Gardeniae Fructus (GF) is one of the most commonly used medicinal and edible resources in China, renowned for its anti-inflammatory and antipyretic effects. However, studies of the chemical characteristics, metabolic transformation and pharmacokinetic behavior of GF in vivo remain incomplete. This study utilized mass defect filtering (MDF) combined with UHPLC-ESI-Q-TOF-MS/MS to analyze the in vitro chemical constituents of GF aqueous extracts and its metabolites in vivo in rats, comprehensively characterizing 114 chemical constituents and 181 endogenous substances, including 18 prototype constituents and 163 metabolites (21 phase Ⅰ and 142 phase Ⅱ metabolites). Additionally, a quantitative method using UHPLC-QQQ-MS/MS was developed to analyze the in vivo dynamics of seven bioactive compounds, and the pharmacokinetic parameters of the main active components in the GF aqueous extracts, namely geniposidic acid, deacetyl asperulosidic acid methyl ester, gardenoside, genipin, genipin 1-β-D-gentiobioside, geniposide, and crocetin, were obtained. This study conducted a comprehensive and systematic investigation into the potential material basis and the in vivo biotransformation profile of GF aqueous extracts based on UHPLC-ESI-Q-TOF-MS/MS coupled with MDF technology and UHPLC-QQQ-MS/MS, providing crucial evidence for further elucidating its pharmacological mechanisms.

Based on extensive research into the current status of understory medicinal herb cultivation and an in-depth analysis of existing problems, this study proposes policy and technical recommendations to promote sustainable and high-quality development. The research team conducted field investigations in advantageous cultivation regions across seven provinces (autonomous regions), including Guangxi, Yunnan, Fujian, and Jilin, supplemented by policy reviews and literature analysis. The findings reveal that although understory medicinal herb cultivation benefits from ecological advantages and policy support, it still faces a series of problems, such as an underdeveloped service system, insufficient regulatory capacity, low market alignment, and immature technical systems. It should be particularly noted that understory cultivation commonly encounters specific challenges, including the economic dilemma of high input and low output, mismatches between forest canopy density and the light requirements of medicinal plants, ambiguous boundaries between ecological protection and utilization in policy implementation, and weak research support, leading to high trial-and-error costs in technology adoption. The following development recommendations are proposed: ① establish a coordination mechanism between forestry and traditional Chinese medicine authorities to integrate planning and policy synergy; ② enhance the alignment of understory medicinal herb cultivation with market demand; ③ develop an independent technical system and standards for understory medicinal herb cultivation, such as establishing a variety suitability framework based on canopy density classification and ecological cultivation protocols; ④ strengthen research focused on industrial development, with priority given to large-scale plantations (e. g., pine and fir forests), dual-purpose food-medicine species (Polygonatum, Gastrodia elata), vine species, and intercropping effects; ⑤ establish a quality certification system and corresponding regulatory framework for understory-cultivated medicinal materials to promote premium pricing; ⑥ improve land-use policies and supporting infrastructure, clarifying utilization rights for different forest types and simplifying approval procedures for temporary facilities.

This study is aimed to investigate the therapeutic effects of Junren Bufei Yixin Granules (JRBF) on hypoxic pulmonary hypertension (HPH) and explore the therapeutic mechanism through the polypyrimidine tract-binding protein 1 (PTBP1)/pyruvate kinase isozyme type M2 (PKM2) signaling pathway. Sixty SPF-grade C57BL/6 male mice were randomized into normal, model, sildenafil, and low/medium/high-dose JRBF groups. HPH was induced by hypoxic exposure (10% O₂, 8 h/day) for 4 weeks. The right ventricular systolic pressure (RVSP) was measured by right cardiac catheterization. Echocardiography was employed record the pulmonary artery acceleration time (PAAT), pulmonary ejection time (PET), tricuspid annular plane systolic excursion (TAPSE), and right ventricular anterior wall thickness at diastole (RVAWd). The histopathological changes were observed by hematoxylin-eosin (HE) and Masson staining. Western blot was employed to measure the expression levels of PTBP1, PKM2, and PKM1 in the lung tissue. The immunofluorescence assay was employed to detect the co-localization of PTBP1 with the marker alpha-smooth muscle actin (α-SMA) of pulmonary arterial smooth muscle cells (PASMCs). The lactate assay kit was used to measure the lactate levels in the serum and lung tissue. In the cell experiments, the hypoxia model was established by exposing human pulmonary artery smooth muscle cells (hPASMCs) to 1% O₂ for 48 h. The optimal (10%) JRBF concentration for intervention was determined by the cell-counting kit-8 (CCK-8). The cell proliferation (EdU), migration (Transwell), PTBP1/PKM2/PKM1, and lactate production were analyzed. The results showed that JRBF significantly reduced the RVSP, improved the PAAT/PET ratio and TAPSE, and attenuated pulmonary arteriolar remodeling and myocardial fibrosis. Furthermore, JRBF suppressed PTBP1 and PKM2 expression and reduced the lactate accumulation in the lung tissue and PASMCs. The cell experiment results showed that the 10% JRBF-containing serum inhibited the proliferation and migration of hPASMCs, while decreasing the PTBP1/PKM2 expression and lactate production. In conclusion, JRBF mitigates HPH progression by suppressing the PTBP1/PKM2 axis and restoring the glycolytic flux.

This study aimed to elucidate the mechanisms of diosgenin, a natural compound derived from traditional Chinese medicine, on the triple-negative breast cancer cell line MDA-MB-231, with a focus on its induction of cell cycle arrest and inhibition of cell migration. Multiple experimental approaches were employed, including RNA sequencing analysis, flow cytometry for cell cycle detection, wound healing assays to evaluate migration capacity, F-actin staining to observe cytoskeletal changes, transmission electron microscopy (TEM) to examine cellular morphology and filopodia alterations, as well as Western blot and immunofluorescence staining to detect the expression of related proteins. RNA sequencing revealed significant gene expression differences between the diosgenin-treated group and the control group, with KEGG and GO analyses showing enrichment of differentially expressed genes mainly in pathways related to cell cycle and migration. Flow cytometry demonstrated that diosgenin induced G₀/G₁ phase arrest in MDA-MB-231 cells in a dose-dependent manner. Further Western blot and immunofluorescence assays indicated that diosgenin regulated the cell cycle via the CDC25A-CDK2/4/6 axis. Wound healing assays showed that diosgenin significantly inhibited cell migration. F-actin staining indicated that diosgenin suppressed F-actin formation and disrupted its structure. TEM observations revealed a reduction in filopodia formation on the cell surface after diosgenin treatment. Moreover, Western blot and immunofluorescence results demonstrated that diosgenin inhibited migration by suppressing epithelial-mesenchymal transition (EMT) and the RhoA-ROCK1 signaling pathway. In conclusion, diosgenin induces G₀/G₁ phase arrest in MDA-MB-231 cells by regulating cell cycle-related proteins and significantly inhibits cell migration by suppressing F-actin formation, reducing filopodia on the cell surface, and inhibiting EMT and the RhoA-ROCK1 pathway.

Chronic obstructive pulmonary disease (COPD) characterized by persistent airflow limitation is a heterogeneous lung condition prone to exacerbations and progression. Recent studies have revealed that gut microbiota dysbiosis can trigger metabolic disorders, immune abnormalities, and inflammatory responses, contributing to the pathogenesis and progression of COPD through the gut-lung axis. The spleen-tonifying and lung-replenishing therapy originates from the five elements theory of TCM, specifically the principle of tonifying the source in the case of deficiency. Enhancing the function of the spleen and stomach (earth element) indirectly nourishes the lungs (metal element), embodying the holistic concept of organ interdependence. The gut, as an extension of the transformation function of the spleen and stomach, reflects the modern interpretation of the spleen's role in transformation and transportation. When the spleen is deficient, gut microbiota dysbiosis leads to the accumulation of turbid toxins, which rise to affect the lungs, resulting in impaired flow of healthy Qi and the interplay of phlegm and stasis. The concept of tonifying the spleen not only involves tonifying the middle Qi but also encompasses multidimensional interventions such as improving gastrointestinal functions and regulating the gut microbiota to restore lung-spleen coordination. The spleen-tonifying and lung-replenishing therapy can influence the gut microbiota in COPD patients, effectively interrupting the pathological vicious cycle of spleen deficiency-microbiota dysbiosis-lung damage, slowing down disease progression, and reducing acute exacerbations. This method highlights the scientific value of the holistic thinking in TCM and provides a key pathway for integrating TCM and Western medicine in the prevention and treatment of COPD, underscoring the core clinical significance of tonifying the spleen and replenishing the lung.

TCM volatile oil exhibits excellent biological activities and wide application scenarios. However, its volatility and susceptibility to oxidation and deterioration severely restrict the quality of its preparations and clinical efficacy. Therefore, stabilizing TCM volatile oil is extremely necessary. Current research mainly focuses on the development of stabilization techniques and carrier materials, aiming to enhance its stability and endow it with sustained-release and controlled-release properties. In recent years, researchers have increasingly paid attention to the intrinsic mechanisms and potential interactions during the stabilization process, which is of great significance for the development of new stabilization technologies for volatile oil and the research on new dosage forms containing volatile oil. This article systematically reviews the mechanisms of action during the stabilization of TCM volatile oil and summarizes the key methods for characterizing interactions, with the aim of providing references for the development of new stabilization technologies for TCM volatile oil and the theoretical research on its stabilization.

Poria cocos is a commonly used bulk traditional Chinese medicinal material, with multiple parts used medicinally, such as Poriae Cutis, Rubra Poria, White Poria, and Poria cum Radix Pini. Polysaccharides are their main active components. Clarifying the composition and content differences of polysaccharides in different medicinal parts of P. cocos can provide a reference for processing and clinical application of P. cocos medicinal materials and decoction pieces. In this paper, high-performance gel permeation chromatography (HPGPC) and nuclear magnetic resonance (NMR) spectroscopy were employed to qualitatively compare the relative molecular mass distribution and chemical composition of alkali-soluble polysaccharides from different parts of crude P. cocos. The results showed that the composition of alkali-soluble polysaccharides in Rubra Poria and Poriae Cutis was consistent with that in White Poria, all of which were β-(1→3) -D-glucans. The relative molecular mass distribution was also relatively close, ranging approximately from 9.13×10⁴ to 1.04×10⁵. On the basis of the content determination method of β-(1→3) -D-glucan in P. cocos according to the 2025 edition of Chinese Pharmacopoeia, the preparation method of the test sample solution was optimized. Firstly, a desalination step was added, which can enable the test sample chromatogram to present only the chromatographic peak of glucose, thereby reducing the difficulty of separation. Secondly, this experiment discovered for the first time that under acidic conditions, the hydrolysis of β-(1→3) -D-glucan to glucose was accompanied by the generation of a small amount of 5-hydroxymethylfurfural (5-HMF) as a by-product. A more intense acid hydrolysis reaction condition indicated a greater conversion yield of 5-HMF. Therefore, according to the results of single-factor experiments and response surface methodology experiments, the acid hydrolysis time was shortened from 6 h to 1.5 h, which improved the analysis efficiency. After verification, the optimized method was simple and stable, and had good repeatability and accuracy. Then, the optimized quantitative method was used to evaluate the content of β-(1→3) -D-glucan in different parts of crude P. cocos and decoction pieces. The results demonstrated that the content of β-(1→3) -D-glucan in different medicinal parts of P. cocos was in the order of White Poria, Poria cum Radix Pini, Rubra Poria, and Poriae Cutis. Among the commercially available Poria decoction pieces, the content of β-(1→3) -D-glucan in the white and hard decoction pieces was higher than that in the dark and loose-textured decoction pieces.

Based on the adiponectin receptor/5′-AMP-activated protein kinase catalytic subunit α-1/carnitine palmitoyltransferase 1b (AdipoR/AMPKα/Cpt1b) signaling axis, this study investigated the therapeutic mechanisms of Jianpi Huogu Formula (JPHGF) in alcohol-induced osteonecrosis of the femoral head (AONFH). A total of 56 Sprague-Dawley rats were randomly divided into a normal group, a model group, and a JPHGF group (5.0 g·kg^-1). Except for the normal group, rats in the other two groups were administered 46% ethanol by gavage to establish the AONFH model, and JPHGF intervention was initiated in the treatment group at week 4 after model induction. After 4 and 8 weeks of intervention, samples were collected. Mechanical and cold pain thresholds were assessed using Von Frey filaments and the acetone drop test, respectively. Hindlimb muscle strength was evaluated by the inclined plane test. Micro-computed tomography (micro-CT) was used to determine bone mineral density (BMD), bone volume fraction (BV/TV), trabecular thickness (Tb. Th), and other bone morphometric parameters. Hematoxylin-eosin (HE) staining was performed to observe histopathological changes. Transcriptomic sequencing was conducted to identify differentially expressed genes (DEGs) regulated by JPHGF in AONFH, followed by Gene Ontology (GO) functional and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. Western blot was used to detect the protein expression of AdipoR1, AdipoR2, phosphorylated AMPKα, and Cpt1b in femoral head tissues. The results showed that after 8 weeks of modeling, rats in the model group exhibited significantly decreased mechanical pain thresholds and increased cold sensitivity (P<0.05, P<0.01), indicating hyperalgesia. The maximum inclined angle was markedly reduced (P<0.01), suggesting weakened hindlimb muscle strength. The femoral head surface appeared rough, with enlarged dark-red cartilage areas and sparse, disrupted trabeculae; the proportion of empty lacunae and the number of adipocytes were significantly increased (P<0.01), while BMD, BV/TV, Tb. Th, and trabecular number (Tb. N) were significantly decreased (P<0.01). After 4 weeks of JPHGF intervention, mechanical and cold hyperalgesia were significantly alleviated (P<0.05), hindlimb strength was restored (P<0.01), and surface morphology of the femoral head was improved. After 8 weeks, trabecular structure was further restored, with decreased empty lacunae and reduced adipocyte numbers, and BMD, BV/TV, Tb. Th, and Tb. N significantly increased (P<0.05, P<0.01); cystic degeneration and collapse were markedly alleviated. Transcriptomic analysis revealed that JPHGF significantly regulated 231 key DEGs, which were mainly enriched in adipocytokine signaling pathways and closely associated with AdipoR1, AdipoR2, p-AMPKα, and Cpt1b. Western blot analysis showed that AdipoR1, AdipoR2, p-AMPKα, and Cpt1b expression levels were significantly downregulated in the AONFH model group compared with the normal group (P<0.01), but were markedly upregulated following JPHGF treatment (P<0.05, P<0.01). In summary, this study demonstrates that JPHGF exerts therapeutic effects against AONFH by activating the AdipoR/AMPKα/Cpt1b signaling axis, thereby improving bone marrow lipid homeostasis and restoring femoral head microarchitecture, effectively relieving pain and functional impairment. These findings provide new experimental evidence and molecular targets for the prevention and treatment of AONFH in clinical practice.

Attention deficit hyperactivity disorder (ADHD), a common neurodevelopmental disorder in children, is characterized by inattention, hyperactivity, and impulsivity. Epidemiological surveys show that the prevalence of ADHD in children is gradually increasing worldwide, and it is the most common childhood mental disorder in China. Because of the complex clinical symptoms, multiple co-morbidities, and unknown etiology, ADHD has far-reaching negative impacts on individuals, families, and the society. Behavioral interventions, as a pillar in the management of ADHD, play a targeted role in improving children's social functioning, with significant benefits supported by evidence. However, they are constrained by uneven resources, poor compliance, and insufficient continuity, Western medicine has multiple adverse effects and unclear long-term effects in the treatment of ADHD despite the definite efficacy. Accordingly, there is an urgent need to find safe and effective therapies suitable for children. With a holistic view and treatment based on syndrome differentiation, traditional Chinese medicine (TCM) has significant advantages in treating ADHD via multiple targets, which involves dopamine (DA), norepinephrine (NE), 5-hydroxytryptamine (5-HT), cyclic adenosine monophosphate (cAMP), brain-derived neurotrophic factor (BDNF) and other signaling pathways. Through these pathways, TCM can treat ADHD through the regulation of neurotransmitters, enhancement of prefrontal and striatal functions, enhancement of neuronal protection, attenuation of neuroinflammation, and reduction of neuronal apoptosis. However, a systematic study remains to be conducted. This paper summarizes the signaling pathways related to the treatment of ADHD by TCM in the past two decades, aiming to provide reference for delving into the mechanism and exploring effective TCM prescriptions for ADHD in children and to give full play to the advantages of the efficacy and characteristics of TCM.

Mitochondrial dysfunction is a key pathological mechanism in metabolic-associated fatty liver disease (MAFLD), and regulating mitochondrial function to restore normal activity is an important therapeutic strategy. The theory of "harmful hyperactivity and responding inhibition" is a classical TCM principle that explains cyclical patterns in nature, interprets physiological and pathological phenomena in the human body, and guides TCM clinical diagnosis and treatment. The mechanism of mitochondrial dysfunction closely aligns with the process described in this theory as when the responding element fails to control, the hyperactive element becomes harmful. Based on the relationship between mitochondrial function and the TCM pathogenesis of MAFLD, and applying the "harmful hyperactivity and responding inhibition" framework, this study proposes that MAFLD originates from spleen deficiency impairing nutrient transport and failing to disperse essence, kidney Yang deficiency leading to impaired Qi transformation, and insufficient mutual regulation of the two, resulting in pathological products such as excessive accumulation of phlegm-turbidity, dampness, and blood stasis. These pathological changes manifest as mitochondrial dysfunction, including mtDNA damage, hepatocyte injury, lipid peroxidation, and mitochondrial accumulation. Clinically, MAFLD treatment follows the principle of regulating the responding element and restraining the hyperactive element: reinforcing the spleen earth to restore regulation, strengthening kidney water to nourish the kidneys and harmonize the liver, and addressing phlegm-stasis obstruction and hyperactivity through blood-activating and phlegm-resolving therapies. By modulating mitochondrial structure and function, this approach improves hepatic lipid metabolism, reduces oxidative stress, and alleviates inflammatory responses, achieving multi-target therapeutic effects. This study provides new theoretical foundations and practical strategies for integrated TCM-western medicine treatment of MAFLD.