ObjectiveAbnormal lipids in neurons can cause the accumulation of α-synuclein（α-syn）. This study aimed to explore the mechanism of Acanthopanacis Senticosi Radix et Rhizoma seu Caulis extract （ASH） in treating Parkinson's disease （PD） mice using lipidomics combined with network pharmacology. MethodsMice were divided into the blank group， model group and ASH （45.5 mg·kg^-1） group. Motor ability was evaluated by pole climbing time and autonomous activity count； The oxidative stress indicators were detected by enzyme-linked immunosorbent assay （ELISA）. Lipid biomarkers in brain tissues were screened and identified by ultra-performance liquid chromatography-tandem mass spectrometry （UPLC-MS/MS）， and metabolic pathway analysis was conducted. The key targets of ASH for PD treatment were explored using network pharmacology. The Kyoto Encyclopedia of Genes and Genomes （KEGG） database was used for pathway enrichment analysis， and the "compound-reaction-enzyme-gene" network was constructed using the MetScape plugin. The protein expression levels of glutathione S-transferase P1 （GSTP1）， glutathione S-transferase Mu 2 （GSTM2）， prostaglandin peroxide synthase 1 （PTGS1）， prostaglandin peroxide synthase 2 （PTGS2）， and prostaglandin E synthase （PTGES） were validated by Western blot. ResultsCompared with the blank group， the model group showed significantly prolonged pole climbing time and reduced autonomous activity count （P<0.01）. Compared with the model group， the ASH group demonstrated significantly faster pole climbing and increased autonomous activity count （P<0.01）. The model group exhibited significantly decreased superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px） levels， and increased malondialdehyde （MDA） level in brain tissues compared with the blank group （P<0.01）. The ASH group showed increased SOD and GSH-Px levels and decreased MDA level compared with the model group （P<0.05， P<0.01）. Lipidomics analysis identified 10 differential metabolites and 8 differential metabolic pathways. Network pharmacological analysis revealed 213 intersection targets between ASH components and PD， with KEGG enrichment involving the sphingolipid signaling pathway， lipid arteriosclerosis， phosphoinositide 3-kinase/protein kinase B（PI3K/Akt） signaling pathway， mitogen-activated protein kinase（MAPK） signaling pathway， and hypoxia inducible factor-1（HIF-1） signaling pathway. Integrated lipidomics and network pharmacology analysis highlighted the central role of the arachidonic acid metabolic pathway. The Western blot results showed that ASH effectively up-regulated GSTP1， GSTM2， and PTGS1 protein expression， and down-regulated PTGS2 and PTGES protein expression. ConclusionASH can ameliorate behavioral deficits， exert antioxidant effects， regulate lipid differential metabolites and the arachidonic acid metabolic pathway， thereby exerting therapeutic effects in PD model mice.

Parkinson's disease （PD） is a neurodegenerative disorder primarily characterized by motor dysfunction. Traditionally， its main clinical features include resting tremor， muscular rigidity， bradykinesia， and postural balance disorders. However， an increasing number of studies have shown that its non-motor symptoms （NMS） exert an even greater impact on patients' quality of life than motor symptoms， severely affecting daily functioning and increasing the burden on families and society. Among these， depression is one of the most common and most debilitating NMS， with statistics indicating that the incidence of depression among PD patients reaches as high as 40%-50%. The pathological mechanisms are complex， involving the interplay between degenerative changes in dopaminergic neurons and disruptions in emotional regulatory circuits， which poses a substantial challenge to clinical treatment. Traditional Chinese medicine （TCM）， characterized by holistic regulation and multi-target intervention， has demonstrated significant advantages in the treatment of PD and depression， offering new insights for managing PD-depression comorbidity. This study integrates research extracted from multiple databases， including PubMed， Web of Science， Google Scholar， and China National Knowledge Infrastructure （CNKI）， that investigates the potential mechanisms of PD and depression as well as TCM-based treatments for these conditions. The aim is to elucidate the shared pathological mechanisms underlying PD and depression and to explore the therapeutic potential of TCM in effectively combating PD-depression comorbidity through these shared mechanisms， thereby providing valuable insights for the development of targeted therapies.

ObjectiveTo explore the improving effect of Huangqi Chifengtang（HCT） on atherosclerosis（AS）， and elucidate its mechanism in relation to adenosine monophosphate-activated protein kinase（AMPK）/peroxisome proliferator-activated receptor α（PPARα） signaling pathway and nucleotide-binding oligomerization domain（NOD）-like receptor thermal protein domain associated protein 3（NLRP3） inflammasome. MethodsEight C57BL/6J mice were set as the normal group， and 32 ApoE^-/- mice were randomly divided into the model group， the positive drug group（atorvastatin， 5 mg·kg^-1·d^-1）， HCT low- and high-dose groups（1.95， 3.90 g·kg^-1·d^-1）. ApoE^-/- mice were fed with high-fat and high-cholesterol feed to establish an AS mouse model. After modeling， they were orally administered corresponding dose of drugs for 28 days， while the normal and model groups received an equal volume of physiological saline via oral gavage. Hematoxylin-eosin（HE） staining was used to observe the pathological status of the aorta and liver in mice， Biochemical testing and enzyme-linked immunosorbent assay（ELISA） were used to detect the levels of total cholesterol（TC）， triglycerides（TG）， low-density lipoprotein cholesterol（LDL-C）， alanine aminotransferase（ALT）， aspartate aminotransferase（AST）， C-reactive protein（CRP）， interleukin（IL）-1β， IL-18 in the serum， as well as superoxide dismutase（SOD）， malondialdehyde（MDA）， and reduced glutathione（GSH） in the liver. Real-time fluorescence quantitative polymerase chain reaction（Real-time PCR） was used to measure the mRNA expression levels of NLRP3， apoptosis-associated speck-like protein（ASC）， cysteinyl aspartate specific proteinase-1（Caspase-1）， Toll-like receptor 4（TLR4） in the aorta， and fatty acid synthase（FAS）， stearoyl-CoA desaturase 1（SCD1）， PPARα， and carnitine palmitoyltransferase 1A（CPT1A） in the liver. Immunohistochemistry was used to determine the protein expressions of NLRP3， Caspase-1， and ASC in the aorta， and Western blot was used to measure the protein expressions of AMPK， p-AMPK， sterol regulatory element binding protein-1c（SREBP-1c）， CPT1A， and FAS in the liver. ResultsCompared with the normal group， the model group showed a significant increase in lipid plaque deposition in the aorta and lipid accumulation in the liver， the levels of TC， TG， LDL-C， AST， ALT， IL-1β， IL-18 and CRP in the serum were significantly increased（P<0.01）， and the mRNA and protein expressions of aortic TLR4， NLRP3， Caspase-1 and ASC were significantly upregulated（P<0.01）. The levels of SOD and GSH in the liver were significantly reduced， while the level of MDA was significantly increased（P<0.01）. The mRNA expressions of FAS and SCD1 in the liver were significantly downregulated， while the mRNA expressions of PPARα and CPT1A were significantly upregulated. The protein expressions of p-AMPK/AMPK and CPT1A in the liver were significantly reduced， while the expressions of SREBP-1c and FAS proteins were significantly increased（P<0.01）. Compared with the model group， the low- and high-dose HCT groups showed significant improvements in aortic plaques and hepatic lipid deposition. The levels of TC， LDL-C， AST， IL-1β and IL-18 in the serum of the low-dose HCT group， as well as TC， TG， LDL-C， AST， ALT， IL-1β， IL-18 and CRP in the serum of the high-dose HCT group， were significantly reduced（P<0.01）. The mRNA expressions of TLR4， NLRP3 and Caspase-1 in the aorta of the low-dose HCT group， as well as TLR4， NLRP3， Caspase-1 and ASC in the aorta of the high-dose HCT group， were significantly downregulated（P<0.01）. The protein expressions of Caspase-1 and ASC in the aorta of the low-dose HCT group， as well as NLRP3， Caspase-1 and ASC in the high-dose HCT group， were significantly downregulated（P<0.01）. The levels of SOD and GSH in the liver of the low- and high-dose HCT groups were significantly increased， while the level of MDA in the high-dose HCT group was significantly decreased（P<0.05， P<0.01）. In the HCT-treated group， the mRNA expressions of FAS and SCD1 in the liver were significantly upregulated， while the mRNA expressions of PPARα and CPT1A were significantly downregulated， the protein expressions of p-AMPK/AMPK and CPT1A in the liver were significantly increased， while the protein expressions of SREBP-1c and FAS were significantly decreased（P<0.05， P<0.01）. ConclusionHCT can improve lipid metabolism by activating the AMPK/PPARα pathway and inhibit NLRP3 inflammasome-mediated inflammatory responses， thereby reducing hepatic lipid deposition and AS plaque formation.

Parkinson's disease （PD）， with its incidence increasing year by year and its onset age gradually becoming younger， has become a major chronic multisystem movement disorder that threatens public health. The microbiota-gut-brain axis （MGBA） is a bidirectional communication system connecting the enteric nervous system and the central nervous system. Its core functions rely on the synergistic interactions among gut microbiota， neural signal transmission， endocrine regulation， and immune interactions， and it plays an indispensable role in maintaining gut-brain dynamic homeostasis， regulating neurotransmitter metabolism， and modulating inflammatory responses. Current studies have found that the gut microbiota of patients with PD exhibits dual dysbiosis characterized by the enrichment of opportunistic pathogens and beneficial bacteria， accompanied by abnormal metabolite levels， which accumulate and trigger neuroinflammation， demonstrating the pivotal regulatory role of the MGBA in the early pathology of PD. Furthermore， this article summarizes Chinese medicines， their active components， and compound formulas that may prevent and treat PD through intervention in the MGBA. These agents can modulate microbial composition， suppress inflammation and oxidative stress， protect the intestinal barrier， and ameliorate dopaminergic neuron damage. By systematically summarizing the central mechanisms of the MGBA in PD and reviewing the research progress of traditional Chinese medicine （TCM） mediated regulation of this pathway in PD intervention， this article aims to provide a theoretical reference for the clinical prevention and treatment of PD and scientific research design.

Lung cancer constitutes the most prevalent and lethal malignant tumor in China. Approximately 85% of lung cancer diagnoses correspond to the non-small cell histological subtype [non-small cell lung cancer (NSCLC)]. Despite surgery being the mainstay for early-stage disease, postoperative recurrence remains high and adjuvant chemotherapy offers limited benefit. In recent years, targeted therapy has demonstrated substantial advantages in driver mutation-positive NSCLC. To this end, the Lung Cancer Medical Education Committee of the Chinese Medical Education Association developed guidelines based on a systematic review of evidence through November 2025, using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and a modified Delphi method. Focusing on epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and addressing ROS proto-oncogene 1 (ROS1), B-Raf proto-oncogene serine/threonine kinase (BRAF) V600E mutation, and mesenchymal-epithelial transition factor (MET) exon 14 (METex14) skipping, the guideline covers molecular testing, neoadjuvant/adjuvant therapy, perioperative strategies, minimal residual disease monitoring, and postoperative surveillance. It defines testing requirements, specifies stage-directed and subtype-specific treatments, and standardizes minimal residual disease monitoring. These recommendations emphasize precision and feasibility to improve survival and quality of life.

Nervous system diseases， also known as neuropathies， encompass a wide range of conditions， primarily including Alzheimer's disease （AD）， Parkinson's disease （PD）， Huntington's disease， and other neurodegenerative disorders， as well as depression， subarachnoid hemorrhage， cerebral ischemia-reperfusion injury， vascular dementia， and other neurological diseases. These diseases pose serious threats to the health and lives of patients， bringing heavy burdens to society and families. The pathogenesis of nervous system diseases is highly complex， involving mechanisms such as neuroinflammation， oxidative stress， apoptosis， endoplasmic reticulum stress， mitochondrial dysfunction， brain-derived neurotrophic factor deficiency， reduced cholinergic activity， axonal injury， and demyelination. In recent years， the incidence and mortality of nervous system diseases have been rising annually. Currently， western medicine primarily focuses on symptomatic treatment， often accompanied by many adverse reactions， including lethargy， excessive sedation， dizziness， headaches， tachycardia， liver function damage， metabolic disorders， and incomplete recovery after surgery. As a traditional Chinese medicine， Salviae Miltiorrhizae Radix et Rhizoma has effects such as promoting blood circulation， removing blood stasis， cooling the blood， clearing the heart， nourishing the blood， and calming the nerves. It can play a role in the treatment and protection against nervous system diseases through multiple targets， pathways， and mechanisms. Studies have found that the water-soluble phenolic acids and fat-soluble diterpenoid quinones in Salviae Miltiorrhizae Radix et Rhizoma are the main active ingredients for the treatment of nervous system diseases. This paper summarized the effects of the active components and compounds of Salviae Miltiorrhizae Radix et Rhizoma on nervous system diseases over the past ten years， aiming to provide a theoretical basis and research ideas for the development and application of active components and compounds of Salviae Miltiorrhizae Radix et Rhizoma in nervous system diseases.

This paper comprehensively discusses on the potential neurobiological mechanisms of acupuncture in the treatment of tobacco dependence， focusing on three important aspects， including acupuncture's regulation of tobacco dependence behavior， effects of acupuncture on withdrawal syndrome， and the role of acupuncture in preventing relapse. It is found that acupuncture can inhibit drug-seeking behavior by regulating the reward pathway and related neurons， such as dopamine， thus modulating tobacco dependence behavior. It also alleviates withdrawal symptoms by improving the oral environment of smokers and reducing negative emotions after quitting. Furthermore， acupuncture can prevent relapse by decreasing brain network activity related to smoking cravings and improving cognitive brain functions like addiction memory. Currently， research on the specific neurobiological mechanism of acupuncture in treating tobacco dependence and the involved neural circuits is limited. Future research directions are proposed， including the evaluation of clinical effects， exploration of specific therapeutic mechanisms， investigation of brain pathology， and strengthening the exploration of brain functions. Additionally， combining modern technologies to clarify the neural circuits involved in acupuncture intervention will provide a basis for acupuncture treatment of tobacco addiction.

ObjectiveTo explore the mechanism of action of Wuwei Shenqintang in improving pulmonary fibrosis by using ultra-performance liquid chromatography-quadrupole-time-of-flight mass spectrometry （UPLC-Q-TOF-MS） for metabolomic analysis of lung tissue and feces. MethodsA rat model with pulmonary fibrosis was established by intratracheal injection of 5 mg·kg^-1 bleomycin. The successfully modeled rats were randomly divided into a blank group， a model group， a prednisone （3.15 mg·kg^-1） group， and low-dose， medium-dose， and high-dose groups of Wuwei Shenqintang （4.586， 9.172， 18.344 g·kg^-1）. The rats were given intragastric administration once a day for 28 consecutive days. Hematoxylin-eosin （HE） staining was used to measure the pathological changes in lung and colon tissue， and Masson staining was used to detect the degree of pulmonary fibrosis. Enzyme-linked immunosorbent assay （ELISA） was used to detect the expression of interleukin-1β （IL-1β）， IL-6， IL-8， tumor necrosis factor-α （TNF-α）， and secretory immunoglobulin A （SIgA） in bronchoalveolar lavage fluid and intestinal mucus. Immunohistochemistry and reverse transcription quantitative polymerase chain reaction （Real-time PCR） were used to detect the expression of type Ⅰ collagen （Col-Ⅰ）， fibronectin （FN）， and alpha smooth muscle actin （α-SMA） in lung tissue. UPLC-Q-TOF-MS was used to study the changes in the metabolic network of lung tissue and feces in rats with pulmonary fibrosis treated with Wuwei Shenqintang， screen potential biomarkers for the treatment of pulmonary fibrosis by Wuwei Shenqintang， and perform pathway enrichment analysis. ResultsCompared with the blank group， the model group showed extensive inflammatory cell infiltration and continuous fibrotic lesions in lung tissue， colonic mucosal damage， and connective tissue hyperplasia. The expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus was significantly increased （P<0.01）. The expression of Col-Ⅰ， FN， and α-SMA proteins and mRNAs in lung tissue was significantly upregulated （P<0.01）. Compared with the model group， the groups of Wuwei Shenqintang exhibited significantly reduced inflammatory infiltration and blue collagen deposition in lung tissue， alleviated colonic damage， decreased expression of IL-6， IL-8， IL-1β， TNF-α， and SIgA in bronchoalveolar lavage fluid and intestinal mucus （P<0.01）， and reduced average absorbance values and mRNA expression of Col-Ⅰ， FN， and α-SMA in lung tissue （P<0.05， P<0.01）， with the prednisone group and the medium-dose and high-dose groups of Wuwei Shenqintang showing the most significant effects. The metabolomics results for lung tissue showed that compared with the blank group， the model group had 19 significantly different compounds （P<0.05， P<0.01）. Wuwei Shenqintang could normalize 17 of these compounds compared with the model group （P<0.05， P<0.01）. Fecal metabolomics results showed that compared with those in the blank group， there were 42 compounds with significant differences in the model group （P<0.05， P<0.01）. Compared with the model control group， Wuwei Shenqintang could normalize 41 of these compounds （P<0.05， P<0.01）. The combined analysis results indicated that Wuwei Shenqintang might inhibit pulmonary fibrosis by regulating the biosynthesis of phenylalanine， tyrosine， and tryptophan as well as the retinol metabolism pathway. ConclusionWuwei Shenqintang can ameliorate pulmonary fibrosis， which may be related to the regulation of the "lung-intestine axis".

The pathogenesis of central nervous system （CNS） diseases is complex， seriously affecting patients' physical and mental health and imposing a heavy economic burden on society. Western medicine shows limited efficacy in treating CNS diseases and is often associated with numerous adverse reactions and contraindications. Chinese medicine Lycii Fructus exhibits multiple pharmacological effects， including immune regulation， enhancement of hematopoietic function， liver protection， anti-tumor， hypoglycemic， antipyretic， anti-aging， and anti-radiation activities， and has gradually been applied in clinical treatment. In recent years， the active components of Lycii Fructus have attracted considerable attention for their potential therapeutic effects on CNS diseases. Studies indicate that these active components may exert neuroprotective effects through anti-inflammatory and antioxidant actions， inhibition of neuronal apoptosis， and repair of neuronal damage， involving multiple targets and pathways. This review summarizes the therapeutic effects of Lycii Fructus active components in CNS diseases over the past decade by searching PubMed， CNKI， Wanfang Data， and other electronic databases， aiming to provide new treatment strategies and insights for future research on Lycii Fructus in CNS disorders.

Objective To investigate the predictive value of atherosclerotic index of plasma(AIP)for the risk of coronary heart disease(CHD)in patients with nonalcoholic fatty liver disease(NAFLD).Methods A retrospective analysis was conducted in 299 patients with NAFLD.Based on presence or absence of CHD,the patients were divided into NAFLD with CHD group(n=177)and NAFLD group(n=122).Clinical data were collected from both groups,and AIP was calculat-ed.Multivariate Logistic regression analysis was performed to explore the independent risk factors for CHD in patients with NAFLD.Receiver operating characteristic(ROC)curves were plotted to evalu-ate the predictive value of AIP for the risk of CHD in patients with NAFLD.Results The NAFLD with CHD group had a higher proportion of males,smokers,and higher levels of alanine aminotrans-ferase(ALT),aspartate aminotransferase(AST),fasting plasma glucose(FPG),triglycerides(TG),low-density lipoprotein cholesterol(LDL-C),γ-glutamyltransferase(GGT),uric acid(UA),and AIP than the NAFLD group.The NAFLD with CHD group also had lower levels of high-density lipoprotein cholesterol(HDL-C)than the NAFLD group(P＜0.05).Multivariate Logistic regression analysis revealed that males(OR=2.548,95％CI,1.402 to 4.632,P=0.002),high levels of AST(OR=1.038,95％CI,1.002 to 1.077,P=0.041),high levels of LDL-C(OR=1.811,95％CI,1.242 to 2.640,P=0.002),and high AIP(OR=16.117,95％CI,1.874 to 138.609,P=0.011)were independent risk factors for CHD in patients with NAFLD(P＜0.05).ROC curve analysis showed that AIP had an area under the curve of 0.746(95％CI,0.688 to 0.804)for pre-dicting CHD in patients with NAFLD,with a sensitivity of 76.3％and a specificity of 73.0％.Conclusion AIP is an independent influencing factor for CHD in patients with NAFLD and has certain predictive value for the risk of CHD in these patients.