Objective To investigate the mechanism by which 4-week high-intensity interval training(HIIT)regulates the mitochondrial unfolded protein response(UPRmt)in skeletal muscle and improves mitochondrial function in a rat model of chronic unpredictable mild stress(CUMS).Methods Male SPF-grade SD rats(6～8 weeks old)were divided randomly into control(C),model(M),HIIT+control(HC),and HIIT+model(HM)groups.Rats in the M and HM groups were subjected to CUMS for 8 weeks to establish a depression model,while rats in the HC and HM groups received HIIT for 5 d a week for 4 weeks.The exercise regimen consisted of 3 min high-speed(85％～90％Smax)combined with 1 min low-speed(50％～55％Smax)uninterrupted repetitive training(Smax is maximum training speed).Behavioral changes were evaluated at weeks 4 and 8.Tissue samples were taken 24 h after the last behavioral test and skeletal muscle mitochondria were examined by transmission electron microscopy.The ATP and reactive oxygen species(ROS)contents were measured by enzyme-linked immunosorbent assays and protein expression levels of activating transcription factor(ATF)4,ATF5,C/EBP homologous protein(CHOP),and heat shock protein 60(HSP60)were detected by Western blot.Results(1)The body mass,number of crossing grids,number of upright positions,sugar-water preference rate,and ATP content were significantly decreased in group M compared with group C(P＜0.01),while the number of damaged mitochondria,ROS content,ATF4,ATF5,CHOP,and HSP60 protein expression were significantly increased(P＜0.01).(2)After 4-weeks of HIIT intervention,the ATP content and ATF4 and ATF5 protein expression levels were significantly increased in the HC group compared with C group(P＜0.05,P＜0.01).The number of crossing grids,number of upright positions,sugar-water preference rate,ATP content,and ATF4 protein expression were significantly increased in the HM group compared with M group(P＜0.01),while the number of damaged mitochondria,ROS content,and ATF5,CHOP,and HSP60 protein expression levels were significantly decreased(P＜0.01).(3)After 4 weeks of HIIT intervention,the number of crossing grids in CUMS rats was significantly positively correlated with ATF4 protein expression,and ROS content was correlated with CHOP protein expression,number of damaged mitochondria,and ATF5 protein expression(|r|＞0.75,P＜0.01;|r|＞0.75,P＜0.05).Upright frequency was significantly negatively correlated with ATF5 and HSP60 protein expression,the number of crossing grids,the sugar-water preference rate,and the expression of CHOP and HSP60 proteins(|r|＜0.75,P＜0.05).Conclusions 4-week HIIT intervention can improve mitochondrial dysfunction and alleviate depressive-like behavior in CUMS rats by regulating skeletal muscle UPRmt.

Guided by Zhang Zhongjing's axiom that"blood stasis induces water",this study develops stage-specific treatment strategies for edema in Kidney Consumption Disorder by examining its four-stage pathogenic progression:Sluggish Flow → Stagnant Obstruction → Depressed Accumulation → Stasis Congelation.We propose an integrated approach that reinforces the root by warming the kidney and replenishing essence,while addressing the branch by activating blood circulation and promoting diuresis.Stage-specific interventions include:for the Sluggish Flow Phase,warming and tonifying kidney Yang combined with unblocking Yang to promote uri-nation;for the Stagnant Obstruction Phase,warming the kidney and replenishing essence supported by activating blood circulation and freeing the collateral channels;for the Depressed Accumulation Phase,quickening blood and resolving stasis,regulating Qi and trans-forming turbidity,along with warming the kidney and strengthening essence;and for the Stasis Congelation Phase,expelling stagnant accumulations while simultaneously regulating essence and blood.This framework advances novel pattern-determined strategies for Kid-ney Consumption edema management.

Objective To investigate the mechanism by which 4-week high-intensity interval training(HIIT)regulates the mitochondrial unfolded protein response(UPRmt)in skeletal muscle and improves mitochondrial function in a rat model of chronic unpredictable mild stress(CUMS).Methods Male SPF-grade SD rats(6～8 weeks old)were divided randomly into control(C),model(M),HIIT+control(HC),and HIIT+model(HM)groups.Rats in the M and HM groups were subjected to CUMS for 8 weeks to establish a depression model,while rats in the HC and HM groups received HIIT for 5 d a week for 4 weeks.The exercise regimen consisted of 3 min high-speed(85％～90％Smax)combined with 1 min low-speed(50％～55％Smax)uninterrupted repetitive training(Smax is maximum training speed).Behavioral changes were evaluated at weeks 4 and 8.Tissue samples were taken 24 h after the last behavioral test and skeletal muscle mitochondria were examined by transmission electron microscopy.The ATP and reactive oxygen species(ROS)contents were measured by enzyme-linked immunosorbent assays and protein expression levels of activating transcription factor(ATF)4,ATF5,C/EBP homologous protein(CHOP),and heat shock protein 60(HSP60)were detected by Western blot.Results(1)The body mass,number of crossing grids,number of upright positions,sugar-water preference rate,and ATP content were significantly decreased in group M compared with group C(P＜0.01),while the number of damaged mitochondria,ROS content,ATF4,ATF5,CHOP,and HSP60 protein expression were significantly increased(P＜0.01).(2)After 4-weeks of HIIT intervention,the ATP content and ATF4 and ATF5 protein expression levels were significantly increased in the HC group compared with C group(P＜0.05,P＜0.01).The number of crossing grids,number of upright positions,sugar-water preference rate,ATP content,and ATF4 protein expression were significantly increased in the HM group compared with M group(P＜0.01),while the number of damaged mitochondria,ROS content,and ATF5,CHOP,and HSP60 protein expression levels were significantly decreased(P＜0.01).(3)After 4 weeks of HIIT intervention,the number of crossing grids in CUMS rats was significantly positively correlated with ATF4 protein expression,and ROS content was correlated with CHOP protein expression,number of damaged mitochondria,and ATF5 protein expression(|r|＞0.75,P＜0.01;|r|＞0.75,P＜0.05).Upright frequency was significantly negatively correlated with ATF5 and HSP60 protein expression,the number of crossing grids,the sugar-water preference rate,and the expression of CHOP and HSP60 proteins(|r|＜0.75,P＜0.05).Conclusions 4-week HIIT intervention can improve mitochondrial dysfunction and alleviate depressive-like behavior in CUMS rats by regulating skeletal muscle UPRmt.

The heart serves as the "energy factory" of the human body and is responsible for maintaining blood circulation and oxygen supplies.Its normal functioning thus relies on the generation of substantial amounts of ATP to support its mechanical activities.Under pathological conditions such as myocardial infarction,coronary artery sclerosis,and pulmonary hypertension,however,an insufficient blood supply leads to a reduced oxygen supply,subsequently activating a series of compensatory protective mechanisms.Hypoxia-inducible factor-1α(HIF-1α),as a nuclear transcription factor stably expressed under hypoxic conditions,has been shown to regulate oxygen transport by promoting angiogenesis and vasodilation,and to optimize oxygen utilization by regulating the balance of glucose and lipid metabolisms,thus participating in the regulation of various cardiac diseases.HIF-1α plays a crucial role in regulating cardiac energy metabolism and oxidative stress.This review systematically summarizes recent research regarding the various mechanisms of action of HIF-1α in reprogramming cardiac energy metabolism,explores its potential clinical applications in cardiovascular diseases,and proposes future research directions and possible treatment strategies.By comprehensively summarizing the mechanism of HIF-1α in ischemic heart disease,this article aims to provide new ideas and therapeutic targets for the prevention and treatment of cardiovascular diseases.

Objective:To investigate a novel coating technology for artificial blood vessel pipelines, conducting preliminary tests on the mechanical stability, hemocompatibility, and biocompatibility of the coating.Methods:The polyester braided artificial blood vessels produced by Terumo Corporation were subjected to three different experimental treatments and divided into three groups. Model group: The uncoated artificial blood vessels were thoroughly cleaned and freeze-dried. Experimental group: The artificial blood vessels were first immersed in a dopamine solution to form a polydopamine(PDA) coating on their surface, and then further immersed in an earthworm active protein/gelatin(EWAP/GT) solution to create PDA/GT/EWAP-modified artificial blood vessels. Collagen group: The untreated polyester woven artificial blood vessels served as the control. The study detailed the characterization, porosity, water permeability, degradation rate, blood compatibility, and cytotoxicity of the PDA/GT/EWAP-coated artificial blood vessels. Additionally, a 2-week in vivo study was conducted to evaluate the biocompatibility of the PDA/GT/EWAP-coated artificial blood vessels implanted subcutaneously in SD rats.Results:The PDA/GT/EWAP-coated artificial vascular grafts were successfully fabricated. The artificial blood vessels in the PDA/GT/EWAP group exhibited a porosityof(50.53±1.10)%, with water permeability showing a gradual decreasing trend over time. The overall in vitro degradation rate at 4 weeks was(1.83±0.08)%, and the PDA/GT/EWAP group demonstrated favorable mechanical stability. The activated partial thromboplastin time(APTT) of the PDA/GT/EWAP group was(26.30±0.46)s, the thrombin time(TT) was(18.83±0.49)s, the hemolysis rate was(2.15±0.09)%, and the plasma recalcification time(PRT) was(191.00±10.54)s, indicating excellent blood compatibility and anticoagulant properties. MTT assay evaluation of the PDA/GT/EWAP group revealed no significant cytotoxicity. After subcutaneous implantation of vascular samples in rats for 2 weeks, analysis of blood immune parameters and hematoxylin-eosin(HE) staining of the artificial vascular samples showed that the immune response in the PDA/GT/EWAP group exhibited no significant difference compared to the collagen group and was superior to the model group. Conclusion.Conclusion:The PDA/GT/EWAP composite-coated artificial blood vessel demonstrates excellent mechanical properties, good hemocompatibility, biocompatibility, and low cytotoxicity. It also shows remarkable stability. This research offers a new approach for domestic technological breakthroughs in related fields.

Parkinson disease is a progressive neurodegenerative disease whose incidence increases year by year as the population ages.TCM compounds for the treatment of Parkinson disease has the characteristics of multiple components,targets,and pathways.Combined treatment with Western medicine can achieve synergistic effects and reduce adverse drug reactions.This article focused on the mechanism of TCM compounds for the treatment of Parkinson disease,reviewed relevant experimental studies in recent years.TCM compounds may exert therapeutic effects on Parkinson disease by regulating oxidative stress,mitochondrial dysfunction,neurotransmitters,neuroinflammation,abnormal protein aggregation,cell apoptosis,stem cell transplantation,neurotrophic factors,second messengers,and other mechanisms,in order to provide basis for clinical treatment of Parkinson disease.

Parkinson disease is a progressive neurodegenerative disease whose incidence increases year by year as the population ages.TCM compounds for the treatment of Parkinson disease has the characteristics of multiple components,targets,and pathways.Combined treatment with Western medicine can achieve synergistic effects and reduce adverse drug reactions.This article focused on the mechanism of TCM compounds for the treatment of Parkinson disease,reviewed relevant experimental studies in recent years.TCM compounds may exert therapeutic effects on Parkinson disease by regulating oxidative stress,mitochondrial dysfunction,neurotransmitters,neuroinflammation,abnormal protein aggregation,cell apoptosis,stem cell transplantation,neurotrophic factors,second messengers,and other mechanisms,in order to provide basis for clinical treatment of Parkinson disease.

The heart serves as the "energy factory" of the human body and is responsible for maintaining blood circulation and oxygen supplies.Its normal functioning thus relies on the generation of substantial amounts of ATP to support its mechanical activities.Under pathological conditions such as myocardial infarction,coronary artery sclerosis,and pulmonary hypertension,however,an insufficient blood supply leads to a reduced oxygen supply,subsequently activating a series of compensatory protective mechanisms.Hypoxia-inducible factor-1α(HIF-1α),as a nuclear transcription factor stably expressed under hypoxic conditions,has been shown to regulate oxygen transport by promoting angiogenesis and vasodilation,and to optimize oxygen utilization by regulating the balance of glucose and lipid metabolisms,thus participating in the regulation of various cardiac diseases.HIF-1α plays a crucial role in regulating cardiac energy metabolism and oxidative stress.This review systematically summarizes recent research regarding the various mechanisms of action of HIF-1α in reprogramming cardiac energy metabolism,explores its potential clinical applications in cardiovascular diseases,and proposes future research directions and possible treatment strategies.By comprehensively summarizing the mechanism of HIF-1α in ischemic heart disease,this article aims to provide new ideas and therapeutic targets for the prevention and treatment of cardiovascular diseases.

Guided by Zhang Zhongjing's axiom that"blood stasis induces water",this study develops stage-specific treatment strategies for edema in Kidney Consumption Disorder by examining its four-stage pathogenic progression:Sluggish Flow → Stagnant Obstruction → Depressed Accumulation → Stasis Congelation.We propose an integrated approach that reinforces the root by warming the kidney and replenishing essence,while addressing the branch by activating blood circulation and promoting diuresis.Stage-specific interventions include:for the Sluggish Flow Phase,warming and tonifying kidney Yang combined with unblocking Yang to promote uri-nation;for the Stagnant Obstruction Phase,warming the kidney and replenishing essence supported by activating blood circulation and freeing the collateral channels;for the Depressed Accumulation Phase,quickening blood and resolving stasis,regulating Qi and trans-forming turbidity,along with warming the kidney and strengthening essence;and for the Stasis Congelation Phase,expelling stagnant accumulations while simultaneously regulating essence and blood.This framework advances novel pattern-determined strategies for Kid-ney Consumption edema management.

Objective:To investigate the effect of p38MAPK signaling pathway mediating progesterone regulation on IL-8 protein secretion by decidual stromal cells(DSCs)on early spontaneous miscarriage.Methods:IHC and Western blot were applied to detect protein expressions of p38MAPK and p-p38MAPK in decidual tissues of miscarriage group and control group.Human DSCs in early pregnancy were isolated in vitro and cultured to be treated with different concentrations of progesterone(0.01 μmol/L,0.1 μmol/L,1 μmol/L and 10 μmol/L),with ELISA measuring IL-8 protein secretion from DSCs and Western blot measuring protein expressions of p38MAPK and p-p38MAPK in DSCs.After treatment with p38MAPK inhibitor SB203580,IL-8 protein secretion was detected by ELISA in progesterone+inhibitor group,progesterone group and control group.Results:Protein expression of p-p38MAPK in decidual tissues of miscarriage group was significantly higher than that of control group(P=0.002 3).Protein secretion of IL-8 in DSCs of 0.01 μmol/L progesterone group was lower than that of control group(P=0.027 6),protein expression of p-p38MAPK in DSCs of 0.1 μmol/L proges-terone group was lower than that of control group(P=0.025 3),IL-8 protein expression was significantly lower than that in control group(P=0.007 0),and protein expressions of both IL-8 and p-p38MAPK from DSCs in 1 μmol/L and 10 μmol/L progesterone groups were significantly lower than those in control group(P=0.003 2,P=0.001 9;P=0.002 2,P=0.001 3).IL-8 protein secretion in proges-terone+p38MAPK inhibitor group was further reduced compared to progesterone group(P=0.046 6).Conclusion:Abnormal activation of p38MAPK signaling pathway is involved in early spontaneous miscarriage,and progesterone may down-regulate IL-8 expression in DSCs by inhibiting p38MAPK phosphorylation to correct early spontaneous miscarriage caused by Th1/Th2 cytokine imbalance.