Cardiovascular diseases， a group of major non-infectious diseases， are characterized by high morbidity and mortality， significantly influencing patients' quality of life. Hence， it is imperative to discover a secure and efficacious treatment approach. As a form of programmed cell death， autophagy has been demonstrated to be associated with the pathogeneses of hypertension， diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， atherosclerosis， and other cardiovascular disorders. It serves as one of the potential targets for the clinical intervention in cardiovascular diseases by traditional Chinese medicine （TCM）. Autophagy exerts dual regulatory effects on the occurrence and development of cardiovascular diseases， and its specific effect predominantly depends on the extent of autophagy and the pathological stage of diseases. Recent studies have confirmed that TCM can prevent and treat cardiovascular diseases by directly regulating autophagy or interacting with oxidative stress， inflammation， and apoptosis under the regulation of autophagy， exhibiting the unique advantages of multiple targets， multiple components， and mild adverse reactions. This article reviews the experimental research progress in the role of autophagy and the intervention by active components and compound prescriptions of TCM and Chinese patent medicines in common cardiovascular diseases （such as diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， and atherosclerosis） in recent years and summarizes the research shortcomings， providing a theoretical basis and strategies for the clinical treatment of cardiovascular diseases.

Cardiovascular diseases， a group of major non-infectious diseases， are characterized by high morbidity and mortality， significantly influencing patients' quality of life. Hence， it is imperative to discover a secure and efficacious treatment approach. As a form of programmed cell death， autophagy has been demonstrated to be associated with the pathogeneses of hypertension， diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， atherosclerosis， and other cardiovascular disorders. It serves as one of the potential targets for the clinical intervention in cardiovascular diseases by traditional Chinese medicine （TCM）. Autophagy exerts dual regulatory effects on the occurrence and development of cardiovascular diseases， and its specific effect predominantly depends on the extent of autophagy and the pathological stage of diseases. Recent studies have confirmed that TCM can prevent and treat cardiovascular diseases by directly regulating autophagy or interacting with oxidative stress， inflammation， and apoptosis under the regulation of autophagy， exhibiting the unique advantages of multiple targets， multiple components， and mild adverse reactions. This article reviews the experimental research progress in the role of autophagy and the intervention by active components and compound prescriptions of TCM and Chinese patent medicines in common cardiovascular diseases （such as diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， and atherosclerosis） in recent years and summarizes the research shortcomings， providing a theoretical basis and strategies for the clinical treatment of cardiovascular diseases.

BACKGROUND:Targeted therapy based on nuclear transcription factor kappa B signaling pathway to explore neuroinflammation is increasingly worth exploring,and the advantages of Chinese medicine such as many targets,wide range,rich mechanisms,and few side effects have great potential in the treatment of various diseases. OBJECTIVE:Based on the nuclear transcription factor kappa B signaling pathway,this paper systematically expounded and summarized the research progress of kaempferol,safflower yellow,baicalin,and triptolide in the treatment of neuroinflammation after spinal cord injury. METHODS:Search terms"spinal cord injury,inflammation,anti-inflammatory,traditional Chinese medicine monomer,monomeric compound,NF-κB signaling pathway,flavonoids,glycosides,phenols,esters,alkaloids"were searched in CNKI and PubMed databases.Totally 67 articles were finally included. RESULTS AND CONCLUSION:(1)The role of nuclear transcription factor kappa B signaling pathway in the nervous system is complex and diverse,which can regulate neutrophils,microglia,astrocytes,and macrophages,and mediate the occurrence and development of inflammation after injury.(2)The effects of traditional Chinese medicine monomers such as baicalin on the degradation of nuclear transcription factor kappa B inhibitory protein,the inhibition of phosphorylation process by safflowerin on nuclear transcription factor kappa B signaling pathway,and the inhibition of kaempferol on nuclear transcription factor kappa B signaling pathway p65 nuclear translocation can reduce the impact of inflammatory response on the body,thereby promoting the recovery of neurological function.(3)The nuclear transcription factor kappa B signaling pathway can promote inflammation and immune cell migration and activation in the early stage of injury,and can promote the repair of injury site and the occurrence of fibrosis in the middle and late stages of injury.Appropriate activation of the nuclear transcription factor kappa B signaling pathway can promote the release of inflammatory factors,improve the antioxidant capacity of cells,and promote the activation of immune cells,but the over-activated nuclear transcription factor kappa B signaling pathway can easily lead to the occurrence and continuation of chronic inflammation and the inhibition of apoptosis.(4)Future research can further explore how to accurately regulate the activation level of nuclear transcription factor kappa B signaling pathway,how to achieve precise intervention for nervous system inflammation and injury,and can also focus on the preparation of traditional Chinese medicine monomers and the mechanism of action of traditional Chinese medicine monomers on signaling pathways,in order to provide more effective treatment strategies for the rehabilitation and functional recovery of neurological diseases.

BACKGROUND:Ferroptosis is an iron-dependent regulatory form of cell death characterized by iron-dependent lipid peroxidation.Long-chain acyl-coenzyme A synthase 4(ACSL4)is involved in the formation of lipid peroxidation substrates,thereby resulting in ferroptosis.Recent studies have shown that ACSL4-mediated ferroptosis plays a key role in atherosclerotic cardiovascular disease. OBJECTIVE:To summarize the structural function and regulatory mechanism of ACSL4 and its potential molecular mechanism mediating ferroptosis,and to elaborate the application of ACSL4 driving ferroptosis in atherosclerosis,ischemic stroke and myocardial infarction,in order to provide a new therapeutic strategy for the treatment of atherosclerotic cardiovascular diseases. METHODS:Relevant literature was searched in PubMed database from database inception to August 2023 using the keywords of"atherosclerosis,ferroptosis,long-chain acyl-coenzyme A synthase 4,ACSL4,glutathione peroxidase 4,ischemic stroke,myocardial infarction,endothelial cell,smooth muscle cells,foam cell."Finally,76 documents were included for review and analysis. RESULTS AND CONCLUSION:ACSL4 participates in the formation of coenzyme derivatives of polyunsaturated fatty acids and inserts them into phospholipids to provide substrates for lipid peroxidation,the core mechanism of iron death.Among the regulatory factors of ACSL4 expression,integrin α6β4,intracellular vesicular transport factor p115,and zinc lipoprotein A20 negatively regulate its expression.Meanwhile,multiple miRs down-regulate its expression by binding to 3'-UTR.On the contrary,up-regulation of ACSL4 is mostly regulated by transcription factors.ACSL4-dependent production of phospholipids containing polyunsaturated fatty acids is an essential prerequisite for lipid peroxidation and ferroptosis.Moreover,ACSL4 and glutathione peroxidase 4 are mutually dependent as positive and negative regulators of ferroptosis,and their specific mechanisms remain to be further studied.ACSL4-mediated ferroptosis is involved in the pathological mechanism of atherosclerosis,ischemic stroke,and myocardial infarction.Endothelial cell injury in atherosclerosis is closely related to ACSL4-mediated ferroptosis,but there are no reports on the involvement of ACSL4 in foam cell formation,smooth muscle cell phenotype transformation,and calcification.ACSL4 has become a research hotspot as a biomarker and potential target of ferroptosis.Targeting ACSL4 to inhibit ferroptosis may become a new direction for the treatment of atherosclerotic cardiovascular diseases.However,there are few studies on drugs inhibiting ACSL4,and further studies are needed in the future.

BACKGROUND:Research has demonstrated a close association between ferroptosis and vascular dementia.Tongmai Kaiqiao Pill has a certain effect on improving the cognitive function of vascular dementia patients,but its mechanism is unclear. OBJECTIVE:To explore the interventional effects and molecular mechanisms of Tongmai Kaiqiao Pill for vascular dementia based on the regulation of ferroptosis by the nuclear factor erythroid-2-related factor 2(Nrf2)/heme oxygenase-1(HO-1)/glutathione peroxidase 4(GPX4)signaling pathway. METHODS:Among eighty-four SD male rats,12 rats were used as the sham-operated group,and the rest of them were prepared as a model of vascular dementia by the modified 2-VO method,and then randomly divided into the model group,the Tongmai Kaiqiao Pills high-,moderate-,and low-dosage(27.6,13.8,and 6.9 g/kg)groups,the combined group(Tongmai Kaiqiao Pill high-dosage+ML385,20 mg/kg),and the donepezil hydrochloride group(0.45 mg/kg).The drug was given once a day by intragastric administration.The combined group was also intraperitoneally injected Nrf2 inhibitor ML385,once a day,for 4 weeks.Morris water maze was used to detect the learning memory ability of rats.Hematoxylin-eosin staining was used to observe the histopathological changes in the hippocampus of rats in each group.Colorimetric assay was used to detect the content of reduced glutathione,ferrous ion(Fe2+),and malondialdehyde in the serum of rats.Prussian blue staining was used to detect the iron deposition in the hippocampal tissue of rats.Transmission electron microscopy was used to observe the ultrastructural changes of mitochondria in rat hippocampal tissues.Western blot assay was used to detect the protein expression levels of Nrf2,HO-1,GPX4,XCT,and ferritin heavy chain 1(FTH1)in rat hippocampal tissues. RESULTS AND CONCLUSION:(1)In comparison to the sham operation,rats in the model group exhibited a significantly prolonged latency period(P<0.05)and a reduced number of platform crossings(P<0.05).Additionally,the hippocampal tissues of these rats displayed loosely organized structure,deeply stained cell nuclei,and solidified or lysed chromatin.Ferri ions aggregated in CA1 region.There were atrophied mitochondria with dissolved cristae and thickened mitochondrial membranes.Fe2+,malondialdehyde,and reduced glutathione levels in rat serum were found to be elevated(P<0.05).A significant reduction in the expression of GPX4,HO-1,XCT,Nrf2,and FTH1 proteins was detected in the hippocampus(P<0.05).(2)Compared to the model group,the average escape latency of the rats was significantly reduced following intervention with Tongmai Kaiqiao Pills and donepezil hydrochloride(P<0.05),with an increased number of platform crossings(P<0.05).Hippocampal neurons showed significant recovery.Notably,iron aggregation in the CA1 region was significantly reduced,and mitochondrial structure and function were improved.There were significant reductions in Fe2+and malondialdehyde levels,while the levels of GPX4,HO-1,XCT,Nrf2,and FTH1 in rat hippocampal tissues,and reduced glutathione in serum were significantly increased(P<0.05).(3)The high-dose Tongmai Kaiqiao Pills exhibited a treatment effect comparable to that of donepezil hydrochloride(P>0.05),with a significant prolongation of water maze escape latency(P<0.05),a reduced number of platform crossings(P<0.05),and insignificant neuronal pathological changes in the CA1 area.However,the combined group showed increased iron deposition,elevated malondialdehyde and Fe2+levels in blood serum(P<0.05),reduced glutathione content(P<0.05),hippocampal tissue mitochondrial atrophy,and reduced expression of Nrf2,XCT,HO-1,GPX4,and FTH1 proteins(P<0.05).Within a certain range,higher doses of Tongmai Kaiqiao Pills demonstrated a more pronounced effect,comparable to the efficacy of high-dose donepezil hydrochloride.(4)It is concluded that Tongmai Kaiqiao Pills have been shown to mitigate histopathological changes in the rat hippocampus and enhance cognitive function in rats with vascular dementia.The mechanism of action is likely associated with the suppression of ferroptosis through the activation of the Nrf2/HO-1/GPX4 signaling pathway.

BACKGROUND:In recent years,with the in-depth study of programmed cell death,new models of programmed cell death(mitophagy,ferroptosis,cuproptosis,and disulfidptosis)involved in Alzheimer's disease injury are gradually emerging and have large research space in the future. OBJECTIVE:To review the molecular mechanism of novel programmed cell death mode(mitophagy,ferroptosis,cuproptosis,and disulfidptosis),the crosstalk mechanism of novel cell death mode,and clinical transformation in Alzheimer's disease,aiming to provide a new perspective for exploring the mechanism of action and drug targets in Alzheimer's disease. METHODS:The first author used the computer to search the literature published between 1991 and 2024.101 articles were finally included according to the inclusion criteria. RESULTS AND CONCLUSION:(1)Programmed cell death is a necessary regulatory pathway to maintain normal cell renewal and homeostasis.Among them,new types of programmed cell death such as mitophagy,ferroptosis,cuproptosis,and disulfidptosis are hot research fields in life science.(2)Mitophagy can clear damaged mitochondria in Alzheimer's disease neurons,reduce intracellular reactive oxygen species,restore the energy metabolism and signal transduction of neurons in Alzheimer's disease,and play a crucial role in regulating the health and function of neurons.(3)Studies on ferroptosis in Alzheimer's disease have attracted much attention.It can regulate Alzheimer's disease through various ways such as cystine/glutamate,iron metabolism,and polyunsaturated fatty acids,thus affecting Aβ deposition and Tau protein phosphorylation.Recent studies have shown that natural polyphenols,Suanzoren decoction,poria acid,and vitamin E can resist ferroptosis in Alzheimer's disease.(4)Cuproptosis is a new and unique form of cell death involving copper dependence,accumulation of fatty acylated proteins,and reduction of iron-sulfur tufting proteins.Excessive copper exposure may directly interact with Aβ plaques and amyloid precursor proteins,exacerbating cognitive impairment in Alzheimer's disease.Currently,the research field of cuproptosis is emerging,and the mechanism of action has not been fully clarified.(5)Disulfidptosis,as an emerging form of programmed cell death,is caused by disulfide stress due to excessive cystine accumulation and glucose starvation,resulting in damage to the actin skeleton associated with Alzheimer's disease.(6)Various patterns of programmed cell death have a tandem mechanism in the pathogenesis of Alzheimer's disease,forming an interaction network of various programmed cell death with autophagy as the core,providing great potential for multi-level and multi-target regulation of Alzheimer's disease.The crosstalk network mechanism between autophagy,necroptosis,and pyroptosis/ferroptosis co-regulates Alzheimer's disease.(7)Cuproptosis and disulfidptosis,as a new mode of programmed death,have not been reported deeply enough in Alzheimer's disease,and further research and continuous attentions are still needed in the future.(8)Since most studies on mitophagy,ferroptosis,cuproptosis,and disulfidptosis are based on basic experiments or biogenic analysis,there is a lack of large-scale and long-term clinical research validation.Further in-depth studies are needed in the future to provide new ideas and effective strategies for the treatment of Alzheimer's disease.

BACKGROUND:Preliminary clinical observations found that Jiawei Chunze Decoction is an effective formula for clinical treatment of urinary retention after spinal cord injury.Animal experiments have found that the phosphatidylinositol 3-kinase/protein kinase B(PI3K/Akt)signaling pathway is closely related to the degree of bladder dysfunction. OBJECTIVE:To further investigate the effects of Jiawei Chunze Decoction on bladder function and PI3K/Akt signaling pathway in rats with urinary retention. METHODS:Sixty female Sprague-Dawley rats were randomly divided into sham operation group,model group,Jiawei Chunze Decoction low-dose group,Jiawei Chunze Decoction high-dose group and agonist group.In the sham operation group,the spinal cord was exposed but not transected.In the other groups,the modified Hassan Shaker spinal cord transection method was used to prepare the model of sacral medullary injury.At 24 hours after modeling,the sham operation group and model group were intragastrically given equal volume of normal saline,Jiawei Chunze Decoction low-dose and high-dose groups were given Jiawei Chunze Decoction granules containing 14.4 and 28.8 g/kg,respectively,via intragastric administration for 4 weeks,and the agonist group was treated with an intraperitoneal injection of PI3K/Akt signaling pathway agonist 740Y-P at a dose of 0.02 mg/kg.After 4 weeks of treatment,the maximum bladder capacity,leakage point pressure and bladder compliance of rats in each group were detected by urine flow dynamics.The minimum bladder contraction tension and frequency of rats in each group were detected by detrusor pull test.The pathological changes of the rat bladder in each group were observed by hematoxylin-eosin staining.The concentrations of GRP78,CHOP and Caspase-12 in serum were detected by ELISA,and the mRNA and protein expressions of PI3K,Akt,GRP78,CHOP and Caspase-12 in bladder tissues were detected by RT-PCR and western blot,respectively. RESULTS AND CONCLUSION:Compared with the sham operation group,the maximum bladder volume,bladder compliance and minimum systolic tension of rats in the model group were increased(P<0.05),and the leakage point pressure and bladder contraction frequency were decreased(P<0.05);serum GRP78,CHOP,and Caspase-12 levels were also increased(P<0.05).The arrangement of bladder epithelial cells in the model group was disordered,and there was monocyte infiltration between cells,tissue edema,and detrusor tract atrophy.The mRNA and protein expressions of PI3K and Akt in bladder tissues were significantly decreased in the model group compared with the sham operation group,while those of GRP78,CHOP and Caspase-12 were increased(P<0.05).Compared with the model group,the maximum bladder volume,bladder compliance and minimum systolic tension of rats were decreased in the Jiawei Chunze Decoction low-dose,high-dose and agonist groups after 4 weeks of intervention(P<0.05),while the leakage point pressure and bladder contraction frequency were increased(P<0.05);serum GRP78,CHOP,Caspase-12 levels were decreased(P<0.05).The bladder epithelial cells in the three intervention groups were distributed evenly,arranged neatly,with less inflammatory cell infiltration and fuller detrusor muscle bundle.Compared with the model group,the mRNA and protein expressions of PI3K and Akt were increased in the three intervention groups,while those of GRP78,CHOP and Caspase-12 were decreased(P<0.05).The Jiawei Chunze Decoction high-dose group was better than the Jiawei Chunze Decoction low-dose group and shared the similar results with the agonist group.To conclude,Jiawei Chunze Decoction can improve the bladder function of rats with urinary retention after spinal cord injury,and the mechanism may be related to reducing the occurrence of endoplasmic reticulum stress in bladder tissue through the PI3K/Akt signaling pathway,and then alleviating apoptosis.

ObjectiveTo investigate the effects of modified Chunzetang on urinary retention in rats with spinal cord injury （SCI） and the c-Jun N-terminal kinase/p38 mitogen-activated protein kinase （JNK/p38 MAPK） signaling pathway. MethodBefore modeling， 10 of the 70 female SD rats were randomly selected to assign to the blank group， and 10 to the sham group. The remaining 50 rats were used to prepare a SCI-induced urinary retention model using the spinal cord transection method. The model rats were randomly divided into model group， low-dose modified Chunzetang group， high-dose modified Chunzetang group， and inhibitor group. After modeling， the blank group， sham group， and inhibitor group were given 2 mL of saline by gavage. The high-dose and low-dose groups of modified Chunzetang were given modified Chunzetang at 28.8 g·kg^-1 and 14.4 g·kg^-1 by gavage， respectively. The inhibitor group was injected intraperitoneally with the JNK inhibitor SP600125 twice a week at a dose of 15 mg·kg^-1. All rats were gavaged for a total of 28 days. Urodynamic and bladder muscle tension tests were conducted to evaluate bladder function. Hematoxylin-eosin （HE） staining was performed to observe the morphology of bladder smooth muscle tissue. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of JNK， phosphorylated （p）-p38 MAPK， B cell lymphoma-2 （Bcl-2）， and cysteinyl aspartate-specific proteinase-3 （Caspase-3）. Western blot was used to detect the expression levels of p-JNK， p-p38 MAPK， ETS-like protein-1 （ELK-1）， and activator protein-1 （AP1） in the detrusor muscle. Immunofluorescence was used to detect the expression levels of p-JNK， p-p38 MAPK， and AP1. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling （TUNEL） assay was conducted to measure cell apoptosis. ResultCompared with blank group and sham group， the model group showed a significant increase in maximum bladder capacity and bladder compliance， and a significant decrease in leak point pressure. The minimum contraction force was increased， and the contraction frequency was significantly decreased （P<0.01）. The structure of bladder smooth muscle was disordered， with a large number of vacuolar cells， tissue edema， mononuclear cell infiltration， obvious hemorrhage， and a trend towards fibrosis in connective tissue. TUNEL positive cells increased significantly. The protein expression levels of p-JNK， p-p38 MAPK， AP1， and ELK-1 were significantly increased （P<0.01）. Compared with model group， all intervention groups showed significant improvement in urodynamic and bladder muscle contraction tests. In the low-dose modified Chunzetang group， the levels of p-p38 MAPK and Caspase-3 was decreased （P<0.05，P<0.01）. The levels of JNK, p-p38 MAPK and Caspase-3 in the high-dose group were significantly decreased （P<0.01）， and the level of Bcl-2 was significantly increased （P<0.01）. The expression levels of p-JNK， p-p38 MAPK， and AP1 proteins were significantly reduced （P<0.01）， and ELK-1 protein expression was decreased （P<0.05）. The positive rate of p-JNK and AP1 receptors was significantly decreased （P<0.01）. The positive cell rate was significantly decreased （P<0.01）. The high-dose modified Chunzetang group was positioned between the low-dose group and the inhibitor group， with no significant difference compared to the inhibitor group. ConclusionModified Chunzetang can improve urinary retention in SCI and enhance the contraction force of bladder smooth muscle. This effect is related to the inhibition of the JNK/p38 MAPK signaling pathway activation， thereby reducing apoptosis of bladder smooth muscle cells.

ObjectiveTo observe the effects of Tongmai Kaiqiao pills on the hypoxia-inducible factor-1α （HIF-1α）/adenovirus E1B 19 kD-interacting protein 3 （BNIP3） signaling pathway and mitochondrial autophagy in the hippocampus of the rat model of vascular dementia （VD）. MethodNinety male SD rats underwent adaptive feeding for one week before the study. Ten rats were randomly assigned to the sham group， where the common carotid artery was isolated without ligation. The remaining rats were subjected to sequential ligation of the common carotid artery for the modeling of VD. The successfully modeled rats were randomly assigned into the following groups： model， high-， medium-， and low-dose （27.6， 13.8， 6.9 g·kg^-1， respectively） Tongmai Kaiqiao pills， donepezil hydrochloride （0.45 mg·kg^-1）， and combination （27.6 g·kg^-1 Tongmai Kaiqiao pills + 2.5 mg·kg^-1 HIF-1α inhibitor YC-1） groups. After 4 weeks of treatment， samples were collected. Nissl staining and hematoxylin-eosin staining were performed to observe the loss of neurons and pathological changes， respectively， in the hippocampal region. Western blot was employed to determine the protein levels of HIF-1α， BNIP3， Beclin-1， and microtubule-associated protein 1 light chain 3B （LC3B） in the hippocampal tissue. Transmission electron microscopy was used to observe the mitochondrial ultrastructure and the number of autophagosomes in the hippocampal tissue. Immunofluorescence was employed to observe the fluorescence intensity of HIF-1α， BNIP3， and LC3B in the hippocampal tissue. ResultCompared with the sham group， the model group showed prolonged escape latency （P<0.01）， decreased number of platform crossings （P<0.01）， reduced and disarranged neuronal layers in the hippocampal region， decreased number of Nissl bodies， disrupted mitochondrial cristae， damaged mitochondrial double-membrane structures， increased number of autophagosomes， upregulated expression of HIF-1α， BNIP3， beclin1， and LC3B （P<0.05， P<0.01）， and enhanced fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.05， P<0.01）. Compared with the model group， Tongmai Kaiqiao pills and donepezil hydrochloride shortened the searching time for the platform （P<0.01） and increased the number of platform crossings （P<0.01）. Moreover， the drugs increased the number of neurons with normal morphology and orderly arrangement and the number of Nissl bodies， alleviated the damage， increased the number of autophagosomes， upregulated the expression of HIF-1α， BNIP3， Beclin1， and LC3B （P<0.05， P<0.01）， and enhanced the fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.05， P<0.01）. Compared with high-dose Tongmai Kaiqiao pills， the combination group prolonged the escape latency （P<0.01）， reduced the number of crossing platforms （P<0.01）， decreased the number of hippocampal neurons， aggravated the damage， decreased the number of Nissl bodies and autophagosomes， downregulated the expression of HIF-1α， BNIP3， beclin1， and LC3B （P<0.01）， and decreased the fluorescence intensity of HIF-1α， BNIP3， and LC3B （P<0.01）. ConclusionTongmai Kaiqiao pills may activate the HIF-1α/BNIP3 signaling pathway to promote the occurrence of mitochondrial autophagy， clear damaged mitochondria， provide energy for healthy cells， reduce neuronal cell death， and restore the brain function， thereby reducing ischemic damage to the hippocampal tissue， improving learning and memory abilities， and exerting therapeutic effects on VD in rats.

Objective:To observe any effect of early recumbent treadmill training on the balance and functional independence during hospitalization of children who have received hematopoietic stem cell transplantation (HSCT).Methods:This was a retrospective analysis of 106 children who had received HSCT. Sixty-nine of them were qualified for study. Of those, 32 had performed recumbent treadmill training and the other 37 had not. The children in both groups received routine clinical treatment and nursing care, and also health education advocating exercise and giving exercise programs before and after the transplantation. The daily exercise was conducted with the help of parents. It lasted 20 to 30 minutes each time, 4 or 5 times a week. The treadmill group additionally spent 30 minutes training on a recumbent treadmill 5 times a week for 6 weeks. Balance, functional independence and fatigue levels were quantified before and after the treatment using the Berg Balance Scale (BBS), the Functional Independence Measure for Children (WeeFIM) and the Pediatric Quality of Life Inventory-Multidimensional Fatigue Scale.Results:After the 6 weeks, significant improvement was observed in the experimental group′s average BBS score, motor function domain score, total WeeFIM score, general fatigue, and sleep/rest fatigue. All were then significantly better than the non-treadmill group′s results.Conclusion:Early recumbent treadmill training can promote the recovery of balance and functional independence of children after HSCT.