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Background The Enoyl-CoA hydratase/isomerase family plays a crucial role in the metabolism of tumors, being crucial for maintaining the energy balance and biosynthetic needs of cancer cells. However, the enzymes within this family that are pivotal in gastric cancer (GC) remain unclear. Methods We employed bioinformatics techniques to identify key Enoyl-CoA hydratase/isomerase in GC. The expression of ECHDC2 and its clinical significance were validated through tissue microarray analysis. The role of ECHDC2 in GC was further assessed using colony formation assays, CCK8 assay, EDU assay, Glucose and lactic acid assay, and subcutaneous tumor experiments in nude mice. The mechanism of action of ECHDC2 was validated through Western blotting, Co-immunoprecipitation, and immunofluorescence experiments. Results Our analysis of multiple datasets indicates that low expression of ECHDC2 in GC is significantly associated with poor prognosis. Overexpression of ECHDC2 notably inhibits aerobic glycolysis and proliferation of GC cells both in vivo and in vitro. Further experiments revealed that overexpression of ECHDC2 suppresses the P38 MAPK pathway by inhibiting the protein level of MCCC2, thereby restraining glycolysis and proliferation in GC cells. Ultimately, it was discovered that ECHDC2 promotes the ubiquitination and subsequent degradation of MCCC2 protein by binding with NEDD4. Conclusions These findings underscore the pivotal role of the ECHDC2 in regulating aerobic glycolysis and proliferation in GC cells, suggesting ECHDC2 as a potential therapeutic target in GC.

β-Elemene, derived from (Wenyujin), is clinically recognized for inducing apoptosis, inhibiting cell cycle progression, and reversing chemotherapy resistance in various cancers. However, its effects on radioresistant gastric cancer (GC) remain unclear. In this study, radioresistant GC cell lines (MKN45/IR and AGS/IR) were established via multiple low-dose radiations. The impact of β-elemene on radiosensitivity was assessed using CCK-8 and clonogenic assays, with ferroptosis markers such as ROS, MDA, and Fe levels measured. Additionally, the influence of β-elemene on GPX4 and its interaction with OTUB1 was examined through qRT-PCR, Western blot, immunofluorescence, co-immunoprecipitation, and in vivo studies. Our findings indicate that β-elemene reverses radioresistance in GC cells and significantly inhibits cell growth when combined with radiotherapy. β-Elemene treatment elevated ROS, MDA, and Fe levels, enhancing ferroptosis, which was confirmed by Ferrostatin-1 and Deferoxamine inhibition studies. Mechanistic analysis revealed that β-elemene disrupts the OTUB1-GPX4 interaction, leading to increased GPX4 ubiquitination and degradation, thus promoting ferroptosis. studies further demonstrated that β-elemene combined with radiotherapy significantly suppressed tumor growth compared to radiotherapy alone. These results suggest that β-elemene effectively modulates radioresistance in GC by targeting the GPX4 pathway and inducing ferroptosis. This highlights its potential as a therapeutic adjunct in radiotherapy for resistant GC cases.

Background Parkinson's disease (PD) is a degenerative neurological disease that worsens over time. Ferroptosis has been proven to contribute to PD pathogenesis. CDG exhibits neuroprotective effects. However, CDG's potential mechanism in PD therapy remains uncertain. Purpose The purpose of this investigation is to ascertain the specific molecular mechanisms of CDG against neuronal ferroptosis and present an alternative option for PD management. Methods Network pharmacology along with LC–MS were used to identify possible targets and candidate pathways. Then RNA-sequencing combined in the in vitro and in vivo experiments were utilized to validate these findings. Results According to network pharmacology prediction, NFE2L2, HMOX1 and PTGS2 may be the key genes for ferroptosis in PD. In the in vivo experiments, CDG ultimately improved the neurobehavior of PD rats by alleviating the damage of dopamine neurons, decreasing the levels of MDA, ROS and Fe 2+ , increasing the GSH level, inhibiting ferroptosis by decreasing ACSL4, TF, and PTGS2 expression levels, and increasing the GPX4, FTH, Nrf2, and HMOX1 levels. RNA-seq analysis showed the differential genes in Model and CDG group were all enriched in Nrf2 and HMOX1, and the enrichment analysis of these differential genes showed they were closely related to the ferroptosis. Subsequently, in vitro experiments, the CDG, OE-Nrf2 and OE-HMOX1 group showed more active cell vitality, with decreasing levels of MDA, ROS, Fe 2+ , ACSL4, TF and PTGS2, and increasing level GSH, GPX4, FTH, Nrf2 and HMOX1. Conclusion CDG has a neuroprotective involvement in alleviating ferroptosis by regulating the Nrf2/HMOX1 pathway. Moreover, this research offers pharmacological evidence supporting the applications of CDG for treating PD.

Terahertz waves are expected to be used in next-generation communications, detection, and other fields due to their unique characteristics. As a basic part of the terahertz application system, the terahertz detector plays a key role in terahertz technology. Due to the two-dimensional structure, graphene has unique characteristics features, such as exceptionally high electron mobility, zero band-gap, and frequency-independent spectral absorption, particularly in the terahertz region, making it a suitable material for terahertz detectors. In this review, the recent progress of graphene terahertz detectors related to photovoltaic effect (PV), photothermoelectric effect (PTE), bolometric effect, and plasma wave resonance are introduced and discussed.

Objectives To discuss the characteristics of TCM syndrome factors and distribution discipline of congestive heart failure, and provide basis for the establishment of diagnosis criteria on essential syndromes. Methods 1) Based on databases of CNKI(1980-2012) and VIP(1989-2012), satisfactory modern documents on congestive heart failure were reorganised and analysed, and factors of compound syndromes were extracted. All the syndromes were classified to deficiency syndrome, excess syndrome, and deficiency complicated with excess syndrome. Compound syndromes were detached to separate syndrome factor in terms of single factor, two factors, three factors and four factors, and then each frequency of occurrence had been counted. 2) 1451 CHF cases from grade 3 and first-class hospitals (from December, 2010 to September, 2012) were collected, with statistical analysing by SPSS18.0. The correlations in CHF syndromes and age, sex, primary illnesses, clinical manifestations, BNP and cardiac functional grading had been studied, and the clinical distribution discipline on common syndromes of CHF had been summarised. Results 1) Literature analysis indicates: Syndrome factors on disease location of CHF are the heart, kidney, lung, and the spleen. Factors on natures of this disease sorted from more to less is qi deficiency, blood stasis, yang deficiency, yin deficiency, yang exhausted, water retention, phlegm, retained fluid, yin exhausted, heat, and blood deficiency. Qi deficiency of the heart was the most common syndrome in single factor of deficiency syndrome, qi and yin deficiency syndrome in two factors of deficiency syndrome, and blood stasis syndrome of the heart in single factor of excess syndrome, blood stasis and water retention in two factors of excess syndrome, qi deficiency and blood stasis in two factors of deficiency complicated with excess syndromes, qi deficiency and blood stasis mixed with water retention in three factors, and yang deficiency of the heart and spleen mixed with blood stasis and water retention in four factors. 2) Retrospective analysis of clinical cases indicates: The primary disease mainly is coronary heart disease. CHF is an ageing disease, patients aged over 80 years old are most common and that less than 50 years old are little. Stagnation of the heart blood syndrome and deficiency of both qi and yin syndrome are mostly seen in female patients. Syndrome of phlegm blocking heart vessel and qi deficiency and blood stasis syndrome are mostly seen in male patients. Deficiency syndrome of the heart qi and qi deficiency and blood stasis syndrome are mostly seen in patients aged 50-60. And that aged over 60 years old are likely manifested with deficiency of both qi and yin syndrome and stagnation of the heart blood syndrome. Syndrome aggravates with the going up of BNP level and cardiac functional grading. Conclusions The essential syndromes of congestive heart failure are qi deficiency and blood stasis syndrome, deficiency of both qi and yin syndrome. Besides, qi deficiency and blood stasis mixed with water retention syndrome can be seen with the extension of disease course. The clinical distribution discipline links to patients’ age and gender. Congestive heart failure mostly develops from coronary heart disease. BNP closely relates to cardiac functional grading and syndromes of CHF, which can be an expected indicator weighting the severity of TCM syndromes.

Compound Formula Rehmannia has been shown to be clinically effective in treating Parkinson's disease and levodopa-induced dyskinesia; however, the mechanisms remain unclear. In this study, we established a model of Parkinson's disease dyskinesia in rats, and treated these animals with Compound Formula Rehmannia. Compound Formula Rehmannia inhibited the increase in mRNA expression of N-methyl-D-aspartate receptor subunits 1 and 2 and excitatory amino acid neurotransmitter genes, and it inhibited the reduction in expression of γ-aminobutyric acid receptor B1, an inhibitory amino acid neurotransmitter gene, in the corpus striatum. In addition, Compound Formula Rehmannia alleviated dyskinesia symptoms in the Parkinson's disease rats. These experimental findings indicate that Compound Formula Rehmannia alleviates levodopa-induced dyskinesia in Parkinson's disease by modulating neurotransmitter signaling in the corpus striatum.

The ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) family of metalloproteinases plays a vital role in various biological and pathological processes, including tissue remodeling, angiogenesis, and cancer progression. Among the 19 ADAMTS family members, our research focused on ADAMTS7, which exhibited significant overexpression in gastric cancer (GC). This overexpression was strongly correlated with poor clinical outcomes, including reduced overall survival and heightened metastatic potential. To investigate the role of ADAMTS7 in GC, we employed an integrated approach encompassing bioinformatics analysis, Western blotting, immunofluorescence, as well as and functional analyses. Our results showed that silencing ADAMTS7 expression significantly inhibited the proliferation, migration, and invasion of GC cells, and furthermore, silencing ADAMTS7 significantly inhibited the growth and metastasis of tumour cells in nude mice, highlighting its critical role in driving the malignant behaviour of GC cells. Further mechanistic studies identified the NF-κB signaling pathway as a key downstream target of ADAMTS7, with ADAMTS7 silencing resulting in a notable reduction in NF-κB pathway activity. These findings establish ADAMTS7 as a significant contributor to the aggressiveness of GC and a pivotal activator of the NF-κB pathway, a major regulator of inflammation and tumor progression. Consequently, ADAMTS7 emerges as a promising therapeutic target and prognostic biomarker for GC. Our study opens new avenues for the development of targeted therapies aimed at inhibiting ADAMTS7 activity, thereby potentially improving treatment outcomes and survival rates for patients with GC.

Parkinson's disease (PD) is a common degenerative disease of the nervous system that seriously affects the quality of life of the patients. The pathogenesis of PD is not yet fully clear. Previous studies have confirmed that patients with PD exhibit obvious gut microbiota imbalance, while intervention of PD by regulating the gut microbiota has become an important approach to the prevention and treatment of this disease. Traditional Chinese medicine (TCM) has been shown to be safe and effective in treating PD. It has the advantages of affecting multiple targets. Studies have shown TCM can regulate gut microbiota. However, the specific mechanism of action is still unclear. Therefore, this article will mainly discuss the association of the alteration of the gut microbiota and the incidence of PD, the advantages of TCM in treating PD, and the mechanism of regulating gut microbiota by TCM to treat PD. It will clarify the target and mechanism of TCM treating PD by acting gut microbiota and provided a novel methodology for the prevention and treatment of PD. Keywords: Parkinson's disease, gut microbiota, traditional Chinese medicine, pathogenesis

Objective To test the effect of Xin Fu Kang Oral Liquid on the activities of respiratory enzyme (I—IV) in pressure overload-induced left ventricular hypertrophy in rats. Methods The models of congestive heart failure (CHF) were established by constricting the abdominal aorta of rats partly. 75 SD rats were randomly divided into Sham operation (SH), Coarctation of abdominal aorta model group (CAA) and Xinfufang Oral Liquid group (XFK). The activities of respiratory enzyme (I—IV) were respectively measured by spectrophotometric method in every group at the 10th, 12th week after the interventional of the drugs. Results The study shows that CAA group the activities of respiratory enzyme significantly decreased, the activities of respiratory enzyme II (SDH), IV (CCO) have obviously difference (p<0.01), In the XFK group the activities of respiratory enzyme obviously increased compared with CAA and by the 10th, 12thweek, SDH, CCO have obviously difference (p<0.01), The activities of respiratory enzyme of the 12th week in XFK group obviously increased compared with that of the 10th week, SDH, CCO have obviously difference (p<0.05). Conclusion XinFuKang Oral Liquid can obviously improve the activities of respiratory enzyme of congestive heart failure rats.

Objective To investigate the effect of Xinfukang Oral Liquid on the expression of ND4 mRNA and Protein of myocardial mitochondria in pressure overload-induced left ventricular hypertrophy rats. Methods Totally, 240 SD rats were randomly divided into three groups, sham operation group (SH) (n=80), coarctation of abdominal aorta model group (CAA) (n=80) and model and Xinfukang liquid treatment group (XFK) (n=80). Congestive Heart Failure rat models were made by partly coarctating the abdominal aorta of rats. Expression of ND4 mRNA and protein were observed at the fourth, eighth and 12th week after the treatment, respectively by RT-PCR and Western Blotting. Results In CAA group at the eighth week after operation, the content of ND4 mRNA and ND4 protein were both decreased compared with SH group (p<0.01); content of ND4 mRNA (p<0.01) and ND4 protein (p<0.05) in XFK group were increased compared with CAA group. And these changes were far more significant at 12 weeks. Conclusion XFK oral liquid can upregulate expression of ND4 mRNA and ND4 protein in myocardial mitochondria of pressure overload rats and improve Myocardial energy metabolism.