Objective To optimize the preparation process parameters of Anshen Dingzhi Pills (ADP, 安神定志丸) and explore its efficacy in alleviating cognitive impairment in sleep deprived model rats. Methods Single factor experiments were conducted on the ratio of powder to honey, drying time and drying temperature. The appearance characteristics, disintegration time limit and six index components (polygalaxanthone III, 3,6′-disinapoylsucrose, ginsenoside Rb₁, β-asarone, dehydrotumulosic acid and pachymic acid) were used as comprehensive evaluation indexes. The AHP-entropy weight method combined with the Box-Behnken design-response surface method (BBD-RSM) were used to optimize the best process parameters for the preparation of ADP. The improved multi-platform water environment method was used to induce a rat model of sleep deprivation. The efficacy of ADP on sleep deprivation rats with cognitive impairment was evaluated by motor function, learning and memory performance, hippocampal histopathological changes, serum levels of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 and oxidative stress markers in brain tissue, such as superoxide dismutase (SOD), reduced glutathione (GSH) and malondialdehyde (MDA). Results The optimal preparation process parameters for ADP was determined as follows, the ratio of honey to medicinal powder of 0.316:1, drying time of 14.0 h and drying temperature of 50 ℃. Pharmacological evaluation demonstrated that the prepared ADP significantly reduced escape latency in sleep deprived rats, increased the number of platform crossings, time spent in the target quadrant, and novel object recognition index. Additionally, it markedly alleviated neuronal structural damage in the hippocampal CA1 region, decreased serum levels of inflammatory factors (TNF-α, IL-1β and IL-6) and effectively regulated the expression levels of oxidative stress (SOD, GSH and MDA) in brain tissue. Conclusion The optimized ADP preparation process is stable and has consistent quality, which can significantly improve the cognitive function and hippocampal nerve cell morphology of sleep-deprived rats, reduce the levels of inflammatory factors, alleviate oxidative stress damage, and also provide a scientific reference basis for the development of ADP preparations and clinical applications.

Objective Drawing on bibliometric and visualization techniques, this study systematically maps the current landscape and emerging hotspots of polysaccharide–gut microbiota research, offering an evidence-based roadmap for future investigations. Methods China National Knowledge Infrastructure (CNKI), VIP, Wanfang and Web of Science (WOS) were searched for Chinese- and English-language publications on “gut microbiota AND polysaccharides”. CiteSpace, VOSviewer and Microsoft Excel were employed to visualize and quantify annual output, leading institutes, prolific authors, highly cited journals, keyword clusters and burst terms. Results A total of 1 684 Chinese and 872 English articles were retained. Over the past decade, the field exhibited an “ascend-descend” pattern, entering a rapid-growth phase after 2017. China (Nanchang University and Nanjing Agricultural University as hubs) and the USA dominate the output; China ranks first globally, benefiting from abundant traditional-Chinese-medicine polysaccharide resources and strong policy support. Chinese and English literatures evolved differently: Chinese papers initially focused on single polysaccharides (e.g., Astragali Radix or Lycium barbarum polysaccharides) modulating microbial abundance, then shifted to structure–activity relationships and veterinary/clinical applications, whereas English papers moved from gut-barrier function to ulcerative colitis mechanisms, with in vitro fermentation models advancing studies linking metabolic syndrome to short-chain fatty acids (SCFAs). Keyword clustering and burst detection identified immunomodulation, structural characterization, metabolic syndrome and SCFAs as core topics, while “high-fat diet” and “precision regulation” emerged after 2022. Conclusion Interactions between polysaccharides and gut microbiota, their structure–activity relationships, and applications in metabolic diseases such as obesity constitute the central research agenda. Complementary Chinese-English collaboration will propel the field toward precision and clinical translation.

Objective To overcome the clinical limitations of selective serotonin reuptake inhibitors (SSRIs), address the inadequate understanding of individual differences and pathological mechanisms in the antidepressant combination of Xiaoyao Powders with SSRIs, achieve precise combination medication, and promote the transformation of depression treatment toward a “data intelligence-driven” model. Methods A systematic search was conducted in CNKI, VIP, and Wanfang databases using combined subject terms: “Xiaoyaosan + Paroxetine” “Xiaoyaosan + Escitalopram/Citalopram” “Xiaoyaosan + Fluoxetine” “Xiaoyaosan + Sertraline” and “Xiaoyaosan + Fluvoxamine”. The search period spanned from the establishment of each database to May 10, 2025. Literatures were screened based on inclusion and exclusion criteria, and key data were extracted. A database titled “Xiaoyao Powders combined with SSRIs for treating depression” was constructed after verification and cleaning. The Apriori algorithm was applied to mine the association rules between “administration regimens and adverse reactions”, with lift used to quantify the association strength. A hypernetwork of “administration regimens-depression types” was built on the basis of hypergraphs, and the PageRank algorithm was integrated to calculate node weights. A comprehensive efficacy factor was introduced to optimize hyperedge weights, enabling precise matching between depression types and optimal traditional Chinese medicine combination regimens. Results A total of 78 literature was valid and included, with the most study on Xiaoyao Powders with Fluoxetine (33) whereas the least study on Xiaoyao Powders with Fluvoxamine (1). When depression subtypes are not differentiated, the combination of Xiaoyao Powders with Fluoxetine exhibits the highest utilization frequency. Jiawei Xiaoyao Powders was the most used among the applicaitons of Xiaoyao Powders with SSRIs (21). Apriori algorithm analysis showed that the combination of Xiaoyao Powders with Paroxetine was associated with a wide range of adverse reactions but weak single-type associations. Strong associations were observed between the combination with Escitalopram/Citalopram and dry mouth or gastrointestinal reactions, as well as between the combination with Sertraline and diarrhea or nausea. Hypergraph analysis revealed that the “Xiaoyao Powders with Fluoxetine” node had the highest hyperdegree, treating seven depression subtypes; the “depression” node also had the highest hyperdegree, matching five combination regimens; the ranking of hyperedge weights clarified the optimal regimens for different depression types. For example, the “Xiaoyao Powders with Escitalopram/Citalopram” combination was prioritized for senile depression patients, while the “Xiaoyao Powders with Fluoxetine” regimen was preferred for postpartum depression patients. Conclusion The Apriori algorithm can accurately analyze the association characteristics between “combination regimens and adverse reactions”, while hypergraphs can effectively achieve high-order matching between “administration regimens and depression types”. The combination of the two methodologies provides a quantitative basis for the precision medication strategy of depression integrating “disease-symptom-medicine”, and lays a foundation for establishing a new evidence-based, quantitative, and predictable paradigm for the combinations of traditional Chinese and Western medicines.

Objective To explore the mechanism of Wutou Decoction (乌头汤) in treating knee osteoarthritis (KOA) by regulating Indian hedgehog factor (Ihh)-glioma associated oncogene homolog (Gli) signaling pathway. Methods Male SD rats were randomly divided into sham group, model group, celecoxib (24 mg/kg) group, Wutou Decoction low-, medium-, and high-dose (1.05, 2.10, 4.20 g/kg) groups, with 10 rats in each group. The improved anterior cruciate ligament resection technique was used to establish a KOA model, after eight weeks of drug intervention, mechanical pain threshold, thermal pain threshold and climbing ability were measured. ELISA was used to detect the levels of matrix metalloproteinase-3 (MMP-3), MMP-13 and type II collagen (Col II) in serum. The morphological changes of knee joint were observed by hematoxylin-eosin (HE) staining. Micro computed tomography (Micro-CT) technology was used to analyze the changes in bone microstructure of knee joint. Western blotting was used to detect the expressions of Ihh, patched 1 (Ptch1), Gli and MMP-13 proteins in knee joint. Results Compared with sham group, rats in model group showed defects and thinning of cartilage surface layer, decreased and disordered cell arrangement, decreased cross-sectional and coronal bone trabeculae, sparse distribution, decreased bone density, thermal pain threshold and mechanical pain threshold were significantly reduced (P < 0.001), slope angle was decreased (P < 0.001), levels of MMP-3 and MMP-13 in serum were significantly increased (P < 0.05, 0.01), Col II level was significantly decreased (P < 0.05), and expression levels of Ihh-Gli signaling pathway related proteins in knee joint were significantly increased (P < 0.001). Compared with model group, the cartilage surface of rats in Wutou Decoction group was smooth, the number of cells was increased, and the morphology was intact. The knee joint cross-section and coronal bone trabeculae were increased, and the distribution was dense. The thermal pain threshold and mechanical pain threshold were significantly increased (P < 0.05, 0.001), slope angle was increased (P < 0.01, 0.001), levels of MMP-3 and MMP-13 in serum were significantly reduced (P < 0.05), level of Col II was significantly increased (P < 0.05), and expression levels of Ihh-Gli signaling pathway related proteins in knee joint were significantly reduced (P < 0.05, 0.001). Conclusion Wutou Decoction protects articular cartilage by inhibiting excessive activation of Ihh-Gli signaling pathway, reducing abnormal proliferation and differentiation of chondrocytes.

The solution environment involved in the pharmaceutical process of traditional Chinese medicine (TCM) is complex, with components coexisting in multiple states—including molecular, ionic, aggregated, and composite forms. This leads to diverse mass transfer patterns during manufacturing and poses challenges in controlling the uniformity and stability of the final preparations. This review summarizes existing analytical techniques for characterizing component states. By establishing the correlation between component states and the solution environment, a confined mass transfer mathematical model is developed to quantitatively describe component states and association coefficients in complex TCM solutions. Combined with strategies for modulating the solution environment and ultrasonic-assisted delamination techniques, this approach provides a methodological framework for resolving supramolecular assemblies in TCM systems. Furthermore, based on the intrinsic relationship among production parameters, component states, and mass transfer behavior, a new concept for regulating TCM preparation processes is proposed, aiming to enhance the orderliness and controllability of TCM production.

Objective To explore the effect and potential mechanism of harpagide on lipid metabolism and bone metabolism in atherosclerosis (AS) mice fed a high-fat diet. Methods AS model was constructed by feeding apolipoprotein E knock-out (ApoE^-/-) mice with high-fat diet for eight weeks, mice were randomly divided into model group, atorvastatin (2.6 mg/kg) group, and harpagide (20 mg/kg) group, with eight mice in each group. Additionally, eight C57BL/6N wild-type mice were included as control group and fed a standard diet. After nine weeks of drug intervention, micro-CT was used to analyze changes in bone microarchitecture. Infrared spectroscopy was employed to examine bone material composition. Hematoxylin-eosin (HE) staining was applied to observe the morphology of femoral trabeculae, and tartrate resistant acid phosphatase (TRAP) staining was used to quantify osteoclast numbers in the femur. Levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), TRAP and C-terminal telopeptide of type I collagen (CTX-1) in serum were measured using biochemical assays. Western blotting was performed to detect protein expression levels of nuclear factor of activated T cells 1 (NFATc1), Fos proto-oncogene (c-Fos), cathepsin K, peroxisome proliferator-activated receptor gamma coactivator-1β (PGC-1β), estrogen-related receptor α (ERRα) and peroxisome proliferator-activated receptor γ (PPARγ) in bone tissue. Results Harpagide significantly improved bone microarchitecture and bone material composition in AS mice (P < 0.05, 0.01), reduced levels of TC, LDL-C, HDL-C in serum and AS index (P < 0.05, 0.01), decreased levels of bone resorption markers CTX-1 and TRAP in serum (P < 0.01), down-regulated the expressions of bone resorption-related proteins c-Fos, NFATc1 and cathepsin K in bone tissue (P < 0.01). Additionally, harpagide suppressed the protein expression levels of PGC-1β, ERRα and PPARγ in bone tissue of AS mice (P < 0.05, 0.01). Conclusion Harpagide ameliorates dyslipidemia and suppresses bone resorption in AS mice, thereby exerting anti-osteoporotic effects. The mechanism may involve the inhibition of PPARγ/ERRα/PGC-1β signaling pathway.

Objective To explore the genetic causal relationship between gastro-esophageal reflux disease (GERD) and chronic obstructive pulmonary disease (COPD) by Mendelian randomization (MR) analysis based on the theory of “gather in stomach and focus on lung”, and to predict potential Chinese herbal medicines that may intervene in GERD-related COPD. Methods The genome-wide association study (GWAS) datasets for GERD and COPD were obtained from the IEU Open GWAS database. A bidirectional two-sample Mendelian randomization (MR) analysis was applied to evaluate the causal relationship between the two conditions, followed by a series of quality control procedures. Subsequently, proximal genes of the instrumental variables were extracted using the Ensembl database, and functional enrichment analysis was performed to explore the potential mechanisms by which GERD influences COPD risk. Furthermore, protein-protein interaction (PPI) analysis was conducted on these proximal genes to identify core genes involved in this process. Potential intervention chemical components and Chinese herbal medicines were predicted using the Comparative Toxicogenomics Database (CTD) and the Coremine Medical database, respectively, and statistical analysis was carried out on the medicinal properties and functions of the identified herbs. The CytoNCA plugin was used to screen core Chinese herbal medicines, and molecular docking of traditional Chinese medicine components with core genes to preliminarily verify the prediction results. Results Forward MR analysis indicated that GERD was causally associated with a significantly increased risk of COPD onset; quality control results confirmed the robustness of this finding. Reverse MR analysis did not reveal evidence supporting a causal effect of COPD on GERD. A total of 135 proximal genes of the instrumental variables were identified, which were primarily enriched in biological pathways such as the regulation of Nuclear Factor-Kappa B (NF-κB) signal transduction, the Interleukin-17 (IL-17) signaling pathway, the Tumor Necrosis Factor (TNF) signaling pathway, the Phosphatidylinositol 3-Kinase-Protein Kinase B (PI3K-Akt) signaling pathway, and natural killer cell-mediated cytotoxicity. The top five genes identified through PPI analysis were determined as core genes. Using the CTD and Coremine Medical databases, 163 chemical components and 167 Chinese herbal medicines were predicted. Statistical analysis of the medicinal properties of the herbs showed that among the Four Natures, cold and warm properties predominated, followed by neutral; among the five flavors, bitter, sweet, and pungent were most common; the primary meridian tropism was the lung meridian, followed by the liver, spleen, and stomach meridians; in terms of functions, tonifying deficiency and resolving phlegm, relieving cough and asthma were primary, followed by clearing heat, relieving exterior syndrome, and regulating qi. After calculation with CytoNCA, key herbs were screened out, including Mahuang (Ephedrae Herba), Baiguo (Ginkgo Semen), Banxia (Pinelliae Rhizoma), Chenpi (Citri Reticulatae Pericarpium), Sangbaipi (Mori Cortex), Gancao (Glycyrrhizae Radix et Rhizoma), Ganjiang (Zingiberis Rhizoma), Shengjiang (Zingiberis Rhizoma Recens), Huangqi (Astragali Radix), Renshen (Ginseng Radix et Rhizoma), Fuling (Poria), and Baizhu (Atractylodis Macrocephalae Rhizoma). Molecular docking demonstrated favorable binding affinity between the core genes and the key components of these Chinese herbal medicines. Conclusion Based on the theory of "accumulation in the stomach and its connection with the lungs," this study not only confirms from a genetic perspective that GERD is a risk factor for COPD, but also reveals that its potential mechanisms are closely associated with inflammatory and immune signaling pathways such as NF-κB, IL-17, TNF, and PI3K-Akt. The predicted Chinese herbal treatment strategies primarily focus on tonifying deficiency, resolving phlegm, relieving cough, and calming asthma.

Ferroptosis, as a new type of programmed cell death characterized by iron dependence and lipid peroxidation, is an important target for inhibiting proliferation, metastasis and reversing drug resistance of urinary tumors. Traditional Chinese medicine (TCM) and its active compounds have unique advantages in the field of regulating ferroptosis due to their multi-target and low toxicity, mainly reflected in the synergistic intervention of key pathways of ferroptosis. Studies have shown that TCM plays an anti-tumor role by targeting the three classical pathways of regulating iron homeostasis, promoting lipid peroxidation and inhibiting the antioxidant defense system with glutathione peroxidase 4 as the core, promoting iron overload in urinary tumor cells and destroying the redox balance to induce ferroptosis. This article aims to systematically review the mechanism of TCM regulating ferroptosis in prevention and treatment of urinary tract tumors, in order to provide reference for its more in-depth molecular mechanisms research and wider clinical application.

Objective To investigate the therapeutic effect and mechanism of total triterpenoid from Cyclocarya paliurus (CPT) on high-fat diet (HFD)-induced metabolic-associated fatty liver disease (MAFLD) mice. Methods C57BL/6J mice were randomly divided into control group, model group, CPT (100 mg/kg) group, metformin (MET, 100 mg/kg) group and CPT + MET group. Except for the control group receiving regular feeding, all other groups were fed HFD for 12 weeks to establish MAFLD models. After successful establishment of MAFLD model, drugs were given eight weeks. During the experiment, the activity levels of mice were observed, their body weight and food intake were measured regularly. One week before the end of medication, the oxygen consumption (VO₂), carbon dioxide production (VCO₂) and energy consumption of mice were measured using indirect calorimetry. After the end of administration, glucose tolerance test and insulin resistance test were conducted to detect glucose tolerance. Liver weight was measured, and liver index was calculated. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), γ-glutamyl transpeptidase (γ-GT), triglycerides (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), fasting blood glucose (FBG), fasting insulin (FINS) in serum were detected, and insulin resistance index (HOMA-IR) was calculated. The levels of TC and TG in hepatic tissues and feces, as well as the levels of total bile acids (TBA) in serum, hepatic tissues and feces were measured. Hematoxylin-eosin and oil red O staining were used to observe the pathological changes in hepatic tissues of mice. Five hepatic tissue and five colon content samples from each group were randomly selected for bile acid (BAs) metabolomics analysis. The mRNA expressions of cholesterol 7α-hydoxylase 1 (Cyp7a1), Cyp7b1, Cyp27a1, Cyp8b1, bile acid coenzyme A synthetase (Bacs), bile acid coenzyme a: amino acid N-acyltransferase (Baat), bile salt export pump (Bsep), recombinant Na⁺ taurocholate cotransporting polypeptide (Ntcp), farnesoid X receptor (FXR), small heterodimeric partner (SHP), fibroblast growth factor receptor 4 (FGFR4), sterol regulatory element-binding protein-1c (SREBP-1c), stearyl coenzyme A desaturation enzyme 1 (SCD1), fatty acid synthetase (FASN), peroxisome proliferator-activated receptor α (PPARα), carnitine palmitoyl transferase 1 (CPT1), lipoprotein lipase (LPL), microsomal triglyceride transfer protein (MTTP) in hepatic tissues and FXR, fibroblast growth factor 15 (FGF15), apical sodium-dependent bile acid transporter (Abst), intestinal bile acid-binding protein (Ibabp), organic solute transporter-α (Ost-α), Ost-β in ileum tissues were determined by qRT-PCR. Western blotting was used to detect the protein expressions of CYP7a1, Cyp7b1, Cyp27a1, Cyp8b1, FXR, SHP, FGFR4, SREBP-1c, SCD1, FASN, PPARα, CPT1, LPL, MTTP in hepatic tissues and FXR, FGF15, Abst in ileum tissues. Results Compared with model group, CPT and its association with MET significantly reduced the body weight, improved glucose tolerance, elevated insulin sensitivity, lowered liver weight and liver index, raised VO₂, VCO₂, VO₂/VCO₂, and daytime and nighttime energy consumptions and total energy consumption in mice (P < 0.01). CPT and its association with MET reduced ALT, AST, ALP, γ-GT, TC, TG, LDL-C, FINS, FBG, TBA levels in serum and TC and TG levels in hepatic tissue as well as HOMA-IR, elevated levels of HDL-C in serum and TC, TG, TBA in feces, reduced liver histopathological scores and lipid deposition (P < 0.01). CPT and its association with MET elevated hepatic tissue TBA level, lowered the contents of unconjugated BAs, primary BAs, secondary BAs and the ratio of primary BAs/secondary BAs in hepatic tissues, as well as the levels of unconjugated BAs and secondary BAs in colon contents, elevated the content of conjugated BAs and the ratio of conjugated BAs/unconjugated BAs in hepatic tissue, as well as the levels of conjugated BAs, primary BAs and the ratios of conjugated BAs/unconjugated BAs, primary BAs/secondary BAs in colon contents (P < 0.01). In addition, CPT and its association with MET elevated Cyp7a1, Cyp7b1, Cyp27a1, Bacs, Baat, FXR, SHP, Bsep, Ntcp, PPARα, CPT1, LPL, MTTP mRNA expressions and Cyp7a1, Cyp7b1, Cyp27a1, FXR, SHP, PPARα, CPT1, LPL, MTTP protein expressions in hepatic tissues, reduced the mRNA and protein expressions of Cyp8b1, FGFR4, SREBP-1c, SCD1, FASN in hepatic tissues, depressed FXR, FGF15, Asbt, Ibabp, Ost-α, Ost-β mRNA expressions and FXR, FGF15, Asbt protein expressions in ileum tissues (P < 0.01). The combination of CPT and MET showed better efficacy than CPT alone (P < 0.05, 0.01). Conclusion CPT may activate the hepatic FXR/SHP pathway by inhibiting intestinal FXR/FGF15 signaling, facilitating the synthesis of BAs in the hepatic intestinal circulation, repressing their ileal reabsorption, and boosting the excretion of BAs with feces. The activated hepatic FXR/SHP pathway restrains lipid synthesis by suppressing SREBP-1c/SCD1/FASN signaling axis, while activated hepatic FXR promotes lipid oxidation and lipid decomposition through activating the PPARα/CPT1 and LPL/MTTP signaling axes to treat MAFLD.

Objective To investigate the therapeutic effect and mechanism of tanshinone II_A on motor function recovery after brachial plexus root avulsion (BPA) using a rat brachial plexus root avulsion (BPA)-replantation model and an hydrogen peroxide (H₂O₂)-induced oxidative damage model in NSC-34 cells. Methods A total of 60 SD rats were randomly divided into sham group, model group, tanshinone II_A low- and high-dose (10, 30 mg/kg) groups, with 15 rats in each group. After modeling, continuous administration was performed for eight weeks. Motor function recovery was evaluated using Terzis grooming test (TGT). The biceps brachii muscle was weighed and processed for hematoxylin-eosin (HE) staining to assess morphological changes. Motor neuron survival in the spinal cord was determined by neutral red staining. Axonal regeneration was assessed by Fluoro-Gold retrograde labeling and immunofluorescence staining for choline acetyltransferase (ChAT) and neurofilament 200 (NF200) in the musculocutaneous nerve. Immunofluorescence was performed to detect ionized calcium-binding adapter molecule 1 (Iba1), glial fibrillary acidic protein (GFAP) and neuronal nitric oxide synthase (nNOS) expressions. Level of malondialdehyde (MDA) and activity of superoxide dismutase in the injured spinal cord were measured. The protein expressions of Ras-related C3 botulinum toxin substrate l (Rac1), cell division control protein 42 (Cdc42), c-Jun N-terminal kinase (JNK) and c-Jun in the injured spinal cord were detected by Western blotting. In vitro, control group, model group, tanshinone II_A group and Rac1 inhibitor group were established. NSC-34 cells were induced with 400 μmol/L H₂O₂ to cause oxidative damage. After intervention with tanshinone II_A or NSC 23766, cell viability was assessed using CCK-8 assay. Levels of MDA, reactive oxygen species (ROS) and activity of SOD were measured, and the expressions of Rac1/JNK pathway-related proteins was analyzed by Western blotting. Results The BPA model was successfully established as evidenced by consistently 0 TGT scores in model group at 1 week post-surgery. Compared with model group, tanshinone II_A significantly improved the TGT scores (P < 0.05, 0.01), enhanced axonal regeneration (P < 0.01), increased motor neuron count (P < 0.01), mitigated muscle atrophy (P < 0.05, 0.01), and reduced the expressions of Iba1 and GFAP (P < 0.05, 0.01). Meanwhile, tanshinone II_A improved oxidative stress damage, including decreased nNOS positive motor neurons (P < 0.05, 0.01), reduced MDA level (P < 0.001), elevated SOD activity (P < 0.01), while up-regulating Rac1, Cdc42, JNK and c-Jun expressions in spinal cord tissue (P < 0.01, 0.001). In vitro, tanshinone II_A significantly increased viability of H₂O₂-injured NSC-34 cells (P < 0.01), elevated SOD activity (P < 0.01), decreased MDA and ROS levels (P < 0.01), up-regulated Rac1, Cdc42, JNK and c-Jun protein expressions (P < 0.05, 0.01, 0.001). Notably, these protective effects of tanshinone II_A were partially attenuated by co-administration of Rac1 inhibitor NSC 23766 (P < 0.05, 0.01). Conclusion Tanshinone II_A promotes motor function recovery following brachial plexus root avulsion by activating Rac1/JNK signaling pathway, which attenuates oxidative stress and neuroinflammation, thereby enhancing motor neuron survival and axonal regeneration.