Background: Adrenocortical hormones, particularly 11-oxygenated androgens, are pivotal in female reproductive health and fertility. Standardized detection kits and population-specific reference intervals are lacking in China, hindering related clinical applications. Methods: A HPLC-tandem mass spectrometry (HPLC-MS/MS) pipeline was developed, rigorously validated, and applied to simultaneously quantify corticosterone, cortisone, cortisol, 18-OH cortisol, androstenedione (A4), 11β-hydroxyandrostenedione (11-OH A4), dehydroepiandrosterone, and dehydroepiandrosterone sulfate in serum samples from 455 reproductive-aged women (18–45 yrs) in Guangxi, China. Age-dependent concentration trends were analyzed, and reference intervals stratified by age (2.5th to 97.5th percentiles) were established. Correlations with body-composition metrics, ethnicity, and the menstrual cycle were investigated. Results: The HPLC-MS/MS method demonstrated high precision (intra- and inter-assay CVs < 15%), accuracy, and sensitivity. All eight hormones exhibited significant age-related declines (P < 0.001 for seven hormones; P = 0.001 for 11-OH A4). Notably, 11-OH A4 levels were significantly lower in the 35–45-yr (3.05 nmol/L) and 25–34-yr (3.09 nmol/L) age groups than in the 18–24-yr (3.57 nmol/L) age group, whereas no significant difference was observed between the 35–45-yr and 25–34-yr age groups. Weak negative correlations were observed between the body mass index and corticosterone and cortisone levels, whereas ethnicity and the menstrual cycle showed no significant associations with hormone levels. Conclusions We developed an HPLC-MS/MS-based method for simultaneously quantifying eight adrenocortical hormones, including 11-OH A4, and defined age-specific reference intervals for reproductive-aged Chinese women. These findings advance the clinical utility of adrenocortical hormones in diagnosing and managing reproductive disorders.

Biomolecular condensates are formed through phase separation of biomacromolecules such as proteins and RNAs. These condensates exhibit liquid-like properties that can futher transition into more stable material states. They form complex internal structures via multivalent weak interactions, enabling precise spatiotemporal regulations. However, the use of inconsistent and non-standardized terminology has become increasingly problematic, hindering academic exchange and the dissemination of scientific knowledge. Therefore, it is necessary to discuss the terminology related to biomolecular condensates in order to clarify concepts, promote interdisciplinary cooperation, enhance research efficiency, and support the healthy development of this field.

The eIF3i gene was amplified from lamb testicular(LT)cells by PCR and cloned into pCold vector to construct the pCold-eIF3i plasmid.Plasmid PCR,double enzyme digestion and se-quencing were used to verify the results.The recombinant eIF3i protein was induced under the op-timized expression conditions.The expression and reactogenicity of the target protein were detected by SDS-PAGE and Western blot.New Zealand white rabbits were immunized with purified recom-binant eIF3i protein combined with Freund's complete and incomplete adjuvants for three times.Se-rum samples were collected after immunization.Indirect ELISA was used to detect antiserum titer,and Western blot was used to analyze antibody specificity.Indirect immunofluorescence assay(IFA)was used to detect the application effect of antibodies.The results showed that the size of LT eIF3i gene was 978 bp.The optimal expression conditions for the eIF3i recombinant protein were as follows:IPTG concentration of 0.2 mmol/L,temperature of 37 ℃,and induction time of 8 h.The recombinant eIF3i protein was expressed as an inclusion body with a size of about 36 kDa.The titer of polyclonal antibody against eIF3i protein was 1∶51 200.Western blot and IFA showed that the prepared polyclonal antibody against eIF3i protein had good reactivity and specificity.In conclusion,we successfully prepared rabbit anti-eif3i polyclonal antibody and confirmed that it could specifically recognize endogenous eIF3i protein,which laid a foundation for further study on the biological function of eIF3i protein.

OBJECTIVE: Glucocorticoid-induced osteoporosis (GIOP) is a common complication of prolonged glucocorticoid therapy. Chlorogenic acid (CGA), a polyphenol with antioxidant properties that is extracted from traditional Chinese medicines such as Eucommiae Cortex, has potential anti-osteoporotic activity. This study aimed to investigate the possible effects of CGA on GIOP in mice and murine long bone osteocyte Y4 (MLO-Y4) cells and explore the underlying molecular mechanisms. METHODS: The protective effects of CGA were initially evaluated in the GIOP mouse model induced by dexamethasone (Dex). The micro-computed tomography, hematoxylin-eosin staining, silver nitrate staining, and serum detection were used to assess the efficacy of CGA for improving bone formation in vivo. Then, network pharmacology analysis was used to predict the potential targets and molecular mechanisms underlying the therapeutic efficacy of CGA against GIOP. After that, 2',7'-dichlorofluorescein diacetate staining, flow cytometry, real-time quantitative reverse transcription polymerase chain reaction, and Western blotting were used to verify the mechanisms of CGA against GIOP in vitro. RESULTS: Animal experiments showed that CGA treatment effectively attenuated Dex-induced decreases in bone mass and strength and improved disrupted osteocyte morphology in mice. The protein-protein interaction analysis highlighted erb-b2 receptor tyrosine kinase (ERBB2), which is also known as human epidermal growth factor receptor 2 (HER2), caspase-3, kinase insert domain receptor, matrix metallopeptidase 9, matrix metallopeptidase 2, proto-oncogene tyrosine-protein kinase Src, and epidermal growth factor receptor as core targets. The Kyoto Encyclopedia of Genes and Genomes analysis revealed several significantly enriched pathways (P < 0.05), including the ERBB, phosphoinositide 3 kinase-AKT serine/threonine kinase 1 (AKT), and mechanistic target of rapamycin kinase (mTOR) pathways. Cellular experiments verified that CGA enhanced bone formation and promoted autophagy while inhibiting apoptosis in MLO-Y4 cells exposed to Dex, which was associated with the upregulated expression of HER2 and activation of the HER2/AKT/mTOR signaling pathway. CONCLUSION CGA exerted anti-osteoporotic effects against GIOP, partially through targeting osteocytes and modulating the HER2/AKT/mTOR signaling pathway. Please cite this article as: Xie AN, Zhang SZY, Zhang Y, Cao JL, Wang CL, Wang LB, Wu HJ, Zhang J, Dai WW. Chlorogenic acid mitigates glucocorticoid-induced osteoporosis via modulation of HER2/AKT/mTOR signaling pathway. J Integr Med. 2025; 23(6):670-682.
Animals ; Chlorogenic Acid/therapeutic use* ; Osteoporosis/metabolism* ; Signal Transduction/drug effects* ; Proto-Oncogene Proteins c-akt/metabolism* ; TOR Serine-Threonine Kinases/metabolism* ; Mice ; Glucocorticoids/adverse effects* ; Receptor, ErbB-2/metabolism* ; Proto-Oncogene Mas ; Dexamethasone/adverse effects* ; Osteocytes/drug effects* ; Osteogenesis/drug effects* ; Male ; Cell Line ; Mice, Inbred C57BL ; Humans

In elderly patients with malignant tumor,sarcopenia frequently co-occurs,which is largely attributed to the cachexia state observed in cancer patients.Although both sarcopenia and cachexia involve muscle loss,there are significant distinctions between the two conditions.Current research indicates that sarcopenia is a multifactorial condition,influenced by factors such as aging,endocrine dysfunction,motor neuron loss,cachexia,inflammation,and malnutrition.With the increasing depth of research into the correlation between sarcopenia and the nervous and immune systems,this article reviews the research progress on sarcopenia in patients with malignant tumors,with a focus on neuroimmunological aspects.It systematically analyzes the mechanisms underlying its onset and progression,as well as the influencing factors and potential intervention strategies for sarcopenia in this patient population.

Objective:Exploring the role and mechanism of CHMP4C in regulating necroptosis during gastric can-cer development and progression.Method:The expression of CHMP4C in pan-cancer was analyzed by bioinformatics methods,and the expression of CHMP4C was detected in human normal gastric epithelial cells and GC cell lines by RT-qPCR and Western blot.Overexpression or knockdown of CHMP4C was performed in GC cell lines,and the effects of CHMP4C on the growth and proliferation of GC cells were detected using CCK-8 and clone formation assays.The CCK-8 experiment and Hoechst/PI double staining experiment were used to detect the changes in GC cell mortality and PI positive cell ratio after treatment with the necroptsis inducer TSZ or inhibitor necrostatin-1(Nec-1).Western blot assay was used to detect the protein and phosphorylation levels of RIPK1,RIPK3,and MLKL in GC cells.Result:CHMP4C was upregulated in GC tissues and cells.The CCK-8 and clone formation experiments showed that overex-pression of CHMP4C significantly improved the proliferation ability and colony formation efficiency of GC cells,while knockdown of CHMP4C significantly weakened GC cells.Moreover,the results of CCK-8 and Hoechst 33342/PI double staining experiments showed that upregulated CHMP4C could inhibit TSZ induced GC cell death;Nec-1 can reverse the decrease in GC cell viability caused by CHMP4C knockdown.Western blot experiment showed that the levels of p-RIPK1,p-RIPK3,and p-MLKL were significantly decreased in overexpressing cells,while they were increased in knockdown cells.After treatment with Nec-1,the expression levels of these three proteins decreased in knockdown cells.Conclusion:CHMP4C may promote GC progression by negatively regulating necroptosis through inhibiting the phosphorylation of the RIPK1/RIPK3/MLKL signaling pathway,suggesting that it is expected to be a potential target for GC therapy.

Aim To explore the mechanism of Cong Rong San on AD model rats based on protein kinase R-like endoplasmic reticulum kinase(PERK)-eukaryotic initiation factor 2α(eIF2α)-nuclear factor kappa B(NF-κB)signaling pathway.Methods Sixty mice were randomly divided into normal group,model group,Cong Rong San groups(4.62,9.24,18.48 g·kg-1)and donepezil group,with 10 mice in each group.All groups of rats received bilateral hippocampal injections of Aβ1-42 to establish the AD model,except the normal group.After the intragastric administration,the Morris water maze behavior test was performed for rats to test-ed the learning and memory abilities.Nissl staining was detected the quantity and Nissl bodies of nerve cells.To detect the nuclear translocation of NF-κB by immu-nofluorescence.To observe the ultrastructure of endo-plasmic reticulum by Transmission electron microsco-py.ELISA for Aβ1-42 and inflammatory cytokines quantification.Western blot was used to detect the ex-pression level of protein in the hippocampus in PERK-eIF2α-NF-κB signaling pathway.Results The morris water maze results showed that Cong Rong San im-proved the escape latency time,increased the number of platform crossings,and prolonged the time spent in the target quadrant in AD rats.(P＜0.05 or P＜0.01).Nissl staining shows the neuronal cells are ar-ranged neatly,nucleus are present and the number of Nissl bodies was numerous and the number of neurons was increased in various doses of Cong Rong San.Im-munofluorescence showed that the expression of NF-κB in the nucleus of rats was decreased(P＜0.05 or P＜0.01).The shape of endoplasmic reticulum was neat,no significantly expanded,and the structure was normal in various doses of Cong Rong San.The levels of Aβ1-42,IL-1,TNF-α and the ratio of p-PERK/PERK,p-eIF2α/eIF2α,p-NF-κB p65/NF-κB p65 in hippo-campus of Cong Rong San group was significantly de-creased in ELISA and Western blot test(P＜0.05 or P＜0.01).Conclusion Cong Rong San can alleviates the immune inflammatory response of neuronal cells in the ERS state for improve the learning and memory a-bility of AD rats,the mechanism of action may through restraint the activation of PERK-eIF2α-NF-κB signa-ling pathway.

Ferroptosis is an iron-dependent cell death modality triggered by the accumulation of lipid peroxides and is closely linked to tumor pathogenesis. Ferritinophagy refers to the selective autophagic degradation of ferritin, releasing intracellular stored iron to maintain iron metabolic homeostasis. This process is also significantly associated with tumor-targeted interventions. This review systematically elucidates the mechanisms of ferroptosis and ferritinophagy, their roles in tumor progression, and the therapeutic potential of pharmacologically induced ferritinophagy in anticancer strategies.

In elderly patients with malignant tumor,sarcopenia frequently co-occurs,which is largely attributed to the cachexia state observed in cancer patients.Although both sarcopenia and cachexia involve muscle loss,there are significant distinctions between the two conditions.Current research indicates that sarcopenia is a multifactorial condition,influenced by factors such as aging,endocrine dysfunction,motor neuron loss,cachexia,inflammation,and malnutrition.With the increasing depth of research into the correlation between sarcopenia and the nervous and immune systems,this article reviews the research progress on sarcopenia in patients with malignant tumors,with a focus on neuroimmunological aspects.It systematically analyzes the mechanisms underlying its onset and progression,as well as the influencing factors and potential intervention strategies for sarcopenia in this patient population.

Establishing a scientific talent classification evaluation mechanism is of great significance for public hospitals to motivate and guide the career development of various types of talents and to promote the high-quality development of the health and medical care industry. However, university-affiliated hospitals had long faced issues such as an imperfect talent classification evaluation system, difficulty in setting evaluation indicators, a relatively monolithic evaluation method, and insufficient application of evaluation results. In 2019, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, initiated a talent stratification and classification management mechanism. The hospital established separate evaluation indicator systems for clinical, research, and teaching talents, and adhered to a value orientation that equally emphasizes medical care, teaching, and research. Additionally, a diversified evaluation mode was constructed, led by the hospital with the participation of peers and the public. Emphasis was also placed on linking evaluation results with talent development, rewards, and excellence awards. The initiative has achieved positive outcomes and can serve as a reference for talent management in other university-affiliated hospitals and relevant departments.