ObjectiveTo investigate the mechanism of action of Kaixinsan in the treatment of Alzheimer's disease （AD） based on network pharmacology， molecular docking， and animal experimental validation. MethodsThe Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform（TCMSP） and the Encyclopedia of Traditional Chinese Medicine（ETCM） databases were used to obtain the active ingredients and targets of Kaixinsan. GeneCards， Online Mendelian Inheritance in Man（OMIM）， TTD， PharmGKB， and DrugBank databases were used to obtain the relevant targets of AD. The intersection （common targets） of the active ingredient targets of Kaixinsan and the relevant targets of AD was taken， and the network interaction analysis of the common targets was carried out in the STRING database to construct a protein-protein interaction（PPI） network. The CytoNCA plugin within Cytoscape was used to screen out the core targets， and the Metascape platform was used to perform gene ontology（GO） functional enrichment analysis and Kyoto encyclopedia of genes and genomes（KEGG） pathway enrichment analysis. The “drug-active ingredient-target” interaction network was constructed with the help of Cytoscape 3.8.2， and AutoDock Vina was used for molecular docking. Scopolamine （SCOP） was utilized for modeling and injected intraperitoneally once daily. Thirty-two male C57/BL6 mice were randomly divided into blank control （CON） group （0.9% NaCl， n=8）， model （SCOP） group （3 mg·kg^-1·d^-1， n=8）， positive control group （3 mg·kg^-1·d^-1 of SCOP+3 mg·kg^-1·d^-1 of Donepezil， n=8）， and Kaixinsan group （3 mg·kg^-1·d^-1 of SCOP+6.5 g·kg^-1·d^-1 of Kaixinsan， n=8）. Mice in each group were administered with 0.9% NaCl， Kaixinsan， or Donepezil by gavage twice a day for 14 days. Morris water maze experiment was used to observe the learning memory ability of mice. Hematoxylin-eosin （HE） staining method was used to observe the pathological changes in the CA1 area of the mouse hippocampus. Enzyme linked immunosorbent assay（ELISA） was used to determine the serum acetylcholine （ACh） and acetylcholinesterase （AChE） contents of mice. Western blot method was used to detect the protein expression levels of signal transducer and activator of transcription 3（STAT3） and nuclear transcription factor（NF）-κB p65 in the hippocampus of mice. ResultsA total of 73 active ingredients of Kaixinsan were obtained， and 578 potential targets （common targets） of Kaixinsan for the treatment of AD were screened out. Key active ingredients included kaempferol， gijugliflozin， etc.. Potential core targets were STAT3， NF-κB p65， et al. GO functional enrichment analysis obtained 3 124 biological functions， 254 cellular building blocks， and 461 molecular functions. KEGG pathway enrichment obtained 248 pathways， mainly involving cancer-related pathways， TRP pathway， cyclic adenosine monophosphate（cAMP） pathway， and NF-κB pathway. Molecular docking showed that the binding of the key active ingredients to the target targets was more stable. Morris water maze experiment indicated that Kaixinsan could improve the learning memory ability of SCOP-induced mice. HE staining and ELISA results showed that Kaixinsan had an ameliorating effect on central nerve injury in mice. Western blot test indicated that Kaixinsan had a down-regulating effect on the levels of NF-κB p65 phosphorylation and STAT3 phosphorylation in the hippocampal tissue of mice in the SCOP model. ConclusionKaixinsan can improve the cognitive impairment function in SCOP model mice and may reduce hippocampal neuronal damage and thus play a therapeutic role in the treatment of AD by regulating NF-κB p65， STAT3， and other targets involved in the NF-κB signaling pathway.

ObjectiveTo investigate the mechanism of modified Si Junzitang and Shashen Maidong Tang ［Yiqi Yangyin Jiedu prescription （YQYYJD）］ in enhancing the sensitivity of cisplatin in epidermal growth factor receptor tyrosine kinase inhibitor （EGFR-TKI）-resistant lung adenocarcinoma cells based on aerobic glycolysis. MethodsThe effects of different concentrations of YQYYJD （0， 2， 3， 4， 5， 6， 7， 8 g·L^-1） and cisplatin （0， 3， 6， 9， 12， 15， 18， 21， 24， 27 mg·L^-1） on the proliferation and activity of PC9/GR cells were detected by the cell counting kit-8 （CCK-8） assay after 24 hours of intervention. The half-maximal inhibitory concentration （IC₅₀） for PC9/GR cells was calculated to determine the concentrations used in subsequent experiments. PC9/GR cells were divided into blank group （complete medium）， YQYYJD group （5 g·L^-1）， cisplatin group （12 mg·L^-1）， and combined group （YQYYJD 5 g·L^-1 + cisplatin 12 mg·L^-1）. After 24 hours of intervention， cell viability was measured using CCK-8 assay. Cell proliferation was assessed by colony formation assay， and cell migration was evaluated by scratch and Transwell assays. Glucose consumption， lactate production， and adenosine triphosphate （ATP） levels were measured by colorimetric assays. The expression levels of glycolysis-related proteins， including hexokinase 2 （HK2）， phosphofructokinase P （PFKP）， pyruvate kinase M2 （PKM2）， lactate dehydrogenase A （LDHA）， glucose transporter 1 （GLUT1）， and monocarboxylate transporter 4 （MCT4）， were determined by Western blot. ResultsBoth YQYYJD and cisplatin inhibited the viability of PC9/GR cells in a concentration-dependent manner. The IC₅₀ of PC9/GR cells for YQYYJD and cisplatin were 5.15 g·L^-1 and 12.91 mg·L^-1， respectively. In terms of cell proliferation， compared with the blank group， the cell survival rate and the number of colonies formed in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group showed a further significant reduction in cell survival rate and colony formation （P<0.01）. In terms of cell migration， compared with the blank group， the cell migration rate and the number of cells passing through the Transwell membrane in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group exhibited a further significant reduction in cell migration rate and the number of cells passing through the Transwell membrane （P<0.01）. In terms of glycolysis， compared with the blank group， glucose consumption， lactate production， and ATP levels in the YQYYJD group， cisplatin group， and combined group were significantly decreased （P<0.01）. Compared with the YQYYJD and cisplatin groups， the combined group showed a further significant reduction in glucose consumption， lactate production， and ATP levels （P<0.05）. Compared with the blank group， the protein expression levels of HK2， PFKP， PKM2， and LDHA in the YQYYJD， cisplatin， and combined groups were significantly decreased （P<0.01）. The combined group showed a further significant reduction in the expression levels of these proteins compared with the YQYYJD and cisplatin groups （P<0.01）. No significant differences were observed in the protein expression levels of GLUT1 and MCT4 among the groups. ConclusionYQYYJD can synergistically inhibit the proliferation and migration of PC9/GR cells and enhance their sensitivity to cisplatin. The mechanism may be related to the downregulation of the expression of glycolysis-related rate-limiting enzymes， including HK2， PFKP， PKM2， and LDHA， thereby inhibiting glycolysis.

ObjectiveTo explore the clinical efficacy and safety of Da Chaihutang （DCH） for the treatment of sepsis with Yang syndrome. MethodsA total of 70 patients suffering from sepsis with Yang syndrome were randomly divided into an observation group and a control group， with 35 cases in each group. They both received standard Western medicine treatment. The observation group was additionally given a dose of DCH， which was boiled into 100 mL and taken twice. The control group was additionally given an equal volume and dosage of warm water. The intervention lasted for three days. The 28-day all-cause mortality and the changes in the following indicators before and after intervention were compared between the two groups， including sequential organ failure assessment （SOFA）， acute physiology and chronic health evaluation Ⅱ （APACHE Ⅱ） score，white blood cell （WBC），the percentage of neutrophils （NEU%），C-reactive protein （CRP），procalcitonin （PCT），alanine transaminase （ALT），aspartate transaminase （AST），total bilirubin （TBil），creatinine （Cr），blood urea nitrogen （BUN），acute gastrointestinal injury （AGI） grade，gastrointestinal dysfunction score （GDS），serum intestinal fatty acid-binding protein （iFABP）， citrulline （CR），platelet （PLT），prothrombin time（PT），activated partial thromboplastin time （APTT），fibrinogen （Fib），international normalized ratio （INR），and D-dimer （D-D）. ResultsThere was no significant difference between the two groups regarding 28-day all-cause mortality. After the intervention，SOFA，WBC，PCT，and Cr were significantly decreased， and PLT was significantly increased in the control group （P<0.05）. SOFA，APACHE Ⅱ，NEU%，CRP，PCT，ALT，AST，Cr，BUN，AGI grade，GDS，and serum iFABP and CR were significantly improved in the observation group （P<0.05）. After the intervention，APACHE Ⅱ，PCT，AGI grade，GDS，and serum iFABP in the observation group were significantly lower than those in the control group ，while CR and PLT were higher （P<0.05，P<0.01）. There were significant differences regarding the gap of SOFA，APACHE Ⅱ，AST，TBil，AGI grade，GDS，iFABP，CR， and PLT between the two groups （P<0.05，P<0.01）. There were slight differences regarding PT，APTT，Fib，INR，and D-D between the two groups，which were in the clinical normal range. ConclusionOn the basis of Western medicine， DCH helped to reduce sepsis severity and improved multiple organ dysfunction with high clinical efficacy and safety， but further research on its impact on the prognosis of patients with sepsis is still required.

ObjectiveTo observe the influence and therapeutic effect of quercetin on cuproptosis in rheumatoid arthritis rats and to explore its possible mechanism based on the solute carrier family 31 member 1 （SLC31A1）/ferredoxin 1 （FDX1） pathway. MethodsSixty male SD rats were divided into six groups： A control group， a model group， high- and low-dose quercetin groups （150 and 50 mg·kg^-1）， a cuproptosis inhibitor （tetrathiomolybdate， TTM） group （10 mg·kg^-1）， and a methotrexate group （2 mg·kg^-1）， 10 rats in each group. Except for the control group， the model of rheumatoid arthritis （CIA） rats was established by type Ⅱ collagen induction method. After successful modeling， each drug group was intervened according to the corresponding dose of drugs， and the control group and the model group were given the same amount of normal saline by gavage， once a day， which lasted for 4 weeks. The swelling degree of rats' feet was observed， and the clinical arthritis scores were determined. The levels of serum rheumatoid factor （RF）， matrix metalloproteinase-3 （MMP-3）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and ceruloplasmin （Cp） were detected by enzyme-linked immunosorbent assay （ELISA）. The content of copper ion （Cu）， malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） in joint tissue was detected. Hematoxylin-eosin （HE） staining was used to observe the pathological changes of joint tissue. The levels of reactive oxygen species （ROS） and dihydrolipoic acid transacetylase （DLAT） were detected by immunofluorescence （IF）. The protein and mRNA expression of SLC31A1， FDX1， lipoic acid synthase （LIAS）， heat shock protein 70 （HSP70）， pyruvate dehydrogenase E1 subunit β （PDHB）， and copper transporting P-type ATPase β （ATP7B） was detected by immunohistochemistry （IHC） and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR）. ResultsCompared to the control group， the model group exhibited joint swelling and deformity， significantly increased clinical arthritis scores， obvious bone destruction， synovial hyperplasia， and inflammatory cell infiltration in joint tissue. In addition， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp showed significant elevation， while the level of IL-10 was significantly reduced. The levels of Cu， MDA， ROS， and DLAT in joint tissue were markedly increased， whereas SOD and GSH content was significantly decreased. The protein and mRNA expression of SLC31A1 and HSP70 was significantly up-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was significantly down-regulated （P<0.01）. Compared to the model group， each treatment group exhibited varying degrees of improvement in joint swelling and deformation as well as clinical arthritis scores in rats. Additionally， there was a reduction in joint bone destruction， inflammatory cell infiltration， and synovial hyperplasia in rats. Furthermore， the serum levels of RF， MMP-3， TNF-α， IL-1β， and Cp significantly decreased， while the level of IL-10 increased significantly. In joint tissue， the levels of Cu， MDA， ROS， and DLAT showed significant decreases， while SOD and GSH content exhibited significant increases. The protein and mRNA expression of SLC31A1 and HSP70 was down-regulated， while the protein and mRNA expression of FDX1， LIAS， PDHB， and ATP7B was up-regulated （P<0.05）. ConclusionQuercetin effectively reduces synovial hyperplasia and inflammatory infiltration in rats with rheumatoid arthritis， thereby alleviating pathological damage to joint tissue. This effect may be attributed to the blockade of the SLC31A1/FDX1 signaling pathway activation and inhibition of excessive cuproptosis.

ObjectiveTo establish a model that can quickly identify the aroma components in different parts of Nardostachys jatamansi， so as to provide a quality control basis for the market circulation and clinical use of N. jatamansi. MethodsHeadspace solid-phase microextraction-gas chromatography-mass spectrometry（HS-SPME-GC-MS） combined with Smart aroma database and National Institute of Standards and Technology（NIST） database were used to characterize the aroma components in different parts of N. jatamansi， and the aroma components were quantified according to relative response factor（RRF） and three internal standards， and the markers of aroma differences in different parts of N. jatamansi were identified by orthogonal partial least squares-discriminant analysis（OPLS-DA） and cluster thermal analysis based on variable importance in the projection（VIP） value >1 and P<0.01. The odor data of different parts of N. jatamansi were collected by Heracles Ⅱ Neo ultra-fast gas phase electronic nose， and the correlation between compound types of aroma components collected by the ultra-fast gas phase electronic nose and the detection results of HS-SPME-GC-MS was investigated by drawing odor fingerprints and odor response radargrams. Chromatographic peak information with distinguishing ability≥0.700 and peak area≥200 was selected as sensor data， and the rapid identification model of different parts of N. jatamansi was established by principal component analysis（PCA）， discriminant factor alysis（DFA）， soft independent modeling of class analogies（SIMCA） and statistical quality control analysis（SQCA）. ResultsThe HS-SPME-GC-MS results showed that there were 28 common components in the underground and aboveground parts of N. jatamansi， of which 22 could be quantified and 12 significantly different components were screened out. Among these 12 components， the contents of five components（ethyl isovalerate， 2-pentylfuran， benzyl alcohol， nonanal and glacial acetic acid，） in the aboveground part of N. jatamansi were significantly higher than those in the underground part（P<0.01）， the contents of β-ionone， patchouli alcohol， α-caryophyllene， linalyl butyrate， valencene， 1，8-cineole and p-cymene in the underground part of N. jatamansi were significantly higher than those in the aboveground part（P<0.01）. Heracles Ⅱ Neo electronic nose results showed that the PCA discrimination index of the underground and aboveground parts of N. jatamansi was 82， and the contribution rates of the principal component factors were 99.94% and 99.89% when 2 and 3 principal components were extracted， respectively. The contribution rate of the discriminant factor 1 of the DFA model constructed on the basis of PCA was 100%， the validation score of the SIMCA model for discrimination of the two parts was 99， and SQCA could clearly distinguish different parts of N. jatamansi. ConclusionHS-SPME-GC-MS can clarify the differential markers of underground and aboveground parts of N. jatamansi. The four analytical models provided by Heracles Ⅱ Neo electronic nose（PCA， DFA， SIMCA and SQCA） can realize the rapid identification of different parts of N. jatamansi. Combining the two results， it is speculated that terpenes and carboxylic acids may be the main factors contributing to the difference in aroma between the underground and aboveground parts of N. jatamansi.

Chronic heart failure （CHF） is the final stage of cardiovascular diseases. It is a complex syndrome， with dyspnea and edema as the main clinical manifestations， and it is characterized by complex disease conditions， difficult cure， and high mortality. Ferroptosis， a new type of programmed cell death， is different from other types of programmed cell death. Ferroptosis is iron-dependent， accompanied by lipid peroxide accumulation and mitochondrial shrinkage， becoming a hot research topic. Studies have confirmed that ferroptosis plays a key role in the occurrence and development of CHF. The regulation of ferroptosis may become a potential target for the treatment of CHF in the future. The theory of Qi deficiency and stagnation refers to the pathological state of original Qi deficiency and abnormal transportation and distribution of Qi， blood， and body fluid， which has guiding significance for revealing the pathogenesis evolution of some chronic diseases. We believe that Qi deficiency and stagnation is a summary of the pathogenesis of ferroptosis in CHF. Deficiency of Qi （heart Qi） is the root cause of CHF， and stagnation （phlegm turbidity and blood stasis） is the branch of this disease. The two influence each other in a vicious circle to promote the development of this disease. Traditional Chinese medicine （TCM） plays an important role in the treatment of CHF， improving the prognosis and quality of life of CHF patients. This paper explores the correlation between the theory of Qi deficiency and stagnation and the mechanism of ferroptosis in CHF. Furthermore， this paper reviews the mechanism of Chinese medicines and compound prescriptions in preventing and treating CHF by regulating ferroptosis according to the principles of replenishing Qi and dredging to remove stagnation， aiming to provide new ideas and methods for the treatment of CHF with TCM.

ObjectiveTo explore the mechanism by which Xiaoyaosan regulates HPT axis dysfunction in the rat model with the syndrome of liver depression and spleen deficiency by observing its effect on the glycoprotein hormone α-subunit （CGA）/glutathione peroxidase 2 （GPX2）/thyroid-stimulating hormone β-subunit （TSHβ） pathway for thyroid hormone synthesis. MethodsSeventy-two male SD rats were randomized into six groups： normal， model， high-dose （16.7 g·kg^-1）， medium-dose （8.35 g·kg^-1）， and low-dose （4.175 g·kg^-1） Xiaoyaosan， and fluoxetine （0.001 8 g·kg^-1） groups， with 12 rats in each group. The rat model of liver depression and spleen deficiency was induced by chronic restraint stress for 21 days. The intervention groups were treated with Xiaoyaosan decoctions or fluoxetine suspension， respectively. After modeling， hematoxylin-eosin staining was employed to observe morphological changes in the thyroid and pituitary tissue of the rats. Serum levels of triiodothyronine （T3）， tetraiodothyronine （T4）， and thyroid-stimulating hormone （TSH） were measured by enzyme-linked immunosorbent assay （ELISA）. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot were employed to determine the mRNA and protein levels， respectively， of TSH receptor （TSHR） in the thyroid tissue， thyrotropin-releasing hormone receptor （TRHR） and TSHβ in the pituitary tissue， and thyrotropin-releasing hormone （TRH）， CGA， GPX2， and TSHβ in the hypothalamic tissue. ResultsCompared with the normal group， the model group showed significant atrophy and irregularity of thyroid follicles， a marked reduction in colloid secretion， extensive vacuolar degeneration of adenocytes in the anterior pituitary， lowered serum levels of T3， T4， and TSH （P<0.01）， and down-regulated mRNA and protein levels of TSHR in the thyroid tissue， TRHR and TSHβ in the pituitary tissue， and TRH， CGA， GPX2， and TSHβ in the hypothalamic tissue （P<0.01）. Compared with the model group， high- and medium-dose Xiaoyaosan and fluoxetine alleviated the pathological changes in the thyroid and pituitary tissue， outperforming the low-dose Xiaoyaosan group. Moreover， they elevated the serum levels of T3， T4， and TSH （P<0.05， P<0.01）. The serum TSH level was also elevated in the low-dose Xiaoyaosan group （P<0.05）. The mRNA and protein levels of TSHR in the thyroid， TRHR and TSHβ in the pituitary， and TRH， CGA， GPX2， and TSHβ in the hypothalamus were up-regulated in the high- and medium-dose Xiaoyaosan groups （P<0.05， P<0.01）. Additionally， the mRNA and protein levels of TSHβ in the hypothalamus were up-regulated in the low-dose Xiaoyaosan group （P<0.01）. In the fluoxetine group， the mRNA and protein levels of TSHR in the thyroid， TRHR in the pituitary， and TRH， CGA， and GPX2 in the hypothalamus were up-regulated （P<0.05， P<0.01）. ConclusionThe downregulation of CGA/GPX2/TSHβ pathway may be one of the biological mechanisms underlying HPT axis dysfunction in the rat model with the syndrome of liver depression and spleen deficiency. Xiaoyaosan may regulate the HPT axis dysfunction by up-regulating the CGA/GPX2/TSHβ pathway.

This article takes the award-winning traditional Chinese medicine（TCM） patents in the China Patent Award as the breakthrough point to analyze the innovative research progress and achievements of TCM in the past thirty years， such as type of patentees， geographical distribution， technology types， international layout and textual features. The China Patent Award has been selected for 24 sessions so far， with 192 patents awarded for TCM， accounting for 2.3% of the total number of awarded patents. Among the award-winning patents of TCM， the patentees are mainly enterprises， and the active geographic regions of TCM innovation include Guangdong， Shandong， Guangxi， Guizhou， Jiangsu and other provinces. The types of award-winning patents mainly focus on TCM compositions， followed by preparation methods and new applications. The main clinical applications include cardiovascular and cerebrovascular diseases， respiratory system diseases and orthopedic diseases. However， there is still much room for improvement in the international layout， and the quality of text has been steadily improving year by year. Obviously， award-winning patents represent a high level in various aspects， including patent quality， technology advancement， protection strength and social benefits. This article analyzes the overall situation of patent awards in TCM， and discusses the gold award-winning patented technologies， the preparation method of HuoXiang Zhengqi liquid oral preparation（CN911072543） and a method of preparing anti-cancer drug elemene from Curcuma wenyujin（CN200910162658.1）， as representative technologies of TCM compounds and extracts， respectively， providing references for future innovation and intellectual property protection related to TCM.

AIM: To investigate the alterations in corneal aberration and relative refractive power following the reduction of back optic zone diameters(BOZD)of orthokeratology lenses.METHODS: Myopic children aged 8-12 years, deemed suitable and willing to wear orthokeratology lenses, were randomly allocated to wear lenses with a 6.0 mm BOZD or a 5.0 mm BOZD. Data collection included changes in higher-order aberrations, relative refractive power and the treatment zone diameter of the two groups after wearing lenses for 1 d, 1 wk, 1, and 3 mo. The correlation of increase in corneal higher-order aberrations with refractive power was analyzed.RESULTS: The increases in total higher-order aberrations, spherical aberrations and coma aberrations varied over time following lens wear(all P<0.001), and there were no statistically significant differences in the changes of total higher-order aberrations and coma aberrations between the two groups of patients(all P>0.05). A significant difference was observed in the increment of spherical aberrations in the 5 mm range between the two groups of patients, which varied over time(Ftime=40.179, Ptime<0.001; Fgroup=11.948, Pgroup=0.001; Finteraction=3.262, Pinteraction=0.03). A significant difference was observed in the increment of spherical aberrations in the 4 mm range between the two patient groups(Ftime=34.462, Ptime<0.001; Fgroup=13.094, Pgroup<0.001; Finteraction=1.372, Pinteraction=0.25). There was no statistically significant distinction in relative refractive power between the two groups(Fgroup=0.048, Pgroup=0.83; Finteraction=1.208, Pinteraction=0.31); however, relative refractive power changed over time(Ftime=40.030, Ptime<0.001). The difference in treatment zone diameter between the two groups was statistically significant, with changes over time(Ftime=11.212, Ptime<0.001; Fgroup=74.073, Pgroup<0.001; Finteraction=0.312, Pinteraction=0.82). The total higher-order aberrations, spherical aberrations, and coma aberrations in 4, 5 and 6 mm range showed a positive correlation with relative refractive power values(all P<0.001). Statistically significant difference was observed in the axial length between the two groups after wearing lenses for 3, 6 and 12 mo(Ftime=185.398, Ptime<0.001; Fgroup=5.618, Pgroup=0.02; Finteraction=2.315, Pinteraction=0.11).CONCLUSION: Orthokeratology lenses leaded to elevated higher-order aberrations. Orthokeratology lenses with smaller BOZD produced significantly greater spherical aberrations at 4 and 5 mm range and smaller treatment zone diameters. The corneal total higher-order aberration was positively correlated with relative refractive power. Wearing orthokeratology lenses with a smaller BOZD can cause slower axial growth and better myopia control.

Tumor drug resistance is an important problem in the failure of chemotherapy and targeted drug therapy, which is a complex process involving chromatin remodeling. SWI/SNF is one of the most studied ATP-dependent chromatin remodeling complexes in tumorigenesis, which plays an important role in the coordination of chromatin structural stability, gene expression, and post-translation modification. However, its mechanism in tumor drug resistance has not been systematically combed. SWI/SNF can be divided into 3 types according to its subunit composition: BAF, PBAF, and ncBAF. These 3 subtypes all contain two mutually exclusive ATPase catalytic subunits (SMARCA2 or SMARCA4), core subunits (SMARCC1 and SMARCD1), and regulatory subunits (ARID1A, PBRM1, and ACTB, etc.), which can control gene expression by regulating chromatin structure. The change of SWI/SNF complex subunits is one of the important factors of tumor drug resistance and progress. SMARCA4 and ARID1A are the most widely studied subunits in tumor drug resistance. Low expression of SMARCA4 can lead to the deletion of the transcription inhibitor of the BCL2L1 gene in mantle cell lymphoma, which will result in transcription up-regulation and significant resistance to the combination therapy of ibrutinib and venetoclax. Low expression of SMARCA4 and high expression of SMARCA2 can activate the FGFR1-pERK1/2 signaling pathway in ovarian high-grade serous carcinoma cells, which induces the overexpression of anti-apoptosis gene BCL2 and results in carboplatin resistance. SMARCA4 deletion can up-regulate epithelial-mesenchymal transition (EMT) by activating YAP1 gene expression in triple-negative breast cancer. It can also reduce the expression of Ca²⁺ channel IP3R3 in ovarian and lung cancer, resulting in the transfer of Ca²⁺ needed to induce apoptosis from endoplasmic reticulum to mitochondria damage. Thus, these two tumors are resistant to cisplatin. It has been found that verteporfin can overcome the drug resistance induced by SMARCA4 deletion. However, this inhibitor has not been applied in clinical practice. Therefore, it is a promising research direction to develop SWI/SNF ATPase targeted drugs with high oral bioavailability to treat patients with tumor resistance induced by low expression or deletion of SMARCA4. ARID1A deletion can activate the expression of ANXA1 protein in HER2+ breast cancer cells or down-regulate the expression of progesterone receptor B protein in endometrial cancer cells. The drug resistance of these two tumor cells to trastuzumab or progesterone is induced by activating AKT pathway. ARID1A deletion in ovarian cancer can increase the expression of MRP2 protein and make it resistant to carboplatin and paclitaxel. ARID1A deletion also can up-regulate the phosphorylation levels of EGFR, ErbB2, and RAF1 oncogene proteins.The ErbB and VEGF pathway are activated and EMT is increased. As a result, lung adenocarcinoma is resistant to epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs). Although great progress has been made in the research on the mechanism of SWI/SNF complex inducing tumor drug resistance, most of the research is still at the protein level. It is necessary to comprehensively and deeply explore the detailed mechanism of drug resistance from gene, transcription, protein, and metabolite levels by using multi-omics techniques, which can provide sufficient theoretical basis for the diagnosis and treatment of poor tumor prognosis caused by mutation or abnormal expression of SWI/SNF subunits in clinical practice.