Helicobacter pylori (Hp) is classified as a group Ⅰ carcinogen and serves as a major pathogenic factor in the development of gastric cancer. Studies have confirmed that eradicating Hp can reduce gastric cancer mortality. Although standard therapies combining proton pump inhibitors with antibiotics have shown some efficacy, increasing drug resistance and adverse effects have led to a continuous decline in the eradication rate of Hp. Therefore, there is an urgent need to develop novel therapeutic strategies to improve the cure rate of Hp infection. This article focuses on the mechanisms by which Hp induces mitochondrial dysfunction, including mediating mitochondrial oxidative stress, alterations in mitochondrial dynamics, mitochondrial autophagy (mitophagy), and mtDNA damage. By delving into the pathogenesis of Hp-related diseases triggered by mitochondrial dysfunction, this review aims to provide a theoretical foundation for identifying new clinical targets for the prevention and treatment of Hp infection.

OBJECTIVE: To investigate the effect and mechanism of Hyssopus cuspidatus Boriss. extract (HCE) in ovalbumin (OVA)-induced allergic asthma. METHODS: Components identification of HCE was conducted using ultra performance liquid chromatography-quadrupole-time of flight-mass spectrometry. Mice were sensitized with OVA to establish asthmatic model, and dexamethasone was used as positive control. Respiratory reactivity, white cells counting in bronchoalveolar lavage fluid and peripheral blood, cytokine level measurement in serum and lung tissue, and histologic examination were performed to evaluate the therapeutic effect of HCE on asthma. Network pharmacology approach was used for mechanism prediction. Western blotting and untargeted lipidomics method were applied for mechanism validation. RESULTS: Fifty-two compounds were identified in HCE, predominantly terpenoids and flavonoids. HCE markedly reduced airway resistance, the eosinophil infiltration in lung tissues, and the levels of immunoglobulin E, interleukin-4, interleukin-5, and interleukin-13. Network pharmacology analysis suggested phosphatidylinositol 3-kinases (PI3K), c-Jun N-terminal kinase (JNK), and p38 Mitogen-activated protein kinase (p38 MAPK) may be key proteins of HCE in the treatment of allergic asthma. Western blot results indicated that the levels of phosphorylated PI3K, JNK, and P38 were downregulated in HCE-treated group. Moreover, HCE significantly upregulated the levels of ceramide and sphingomyelin and downregulated the level of phosphatidylcholine. CONCLUSION HCE inhibited allergic asthma via PI3K/JNK/P38 signaling pathway and lipid homeostasis regulation.

The etiology of tumors is complex and influenced by multiple factors, including the host and environmental conditions. Allergy is primarily driven by the immune response of helper T cell 2 (Th2). Research has shown that the Th2 immune response is closely related to tumors, which is specifically manifested through Th2 antibodies, allergy-related effector cells and mediators within the tumors, as well as tumor immune-related functions. This internal interaction mechanism will increase the complexity and challenges associated with the clinical diagnosis and treatment of tumors and allergy. The formation of allergic constitution is shaped by both congenital and acquired factors, and its physical state is closely linked to the occurrence and progression of allergic diseases. Therefore, this paper aims to explore the relationship between tumors and allergic reactions from the perspective of traditional Chinese medicine (TCM) constitution theory. Based on the four basic principles of the TCM constitution, including endowment inheritance theory, environment constraint theory, body-spirit composition theory, and life process theory, this exploration will focus on four aspects: genetic factors and internal disease causes, inflammatory environments and functional regulation, psychological disorders and emotional pathogenesis, as well as age structure and disease risk. Furthermore, from the perspective of constitution-disease relation of chronic disease prevention, this paper will discuss the significant importance of adjusting allergic constitution to improve both subjective symptoms and objective indicators of allergic reactions in tumor patients.

BACKGROUND:Cardiac dysfunction due to spinal cord injury is an important factor of death in patients with spinal cord injury;however,the specific mechanism is still not clear.Therefore,revealing the mechanism of cardiac dysfunction in spinal cord injury patients is of great significance to improve their quality of life and survival rate. OBJECTIVE:To investigate the mechanism of luteolin in improving serum-induced myocardial cell death in spinal cord injury rats. METHODS:Allen's impact instrument was used to damage the spine T9-T11 of male SD rats to establish a spinal cord injury model meanwhile a sham operation group was set as the control group.The serum of rats of each group was collected.H9c2 cells were divided into a blank control group,a sham operated rat serum group,a spinal cord injury rat serum group and a luteolin pretreatment group.The cells in blank control group were only cultured with ordinary culture medium.The cells in the sham operated rat serum group were treated with medium containing 10%serum from sham operated rat.The cells in the spinal cord injury rat serum group were treated with medium containing 10%serum from spinal cord injury rat.The cells in the luteolin pretreatment group were precultured with a final concentration of 20 μmol/L luteolin for 4 hours and then changed to a medium containing 10%rat serum from spinal cord injury rat.After 24 hours of culture,the survival rate of each group of H9c2 cells was measured by CCK-8 assay.Western blot assay was used to detect the expression of autophagy related protein LC3 and p62 in H9c2 cells in each group. RESULTS AND CONCLUSION:Compared with the blank control group,there was no significant change in cell survival rate in the sham operated rat serum group(P>0.05).Compared with the sham operated rat serum group,the cell survival rate(P<0.01)and the expression of LC3 protein(P<0.05)in spinal cord injury rat serum group was significantly reduced,and the expression of p62 protein was significantly increased(P<0.05).Compared with the spinal cord injury rat serum group,the survival rate of cells in the luteolin pretreatment group significantly increased(P<0.000 1);the expression of LC3 protein significantly increased(P<0.05),and the expression of p62 protein significantly decreased(P<0.05).The results indicate that luteolin may improve myocardial cell death induced by serum from rats with spinal cord injury by promoting autophagy.

Hepatic encephalopathy is a difficult and critical disease with rapid progression and limited treatment methods in the field of liver disease， and it is urgently needed to make breakthroughs in its pathogenesis. Selection of appropriate prevention and treatment strategies is of great importance in delaying disease progression and reducing the incidence and mortality rates. This article reviews the theory of “turbid toxin pathogenesis” and related prevention and treatment strategies for hepatic encephalopathy in traditional Chinese medicine/Zhuang medicine， proposes a new theory of “turbid toxin pathogenesis”， analyzes the scientific connotations of “turbid”， “toxin”， and the theory of “turbid toxin pathogenesis”， and constructs the “four-step” prevention and treatment strategies for hepatic encephalopathy， thereby establishing the new clinical prevention and treatment regimen for hepatic encephalopathy represented by “four prescriptions and two techniques” and clarifying the effect mechanism and biological basis of core prescriptions and techniques in the prevention and treatment of hepatic encephalopathy， in order to provide a reference for the prevention and treatment of hepatic encephalopathy.

Objective To investigate the effects of hypoxia on the transcriptional phenotype and ultrastructure of tumor-associated macrophages(TAMs)in glioma.Methods CD14+monocytes were isolated from healthy human peripheral blood samples collected from the Blood Bank of the First Affiliated Hospital of Army Medical University,and the cells were induced to differentiate into TAMs through co-culture with glioma cell-conditioned medium.Hypoxic TAM models were established using varying concentrations of cobalt chloride hexahydrate(CoCl2,50～400 μmol/L)or hypoxic conditions(1%,5%,10%O2)for 48 h,while normoxic TAM models(21%O2)served as controls.RT-qPCR and transcriptome sequencing were employed to analyze transcriptional changes in TAMs under normoxic and hypoxic conditions.Gene set enrichment analysis(GSEA)was applied to compare the differences in angiogenesis,glycolysis and other hypoxia-responsive pathways between the 2 conditions.Transmission electron microscopy(TEM)or immunofluorescence staining was conducted to assess the ultrastructural alterations in cytoskeleton,endoplasmic reticulum(ER),and mitochondria in normoxic and hypoxic TAMs(1%O2).Results Hypoxic TAMs exhibited up-regulated transcription of hypoxia-responsive markers(oxygen transport,glycolysis,pro-angiogenesis),with the effects correlating with hypoxia severity(P<0.05).GSEA revealed significant up-regulation of hypoxia,angiogenesis regulation,glycolysis and gluconeogenesis,and starvation stress pathways,alongside down-regulation of innate immunity,macrophage activation,cytoskeleton,and protein maturation pathways in hypoxic TAMs(P<0.05).TEM and immunofluorescence staining demonstrated obvious ultrastructure changes,including disrupted cytoskeletal organization,shortened rough ER with reduced ribosomes,mitochondrial swelling with cristae damage,and diminished ER-mitochondria contacts in hypoxic TAMs.Conclusion CoCl2 and hypoxia induce a hypoxic transcriptional phenotype in TAMs,which may potentially associated with ultrastructural remodeling of the cytoskeleton,ER,and mitochondria.

•A strategy for in situ metabolically synthesized active drug-based probes was proposed.•The potential purgative targets of SA were successfully hooked and identified.•The work provided a new insight for studying the direct targets of unstable active drugs.

Objective To explore the effective substances that specifically bind to RSV-F protein in the water extract of Forsythia suspensa,and verify its effect.Methods Surface plasmon resonance(SPR)affinity fishing technology was used to enrich,regenerate and recover the active components that specifically bind to RSV-F protein in the water extract of Forsythia suspensa.The recovered samples were analyzed and identified by UHPLC-MS/MS,and the active components that stably bind to F protein were screened by molecular docking,molecular dynamics simulation and SPR affinity detection,and then returned to animal experiments for pharmacodynamics verification.BALB/c mice were randomly divided into normal group,model group,positive control group,protocatechuic acid group and verbascoside group.In the experimental group,RSV was dripped into the nose to make models.Each drug group began to be given intragastric intervention on the day of modeling,and samples were taken after 4 days.HE staining was used to observe the pathological changes of lung tissue,and ELISA was used to detect the changes of inflammatory factors in lung tissue.Results A variety of active components in the aqueous extract of Forsythia suspensa could bind to RSV-F protein,among which the results of verbascoside and protocatechuic acid were more stable.In vivo pharmacodynamics experiments showed that the lung tissue of the model group had obvious pathological changes and the level of inflammatory factors increased,and the pathological state was improved after the intervention of verbascoside and protocatechuic acid compared with the normal group.Conclusion Forsythia suspensa can interfere with the expression of RSV-F protein through many active components such as verbascoside and protocatechuic acid,which may be the material basis of its anti-RSV.

In recent years,with the advancement of microbial detection technologies,an increasing number of studies have revealed significant differences in the gut microbiota composition of kidney transplant recipients before and after surgery.These changes in the gut microbiota may influence graft function and the occurrence of post-transplant complications through a variety of factors.This article will review the research progress in the relationship between gut microbiota and kidney transplantation.It focuses on the changes in gut microbiota after kidney transplantation.The role of gut microbiota in immune regulation,drug metabolism,graft function protection,and post-transplant complications is also studied.At the same time,these effects may be of great significance in improving the short-term and long-term prognosis of kidney transplant recipients,thus providing a novel idea for further improving kidney transplant prognosis.

Hepatitis B virus(HBV)infection is worldwide and poses a serious threat to human health.Existing conventional therapeutic drugs(e.g.,interferon-alpha,nucleoside analogs)can inhibit intrahepatic replication of HBV,but it is difficult to remove HBV covalently closed circular DNA(cccDNA)from the nucleus of hepatocytes,resulting in the virus not being easily cleared and the formation of a chronic infection that is difficult to cure.However,the emergence of targeted drugs is expected to destroy cccDNA making a cure for HBV infection possible.To achieve this,in vitro cell models of HBV infection and replication are needed to screen for targeted drugs.In recent years,in vitro cell models for HBV research have made fundamental progress,providing a platform for a better understanding of virus-host interactions,in vitro studies of the HBV life cycle,and the screening and evaluation of novel antiviral drugs.In this review,the research progress of HBV infection and replication cell models,and the characteristics and limitations of different cell models are reviewed,aiming to provide a basis for exploring the mechanism of complex chronic HBV infection,screening targeted drugs and selecting suitable HBV cell models in vitro.