To analyze the changing pattern of blood stasis degree in different TCM syndromes of non-traumatic osteonecrosis of femoral head (NONFH), the present study adopted a retrospective cross-sectional design. The clinical and digital subtraction angiography (DSA) data were collected from 60 NONFH patients with blood stasis syndrome treated at the Third Affiliated Hospital of Beijing University of Chinese Medicine from February 2022 to March 2025. According to Chinese Medicine Identification Criteria for Necrosis of the Femoral Head (2019 edition), 60 patients were allocated into three groups of phlegm-stasis obstruction of collaterals, meridian obstruction, and liver-kidney deficiency, with 20 patients in each group. The morphological features of blood vessels were observed by DSA, and the diameter of the profunda femoris artery, diameters of medial/lateral circumflex femoral arteries, and vessel count were recorded. The degrees of blood stasis in different syndrome groups were analyzed. The results showed that there were 38 males and 22 females among the 60 patients, with mean age of (41.18±14.56) years. Two, thirty-three, twenty-two, and one patients were in ARCO stages Ⅰ, Ⅱ, Ⅲ and Ⅳ, respectively. There was no difference in the baseline data (age, BMI, etc.) among the three groups. Regarding the vascular parameters, the meridian obstruction group had the profunda femoris artery diameter of (6.59±0.94) mm, medial circumflex femoral artery diameter of (2.99±0.42) mm, medial/lateral ratio of 0.50 (0.43, 0.58), and total number of arteries being 8.00 (7.00, 8.00), which were all lower than those in the phlegm-stasis obstruction group and the liver-kidney deficiency group (P<0.05, P<0.01). The results indicated that the DSA of NONFH patients with blood stasis presented abnormal vascular morphology, and their vascular images showed a certain pattern throughout the disease course, with lower vessel diameter and count in the middle stage. This result suggested that the degree of blood stasis in the patients varied from mild to severe and back again with the progression of the disease. This study not only provides quantifiable imaging indicators for the macroscopic diagnosis of blood stasis syndrome and verify its dynamic evolution law, but also suggests that in clinical practice, imaging techniques such as DSA can be used to assist in syndrome differentiation and classification. This provides objective references for staged treatment and the optimization of intervention timing and intensity of blood-activating and stasis-resolving regimens.

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.

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.

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.

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.

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.

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.

This study aims to investigate the effects of glycyrrhizic acid and calcium ions from adjuvant solutions on the toxic lectin in Pinelliae Rhizoma Praeparatum and clarify the processing detoxification mechanism. Molecular docking and molecular dynamics simulations were employed to construct a 3D model of lectin and evaluate the interactions of glycyrrhizic acid and/or calcium ions with lectin. Wild-type and mutant lectin proteins were produced via a prokaryotic expression system in Escherichia coli. The interactions of glycyrrhizic acid and/or calcium ions with the lectin proteins were verified by Bio-Layer Interferometry (BLI), and the irritant toxicity was assessed via a rabbit model of conjunctival irritation. The findings revealed that the ternary complex formed by glycyrrhizic acid, calcium ions, and lectin exhibited greater stability. This complex showed significantly reduced root mean square deviation (RMSD), root mean square fluctuation (RMSF), solvent-accessible surface area (SASA), radius of gyration (Rg), Gibbs free energy of solvation (ΔGSOLV), and total binding free energy (ΔTOTAL), but significantly increased number of hydrogen bonds and gas-phase free energy (ΔGGAS). The combined action of glycyrrhizic acid and calcium ions led to a significant increase in the number of interactions in the amino acid residue region 51-56, 170-175, and 232-237 of lectin, with enhanced Coulomb interaction-short range (Coul-SR) and Lennard-Jones-short range (LJ-SR). When the wild-type lectin protein co-bound with glycyrrhizic acid and calcium ions, the affinity constant was 8.10×10^-6 mol·L^-1, which was significantly lower than that of the binary complex of wild-type lectin with glycyrrhizic acid or calcium ions and the ternary complex of mutant lectin with glycyrrhizic acid and calcium ions. Additionally, lectin soaked in a mixed solution of glycyrrhizic acid and calcium ions did not significantly exacerbate the irritation of the rabbit conjunctiva when being combined with toxic needle crystals. In conclusion, glycyrrhizic acid and calcium ions demonstrate a synergistic effect in forming a structurally stable and non-toxic supramolecular complex with lectin, thereby achieving the processing detoxification of Pinelliae Rhizoma Praeparatum.

This study aims to systematically retrieve and sort out the clinical research evidence of oral Chinese patent medicines in the treatment of vascular dementia (VaD) and understand the distribution and quality of the existing evidence in this field. PubMed, Web of Science, Cochrane Library, EMbase, CNKI, VIP, Wanfang, and SinoMed databases were retrieved from their establishment to November 5, 2024. Evidence diagrams were used to comprehensively present the data distribution characteristics. A total of 211 pieces of literature were included, among which 176 were RCTs, 11 were non-RCTs, 3 were retrospective studies, 1 was cohort study, 17 were systematic reviews/Meta-analyses, and 3 were expert recommendations or consensuses. It involves 45 kinds of Chinese patent medicines. Among them, Ginkgo Leave Tablets/Capsules are the most widely used. Most of the research periods are 8-12 weeks, and the sample size is 51-100 cases. The main outcome indicators include clinical efficacy, cognitive function evaluation, quality of life evaluation, safety indicators, neurological function indicators, hemorheological indicators, etc. The literature quality of RCTs, non-RCTs, and systematic reviews/Meta-analyses are generally not high, and the quality level of evidence is relatively low. Most studies have shown that oral Chinese patent medicines have potential efficacy in the treatment of VaD, but there is a lack of high-quality clinical evidence. Chinese patent medicines have advantages in the treatment of VaD, but there is still a lack of high-quality studies. This suggests that in future clinical research, large-sample and multi-center RCTs need to be carried out. Meanwhile, clinical research design and reporting should be standardized in accordance with relevant guidelines or tools to explore the characteristic advantages of oral Chinese patent medicines in the treatment of VaD, select reasonable outcome indicators, and strive to improve the quality of clinical research in TCM. This will help standardize the research plan, produce advanced evidence-based medical evidence with rigor and scientificity, and provide strong support for the prevention and treatment of VaD with TCM.

This study aims to investigate the effects of Naotaifang (NTF) on neuronal ferroptosis and pyroptosis in cerebral ischemia-reperfusion injury (CIRI), with a focus on nuclear factor erythroid 2-related factor 2 (Nrf2). A rat model of CIRI was established by middle cerebral artery occlusion/reperfusion (MCAO/R). Sprague-Dawley rats were randomly assigned to a sham group, a model group, low/medium/high-dose (4.5, 9, 18 g·kg^-1, respectively) NTF groups, and a butylphthalide (60 mg·kg^-1) group (n=15 per group). After modeling, the treatment groups received corresponding agents by gavage once daily for 7 days, and the sham and model groups received an equal volume of normal saline. After treatment, the neurological function was assessed based on the Zea-Longa score, the infarct volume by TTC staining, and cellular morphology by HE staining. The levels of Fe²⁺, interleukin-1β (IL-1β), and interleukin-18 (IL-18) were measured by ELISA, and those of malondialdehyde (MDA) and glutathione (GSH) by biochemical assays. Western blot was employed to examine the expression levels of Nrf2, glutathione peroxidase 4 (GPX4), NOD-like receptor family pyrin domain-containing 3 (NLRP3), and the N-terminal fragment of gasdermin D (GSDMD-N). In the cell experiment, oxygen-glucose deprivation/reperfusion (OGD/R) was used to model CIRI in SH-SY5Y cells. siRNA-mediated Nrf2 knockdown (si-Nrf2) was employed to probe into the role of Nrf2 in OGD/R-induced ferroptosis and pyroptosis and the intervention effect of NTF. Membrane damage was evaluated by Hoechst/propidium iodide staining and LDH release, and GPX4 and GSDMD immunofluorescence was employed to indicate ferroptosis and pyroptosis, respectively. Fe²⁺, MDA, and GSH were quantified biochemically, and the levels of IL-1β and IL-18 by ELISA. The expression of Nrf2, GPX4, NLRP3, and GSDMD-N was quantified by Western blot. The cellular ultrastructure was observed by transmission electron microscopy. The results of the animal experiment showed that NTF promoted the expression of Nrf2 to alleviate neuronal ferroptosis and pyroptosis, thus producing significant neuroprotection against CIRI in a dose-dependent manner. The results of the cell experiment showed that the neuroprotective effects of NTF after CIRI were mediated by Nrf2-dependent suppression of neuronal ferroptosis and pyroptosis. Taken together, NTF attenuates CIRI by suppressing neuronal ferroptosis and pyroptosis through Nrf2-mediated regulation.