This study systematically elucidated the scientific connotation of Jianpi Huogu Formula in treating phlegm-stasis blocking collaterals syndrome in steroid-induced osteonecrosis of the femoral head (SONFH) by integrating clinical transcriptomics, lipid metabolomics, and biomolecular network mining techniques. The invigorating the spleen and resolving phlegm group (Codonopsis Radix, Atractylodis Macrocephalae Rhizoma, Poria, and Citri Reticulatae Pericarpium) targeted effective target genes such as ALDH7A1 and ACOX1 through 115 chemical components, regulated the AMPK and sphingolipid signaling pathways, significantly reduced the levels of diacylglycerol (DAG) and cholesterol esters, and effectively corrected lipid metabolism disorders. The activating blood circulation and dredging collaterals group (Angelicae Sinensis Radix, Chuanxiong Rhizoma, Paeoniae Radix Rubra, Achyranthis Bidentatae Radix, and Cinnamomi Ramulus) exerts effects through 197 chemical components by intervening in the chemokine and NOD-like receptor pathways, inhibiting the formation of neutrophil extracellular traps (NETs), downregulating inflammatory factor expression, and promoting vascular function repair. The tonifying the kidney and strengthening bones group (Rehmanniae Radix Praeparata and Cervi Cornu) regulated the PI3K/Akt and Ras/MAPK signaling pathways, inhibited osteoclast differentiation genes CTSK and MMP9, and facilitated the reconstruction of bone homeostasis. Transcriptomic and lipid metabolomic analyses were performed on clinical blood samples collected before and after treatment with Jianpi Huogu Formula. Multi-omics integration revealed that the three efficacy groups synergistically constructed a multidimensional network involving "lipid metabolism-immunity-bone homeostasis". A total of 594 differentially expressed effector genes (367 downregulated and 227 upregulated) were identified via clinical transcriptomics, and 179 differential lipid metabolites (mainly triglycerides and DAG) associated with the formula's efficacy were identified via lipid metabolomics. Together with 2 657 disease/syndrome-related genes, a "disease-syndrome-symptom-formula" association network was constructed. Topological eigenvalue analysis and functional mining indicated that the core network targets of Jianpi Huogu Formula in intervening SONFH mainly regulated signaling pathways such as osteoclast differentiation, apoptosis, Ras, MAPK, PI3K/Akt, and p53, thereby inhibiting osteoclast activity, promoting osteoblast proliferation, balancing bone resorption and formation, and improving the bone marrow microenvironment. This study systematically reveals the scientific basis of Jianpi Huogu Formula in intervening in the pathological process of SONFH through the synergistic action of "lipid metabolism reprogramming-transcriptional regulatory network" from three key dimensions, i. e., lipid metabolism, inflammation, and bone remodeling. It fully demonstrates the holistic advantages of traditional Chinese medicine (TCM) formulas in multi-component, multi-target, and multi-pathway coordinated regulation, and provides an innovative perspective and data support for elucidating the mechanism of TCM in the prevention and treatment of SONFH.

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.

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.

A long-term follow-up non-randomized controlled study was conducted to evaluate the medium- and long-term efficacy of the Jianpi Huogu (Kanggu) Formula in treating early-stage (ARCO Ⅰ-Ⅱ stage) femoral head necrosis, thereby providing evidence for the early prevention and treatment of the disease with TCM, improvement of symptoms, and delay of disease progression. Patients who received Jianpi Huogu (Kanggu) Formula (experimental group, n = 61) or formula combined with TCM infusion therapy (control group, n = 168) between January 2003 and June 2020, with a follow-up of ≥3 years, were included. Clinical and imaging data at baseline and annual follow-ups were collected, and 40 matched pairs (80 cases) were selected using propensity score matching. The primary endpoints were clinical efficacy (hip pain scores, hip flexion function scores, walking distance scores, and total scores of clinical efficacy) and the Beijing University of Chinese Medicine X-ray Evaluation (BUCMXE), including femoral head morphology scores, osteoarthritis scores, necrotic lesion density scores, and total scores of BUCMXE. The efficacy of the two groups was compared before treatment and at 3, 5, and 10 years post-treatment. Clinical efficacy showed that, compared with pre-treatment, both groups had significantly reduced hip pain scores and improved hip flexion function scores, walking distance scores, and total scores of clinical efficacy at 3, 5, and 10 years (P<0.001). Imaging evaluation showed that, compared with pre-treatment, femoral head morphology scores in experimental group increased at 3 (0.65±1.00, P<0.05), 5 (0.70±1.02, P<0.001) and 10 years (0.80±1.08, P<0.05); osteoarthritis scores increased at 3 (0.32±0.66, P<0.05) and 5 years (0.32±0.67, P<0.05); necrotic lesion density scores decreased at 3 (1.18±0.50, P<0.05) and 5 years (1.19±0.52, P<0.05); total scores of BUCMXE increased at 3 (2.15±1.29, P<0.05) and 5 years (2.22±1.32, P<0.05). Compared with control group, the femoral head morphology scores increased in experimental group (P<0.05). These results confirm that the Jianpi Huogu (Kanggu) Formula can significantly improve clinical symptoms (pain and joint function) in patients with ARCO Ⅰ-Ⅱ stage femoral head necrosis. Medium- and long-term imaging data suggest slow disease progression (scores not reaching grade Ⅰ pathological criteria). For patients with ARCO Ⅰ stage or mild disease, monotherapy with this formula may be considered.

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.

Published in 1856, Catalogus Medicamentorum Sinensium stands as the earliest known modern pharmacological work in existence. Compiled by the Russian scholar Alexander Tatarinov during the 19th century, this groundbreaking study systematically documented and identified the botanical origins of 495 Chinese medicinal materials procured from Beijing, supplemented with plant specimens collected in China. It represents the first application of modern scientific nomenclature, combining Latin binomial names with specified medicinal parts, for the systematic classification of Chinese medicinal materials. This research conducted a comprehensive analysis of the cataloged substances through meticulous examination of relevant literature, archival records, and reference materials. By using methods such as materia medica verification, data analysis, etc., the information of the listed drugs was verified, classified, organized, and examined, and compared with the origins recorded in modern standards or specialized works. The compendium documented 495 medicinal entries (including 33 duplicate medicinal materials), comprising 396 botanical, 35 mineral, 40 zoological, and 24 other substances. This book identified a total of 190 Chinese medicinal materials whose origin was consistent with that recorded in the 2020 edition of the Pharmacopoeia of the People's Republic of China or Chinese Materia Medica. There were 76 cases with completely different origins. Another 189 cases had their origins not fully identified, but only partial information was marked. Lastly, there were 40 cases that were either untested or could not be matched with current Chinese medicinal materials. The research results indicate that this book is the first in modern times to use Linnaean binomial nomenclature to name the origin of Chinese medicinal materials. It laid the foundation for subsequent research on the origin of Chinese medicinal materials and established the methods and annotation formats for such research. It has been subsequently adopted and referenced by subsequent TCM researchers both in China and abroad. The publication of this book can be regarded as a historical turning point in the evolution of the definition of the origin of Chinese medicinal materials from traditional to modern times. It has advanced the description of the name and reality of Chinese medicinal materials in the form of text and pictures to the definition method using modern natural classification systems and labeled with biological Latin names, which is a pioneering work. This research can provide a reference for sorting out the development process of modern research on the origin of Chinese medicinal materials.

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.

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.

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.