to significant functional impairment of motor, sensory and autonomic nerves, while functional impairment was less severe following True Blue tracing. Fluoro-Ruby injection appears to have no effect on neurological function.

Electroacupuncture treatment improves motor function and neurological outcomes after cerebral ischemia/reperfusion injury

Electroacupuncture(EA)has been widely used for functional restoration after stroke.However,its role in post-stroke rehabilitation and the associated regulatory mechanisms remain poorly understood.In this study,we applied EA to the Zusanli(ST36)and Quchi(LI11)acupoints in rats with middle cerebral artery occlusion and reperfusion.We found that EA effectively increased the expression of brain-derived neurotrophic factor and its receptor tyrosine kinase B,synapsin-1,postsynaptic dense protein 95,and microtubule-associated protein 2 in the ischemic penumbra of rats with middle cerebral artery occlusion and reperfusion.Moreover,EA greatly reduced the expression of myelin-related inhibitors Nogo-A and NgR in the ischemic penumbra.Tyrosine kinase B inhibitor ANA-12 weakened the therapeutic effects of EA.These findings suggest that EA can improve neurological function after middle cerebral artery occlusion and reperfusion,possibly through regulating the activity of the brain-derived neurotrophic factor/tyrosine kinase B signal pathway.All procedures and experiments were approved by the Animal Research Committee of Shanghai University of Traditional Chinese Medicine,China(approval No.PZSHUTCM200110002)on January 10,2020.

Bone marrow mesenchymal stem cell therapy regulates gut microbiota to improve post-stroke neurological function recovery in rats

BACKGROUND As a cellular mode of therapy,bone marrow mesenchymal stem cells(BMSCs)are used to treat stroke.However,their mechanisms in stroke treatment have not been established.Recent evidence suggests that regulation of dysregulated gut flora after stroke affects stroke outcomes.AIM To investigate the effects of BMSCs on gut microbiota after ischemic stroke.METHODS A total of 30 Sprague-Dawley rats were randomly divided into three groups,including sham operation control group,transient middle cerebral artery occlusion(MCAO)group,and MCAO with BMSC treatment group.The modified Neurological Severity Score(mNSS),beam walking test,and Morris water maze test were used to evaluate neurological function recovery after BMSC transplantation.Nissl staining was performed to elucidate on the pathology of nerve cells in the hippocampus.Feces from each group of rats were collected and analyzed by 16s rDNA sequencing.RESULTS BMSC transplantation significantly reduced mNSS(P<0.01).Rats performed better in the beam walking test in the BMSC group than in the MCAO group(P<0.01).The Morris water maze test revealed that the BMSC treatment group exhibited a significant improvement in learning and memory.Nissl staining for neuronal damage assessment after stroke showed that in the BMSC group,cells were orderly arranged with significantly reduced necrosis.Moreover,BMSCs regulated microbial structure composition.In rats treated with BMSCs,the abundance of potential short-chain fatty acid producing bacteria and Lactobacillus was increased.CONCLUSION BMSC transplantation is a potential therapeutic option for ischemic stroke,and it promotes neurological functions by regulating gut microbiota dysbiosis.

Stellate ganglion block reduces inflammation and improves neurological function in diabetic rats during ischemic stroke

Diabetes mellitus is an independent risk factor for ischemic stroke.Both diabetes mellitus and stroke are linked to systemic inflammation that aggravates patient outcomes.Stellate ganglion block can effectively regulate the inflammatory response.Therefore,it is hypothesized that stellate ganglion block could be a potential therapy for ischemic stroke in diabetic subjects.In this study,we induced diabetes mellitus in rats by feeding them a high-fat diet for 4 successive weeks.The left middle cerebral artery was occluded to establish models of ischemic stroke in diabetic rats.Subsequently,we performed left stellate ganglion block with 1%lidocaine using the percutaneous posterior approach 15 minutes before reperfusion and again 20 and 44 hours after reperfusion.Our results showed that stellate ganglion block did not decrease the blood glucose level in diabetic rats with diabetes mellitus but did reduce the cerebral infarct volume and the cerebral water content.It also improved the recovery of neurological function,increased 28-day survival rate,inhibited Toll like receptor 4/nuclear factor kappa B signaling pathway and reduced inflammatory response in the plasma of rats.However,injection of Toll like receptor 4 agonist lipopolysaccharide 5 minutes before stellate ganglion block inhibited the effect of stellate ganglion block,whereas injection of Toll like receptor 4 inhibitor TAK242 had no such effect.We also found that stellate ganglion block performed at night had no positive effect on diabetic ischemic stroke.These findings suggest that stellate ganglion block is a potential therapy for diabetic ischemic stroke and that it may be mediated through the Toll like receptor 4/nuclear factor kappa B signaling pathway.We also found that the therapeutic effect of stellate ganglion block is affected by circadian rhythm.

Effects of butyphthalide + rt-PA intravenous thrombolysis on the DWI characteristics, coagulation function and neurological function in patients with acute cerebral infarction

Objective: To investigate the effects of butyphthalide + alteplase (rt-PA) intravenous thrombolysis on the diffusion-weighted imaging (DWI) characteristics, coagulation function and neurological function in patients with acute cerebral infarction. Methods: The patients with acute cerebral infarction who were admitted to our hospital between April 2015 and October 2018 and with the onset time 4.5 hours were selected and divided into the observation group receiving butyphthalide + rt-PA intravenous thrombolysis and the control group receiving rt-PA intravenous thrombolysis by random number table. The differences in DWI parameter apparent diffusion coefficient (ADC), coagulation function indexes and neurological function indexes were compared between the two groups. Results: At 7 and 14 days after treatment, the ADC values of both groups were significantly increased, and the ADC values of the observation group were significantly higher than those of the control group;at 7 days after treatment, the prothrombin time (PT) and activated partial thromboplastin time (APTT) levels in both groups were significantly prolonged whereas fibrinogen (FIB), D-dimer (D-D), platelet activating factor (PAF), P-selectin, von Willebrand factor (vWF), neuron-specific enolase (NSE), S100B protein (S100B), malondialdehyde (MDA) and endothelin-1 (ET-1) contents were significantly decreased, and the APTT and PT levels in the observation group were significantly shorter than those in the control group whereas FIB, D-D, PAF, P-selectin, vWF, NSE, S100B, MDA and ET-1 contents were significantly lower than those in the control group. Conclusion: Butyphthalide + rt-PA intravenous thrombolysis can improve the DWI characteristics, coagulation function and neurological function of patients with acute cerebral infarction.

Effect of argatroban on neurological function in patients with acute cerebral infarction and its mechanism

Objective: Analyze the effect of argatroban on neurological function in patients with acute cerebral infarction and explore its possible mechanisms. Methods: From August 2015 to August 2017, 140 patients with acute cerebral infarction who were admitted to the Department of Neurology in our hospital were divided into a control group and an observation group according to the lottery method, with 70 cases in each group. Patients in the conventional group received routine treatment. Patients in the treatment group received routine treatment plus argatroban. The changes of neurological function, coagulation function and inflammatory factors were observed in the two groups. Result: Before treatment, there were no significant differences in neurological function parameters, coagulation function indexes and inflammatory factors between the two groups. After treatment, the neurological function indexes NT-proBNP, NPY and S-100β levels, coagulation function index FIB level, inflammatory factor indicators MMP-9, Lp-PLA2 and Hcy, vascular endothelial function index ET levels decreased, coagulation Functional indicators PT, TT and APTT are both elevated, and NO and CGRP levels are elevated. The levels of NT-proBNP, NPY and S-100β, FIB level, MMP-9, Lp-PLA2 and Hcy, ET levels in the treatment group were lower than those in the conventional group, while the levels of PT, TT and APTT levels, and NO and CGRP levels were higher than the conventional group. Conclusion: Argatroban treatment can significantly improve neurological function in patients with acute cerebral infarction. The possible mechanism is to improve coagulation function, vascular endothelial function and relieve inflammatory stress response.

Effects of Maixuekang Capsules Combined with Edaravone on Serum MMP-9, S-100β Protein Levels and Neurological Functions in Patients with Hemorrhagic Cerebral Infarction

OBJECTIVE: To investigate the effects of Maixuekang Capsules combined with edaravone on serum matrix metalloproteinase-9(MMP-9), S-100β protein levels and neurological functions in patients with hemorrhagic cerebral infarction. METHOSDS: A total of 76 patients with hemorrhagic cerebral infarction treated in the First Affiliated Hospital of Henan University of Science and Technology from January 2017 to May 2018 were selected and were randomly divided into treatment group and control group, with 38 patients in each group. The control group was given edaravone, and the treatment group was given Maixuekang Capsules on the basis of the control group. The clinical efficacy, serum MMP-9 and S-100β protein levels, neurological function recovery, activity of daily living and incidence rate of adverse reactions were compared between the 2 groups. RESULTS: The total effective rate of the treatment group was 92.11%, which was higher than 71.05% of the control group(P < 0.05); the National Institutes of Health Stroke Scale(NIHSS) score in the 2 groups decreased(P < 0.05), and the Activity of Daily Living Scale(ADL) score increased(P < 0.05), the improvement of the above 2 scores in the treatment group were better than those in the control group(P < 0.05); the level of MMP-9 was gradually decreasing in the 2 groups, on the 7th day, 14 th day after treatment, and the levels of MMP-9 decreased significantly(P < 0.05), and the treatment group was lower than the control group at all time points(P < 0.05); on the 3rd day after treatment, the levels of S-100β protein in the 2 groups increased significantly(P < 0.05); on the 7th day, 14 th day after treatment, the levels of S-100β protein in the two groups decreased significantly(P < 0.05), and the treatment group was significantly lower than the control group(P < 0.05); there was no significant difference in incidence rate of adverse reactions between 7.89% in the control group and 5.26% in the treatment group(P > 0.05). CONCLUSION: The combination of Maixuekang Capsules and edaravone is effective in treating hemorrhagic cerebral infarction, and it can significantly improve neurological function defect and daily living ability, reduce serum MMP-9 and S-100β protein levels, and has higher safety.

Effects of Intravenous Thrombolytic Therapy with Alteplase on Neurological Function,Coagulation Function and Serum Inflammatory Factors in Patients with Acute Cerebral Infarction

Objective:To investigate the effects of intravenous thrombolysis therapy with alteplase on neurological function,coagulation function and serum inflammatory factors in patients with acute cerebral infarction.Methods:A total of 96 patients with acute cerebral infarction admitted to our hospital from September 2017 to October 2019 were randomly divided into two groups,with 48 patients in each group.The control group(n=48)received routine treatment,and the observation group received intravenous thrombolysis therapy with alteplase on the basis of routine treatment.The neurological deficit score,prothrombin time(PT),activated partial thromboplastin time(APTT),tumor necrosis factor-a level(TNF-α),and high-sensitivity C-reactive protein(hs-CRP)were compared between the two groups after 15 days of treatment.Results:After treatment,NIHSS scores in both groups were lower than those before treatment;PT levels were increased,while APTT,TNF-αand hs-CRP levels were all decreased in both groups,and the changes in the observation group were greater than those in the control group,with statistically significant difference(P<0.05).Conclusions:Intravenous thrombolysis therapy with alteplase can improve the neurological function,coagulation function and serum levels of inflammatory factors in patients with acute cerebral infarction,which is worthy of clinical application.

Effects of Yinxingdamo Injection Combined with Oxiracetam Capsule on Cognitive Function and Neurological Deficit in Patients with Acute Cerebral Infarction

OBJETTIVE: To observe the effects of Yinxingdamo Injection combined with oxiracetam capsule on cognitive function and neurological deficit in patients with acute cerebral infarction. METHODS: A total of 76 patients with acute cerebral infarction were randomly divided into observation group and control group, with 38 patients in each group. Patients in the control group were treated with conventional western medicine and oxiracetam capsules while patients in the observation group were given Yinxingdamo injection intravenous drip treatment on the basis of the same treatment. After 4 weeks of treatment, the cognitive function of the two groups before and after treatment was observed [Simple Intelligence Scale(MMSE Score), Montreal Cognitive Assessment Scale(MoCA Score)], Neurological Deficit [Chinese Stroke Scale(CSS Score), Daily Life Activity ability(ADL score)], free radical biochemical indicators [malondialdehyde(MDA), oxide dismutase(SOD)] changes, and statistical effects of two groups. RESULTS: After treatment, the total effective rate of the observation group was 92.1%, which was significantly higher than 73.7% of the control group(P < 0.05). The MMSE score and MoCA score of the two groups were significantly increased after treatment(P < 0.05), and the MMSE score and MoCA score inobservation group were significantly increased after treatment than the control group(P < 0.05). The CSS scores of the two groups were significantly decreased after treatment(P < 0.05), and the ADL scores were significantly increased(P < 0.05). The improvement of CSS score and ADL score in the observation group were significantly better than those in the control group(P < 0.05), and serum MDA levels were significantly decreased in both groups after treatment(P < 0.05), and SOD levels were significantly increased(P < 0.05), and the improvement of MDA and SOD levels in the observation group was significantly better than that in the control group group(P < 0.05). CONCLUSION: Yinxingdamo injection combined with oxiracetam capsule can effectively inhibit the oxygen free radical reaction injury in patients with acute cerebral infarction, and significantly improve the symptoms of cognitive dysfunction and neurological deficit in patients. Its curative effect is exact and worthy of clinical application.

Deferoxamine improves neurological function in a rat model of experimental spinal cord injury

A rat model of spinal cord injury was established using modified Allen＇s method and treated with the ferric iron-chelating agent, deferoxamine. Hematoxylin-eosin, Nissl and Perl＇s Prussian blue staining, at 7 14 days following spinal cord injury, showed that following deferoxamine treatment, glial cells proliferation increased significantly, nerve cell morphology was improved and hemosiderin was significantly reduced in the injury region. At 1 56 days following injury, Basso, Beattie, and Bresnahan Locomotor Rating Scale scores were increased, while latencies of somatosensory-evoked potentials and motor-evoked potentials were decreased. Results demonstrate that deferoxamine can promote neurological functional recovery after experimental spinal cord injury in rats.