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.

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.

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.

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 investigated the secondary metabolites of the endophytic fungus Penicillium sp. RM isolated from the toxic plant Rhododendron molle. Ten compounds were isolated and purified from the ethyl acetate extract of the fungal fermentation broth by silica gel column chromatography, gel column chromatography, and semi-preparative HPLC. The structures of these compounds were elucidated by comprehensive spectroscopic analyses, including NMR, MS, UV, IR, and CD. The identified compounds were as follows: penicidienone A (1), diversonol (2), alternariol (3), alternariol 9-methyl ether (4), methylated dechloromonilicin (5), norliquexantona (6), alternethanoxin A (7), α-diversonolic ester (8), (±) -asperlone A (9), and verruculotoxin (10). Compound 1 was identified as a new cyclopentenone derivative. Compound 9 showed inhibitory activity against the proliferation of HepG2 (IC₅₀=9.7 μmol·L^-1), HGC27 (IC₅₀ = 9.3 μmol·L^-1), and U251 (IC₅₀ = 8.4 μmol·L^-1) cell lines.

This study aims to investigate the antifungal secondary metabolites produced by the endophytic fungus Aspergillus sp. FH-1 isolated from Valeriana officinalis via a high-salt rice medium. Compounds were isolated and purified by silica gel and ODS column chromatography, semi-preparative HPLC, and other techniques. The chemical structures were elucidated through analysis of physicochemical properties and spectroscopic data of nuclear magnetic resonance (NMR), infrared (IR), and mass spectrometry (MS). The inhibitory effects of all the compounds against Colletotrichum gloeosporioides were evaluated via the mycelial growth rate method. Eight compounds were obtained from the ethyl acetate extract of Aspergillus sp. FH-1. They were identified as asperchoried A (1), butyrolactone Ⅱ (2), isobutyrolactone Ⅱ (3), aspernolide A (4), butyrolactone Ⅴ (5), clavatone (6), 1-hydroxy-6,8-dimethoxy-3-methylanthracene-9,10-dione (7), and (S) -7-methoxy-2, 5-dimethyl-2, 3-dihydrobenzofuran-6-ol (8). Among them, compound 1 is a novel chlorinated butanolide derivative and was designated asperchoried A. Compounds 1, 2, 6, and 7 possessed inhibitory effects on C. gloeosporioides, with EC₅₀ values of 15.08, 77.19, 89.94, and 62.02 μg·mL^-1, respectively.

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.

This study aimed to investigate the mechanisms by which Acanthopanax senticosus extract (ASH) exerts effects onα-synuclein (α-syn) overexpressing transgenic mouse model of Parkinson's disease (PD), with a focus on its regulation of brain lipid metabolism. Twenty PD model mice were randomly assigned to a model group or an ASH treatment group (45.5 mg·kg^-1 by gavage for 4 weeks), and 10 C57BL/6 mice served as a normal control group. Behavioral assessments revealed that, compared with controls, PD model mice showed prolonged pole test time, reduced spontaneous locomotor activity, shorter latency to fall in the rotarod test, and decreased total distance traveled in the open field test. Serum levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), caspase-9 were significantly elevated, B-cell lymphoma-2 (Bcl-2), and proliferating cell nuclear antigen (PCNA) expression was reduced, and marked neuronal damage was observed in brain tissue. ASH intervention significantly improved these behavioral and biochemical parameters and attenuated neuronal injury. Untargeted lipidomics analysis revealed significant alterations in sphingomyelin (SM), ceramide (Cer), phosphatidylcholine (PC), and phosphatidylserine (PS) across multiple brain regions (cortex, substantia nigra, cerebellum, and striatum) in PD mice, which were notably restored by ASH treatment. Pathway analysis indicated that these metabolites were predominantly involved in sphingolipid metabolism. Western blot further demonstrated that ASH downregulated the expression of key sphingolipid metabolic enzymes serine palmitoyltransferase long-chain base subunits 1 and 2 (SPTLC1 and SPTLC2) and upregulated UDP-glucose ceramide glucosyltransferase (UGCG), β-galactosylceramidase (GALC), and sphingosine kinase 2 (SPHK2), thereby suppressing abnormal SM and Cer accumulation in the substantia nigra and elevating PS and PC levels in the striatum. Spearman's correlation analysis supported the modulatory effect of ASH on brain lipid metabolic profiles. In conclusion, ASH improves behavioral deficits, exerts anti-inflammatory effects, and regulates sphingolipid metabolism to correct disordered lipid profiles, thereby providing neuroprotective effects in PD mice.

This study aimed to elucidate the therapeutic effects and molecular mechanisms of Periplaneta americana extract (PAE) on ground-glass nodule (GGN) -type early-stage lung adenocarcinoma (LUAD) using patient-derived organoid (PDO) models. GGN-type patient-derived early-stage LUAD organoid (GGN-PDO) were successfully established. At the level of drug quality control and component analysis, the content of free amino acids and peptides in PAE were determined by high-performance liquid chromatography (HPLC), and the main components were further analyzed by liquid chromatography-mass spectrometry (LC-MS). Analysis of variance was used to evaluate the similarity between drugs of the same batch (Pearson correlation coefficient 0.87-0.99) and ensure quality control. At the histopathological level, hematoxylin-eosin (HE) staining and immunohistochemical (IHC) analysis of key molecular markers, including cytokeratin 7 (CK7), thyroid transcription factor-1 (TTF-1), and Ki-67, confirmed that the organoids recapitulated the tumor characteristics of parental tissues. Pharmacodynamic evaluation demonstrated that PAE significantly inhibited the proliferation and viability of GGN-PDOs in a dose-dependent manner, while immunofluorescence (IF) staining showed a marked reduction in the proliferation marker Ki-67. Flow cytometry further confirmed that PAE induced apoptosis in GGN-PDO, and Western blot analysis demonstrated that PAE downregulated the anti-apoptotic protein Bcl-2 and upregulated the pro-apoptotic protein Bax, thereby activating the apoptotic pathway. Notably, for the first time, the pro-apoptotic mechanism of PAE was shown to involve inhibition of the Janus kinase 1 (JAK1)/phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway, as evidenced by markedly decreased protein levels of JAK1, PI3K, p-PI3K, AKT, and p-AKT following PAE treatment. In summary, this study is the first to use a clinically relevant GGN-PDO models to demonstrate that PAE induces apoptosis in early-stage LUAD via JAK1/PI3K/AKT pathway inhibition, providing a solid theoretical and experimental basis for developing innovative pharmacotherapies and non-surgical interventions against GGNs.

The therapeutic effects of Quzhou Aurantii Fructus aqueous extract (QAFA) and Aurantii Fructus aqueous extract (AFA) on functional dyspepsia (FD) in rats were evaluated and compared, and their underlying mechanisms were investigated. The FD rat models were constructed by a combined method of "pinching tail + irregular diet + drinking dilute acidic water". The rats were orally administered QAFA at a dose of 2.05 g·kg^-1(equivalent to 4 g·kg^-1 QAF) and AFA at a dose of 1.93 g·kg^-1(equivalent to 4 g·kg^-1 AF), respectively. After 14-day administration, the gastric emptying and intestinal propulsion were assessed. The pathological changes in the gastric antrum and duodenum were analyzed via histology, and the levels of serum gastrin (GAS) and vasoactive intestinal polypeptide (VIP) were measured by enzyme-linked immunosorbent assay. The underlying mechanisms were investigated by using 16S rRNA sequencing and serum metabolomics. The results showed that QAFA and AFA could increase gastrointestinal motility. Hematoxylin-eosin (HE) staining and immunofluorescence analysis showed that both QAFA and AFA repaired the damaged intestinal barrier, and ELISA analysis showed that they regulated GAS and VIP levels in serum. These results suggest that both can improve symptoms in FD rats. The intestinal microbiota analysis revealed that QAFA and AFA reduced the abundance of the harmful microbe Ruminococcus. AFA increased the abundance of the beneficial bacteria Prevotella and Lactobacillus, and QAFA increased the abundance of Clostridia UCG-014. Metabolomic analysis showed that both QAFA and AFA restored serum metabolites primarily through regulating phospholipid metabolism. Correlation analysis between metabolites and gut microbiota showed that both QAFA and AFA decreased the abundance of Ruminococcus, and AFA increased the abundance of Prevotella, thereby restoring serum metabolite levels. These findings suggest that QAFA and AFA may improve FD symptoms in rats by modulating specific gut microbiota to restore gastrointestinal hormones and phospholipid metabolism. However, there are some differences in the specific microbiotas they regulate.