Functional constipation (FC) in elderly individuals is a significant health issue that adversely affects their quality of life, with recent studies indicating a close relationship between this condition and gut microbiota dysbiosis. This review aims to explore the role of the gut microbiota in FC in elderly individuals, analyze the mechanisms of the gut-brain axis, and evaluate the potential use of microecological agents, including probiotics and prebiotics, in modulating the gut microbiota and alleviating constipation symptoms. By integrating the latest research findings, this study seeks to provide new perspectives and intervention strategies for the management of FC in elderly individuals.

Lupus nephritis is recognized as a common and severe complication of systemic lupus erythematosus, without an optimal therapeutic strategy currently available. While mesenchymal stem cells (MSCs) hold therapeutic promise, their efficacy varies substantially, likely due to their plasticity and capacity to adopt pro-inflammatory (MSC1) or anti-inflammatory (MSC2) functional states in response to different microenvironments. Here, we report for the first time that IL-27, via JAK1–STAT1 signaling, up-regulates indoleamine 2,3-dioxygenase (IDO) in MSCs, driving MSC differentiation toward an IDO-positive MSC2 phenotype with low immunogenicity. These IDO-positive MSC2 cells produce kynurenine and kynurenic acid, the metabolites of tryptophan, which bind to the intracellular aryl hydrocarbon receptor. This interaction stimulates an increase in the anti-inflammatory factor TSG-6 and induces the differentiation of regulatory T cells. Notably, IL-27-conditioned MSC2 demonstrated superior therapeutic efficacy compared to conventional MSCs in a murine lupus nephritis model. In conclusion, this study revealed that IL-27 is a critical modulator of MSC immune plasticity and presented a novel therapeutic strategy utilizing IL-27-enhanced MSC2 for autoimmune diseases.

As a critical component of the tumour immune microenvironment (TIME), the resident microbiota promotes tumorigenesis across a variety of cancer types. Here, we integrated multiple types of omics data, including microbiome, transcriptome, and metabolome data, to investigate the functional role of intratumoral bacteria in gastric cancer (GC). The microbiome was used to categorize GC samples into six subtypes, and patients with a high abundance of Streptococcus or Pseudomonas had a markedly worse prognosis. Further assays revealed that Streptococcus anginosus (SA) promoted tumour cell proliferation and metastasis while suppressing the differentiation and infiltration of CD8+ T cells. However, antibiotic treatment significantly suppressed tumorigenesis in SA+ mice in vivo. We further demonstrated that the SA arginine pathway increased the abundance of ornithine, which may be a major contributor to reshaping of the TIME. Our findings demonstrated that SA, a novel risk factor, plays significant roles in the initiation and progression of GC, suggesting that SA might be a promising target for the diagnosis and treatment of GC.

The liver serves as a crucial organ for detoxification and exhibits a robust regenerative capacity. The improper administration of pharmaceuticals frequently results in drug-induced liver injury (DILI), a condition closely associated with the overproduction of reactive oxygen species (ROS). In addressing DILI, Traditional Chinese Medicine (TCM) often employs plant-based remedies, which have demonstrated favorable therapeutic outcomes. These plant-based treatments are typically rich in antioxidants capable of neutralizing ROS. However, there is a notable lack of comprehensive reviews that synthesize the therapeutic effects of antioxidants derived from medicinal plants on DILI. The present review starts by exploring ROS generation and clearance in human health, then outlines DILI characteristics and treatments, emphasizing its strong link to oxidative stress. Furthermore, we discuss the properties and classification of antioxidants found in plant-based pharmaceuticals, with a particular emphasis on the synergistic effects of these antioxidants and their mechanisms for repairing DILI. Finally, we provide a summary of commonly utilized medicinal plants from TCM for the treatment of DILI. In conclusion, this article explores the future prospects and potential solutions for treating DILI using antioxidants found in plant-based drugs derived from TCM. The objective of this review is to examine the role of antioxidants in TCM and their impact on DILI.

OBJECTIVES:Breast cancer is a common malignancy in women. More than 90% of breast cancer deaths are caused by metastasis. Epimedii Folium (EF) is a commonly used herb with anti-tumor benefits, but its underlying mechanisms and active components for breast cancer prevention are little understood. This study assessed the therapeutic role of Icariside I (ICS I) in Epimedium flavonoids (EF) on lung metastasis of breast cancer, including the underlying mechanism.METHODS:Western blot, RT-qPCR, wound healing assay, colony formation assay, and flow cytometry were used to investigate the inhibition of breast cancer cells growth and migration by EF and ICS I through disrupting the IL-6/STAT3 pathway. Combined with 4T1 breast cancer model in mice, Western blot, RT-qPCR, Hematoxylin and Eosin staining, immunohistochemistry were used to evaluate the therapeutic role of ICS I in proliferation, apoptosis, invasion, and metastasis of breast cancer.KEY FINDINGS:EF can inhibit STAT3 phosphorylation and reduce the colony formation and migration of breast cancer cells. Detecting the active ingredients in EF, we found ICS I can reduce the activation of STAT3 in 4T1 breast cancer cells, impair colony formation and migration. Moreover, ICS I induced cells G1 phase arrest and modulated Cyclin D1, CDK4, bcl-2, and bax to inhibit proliferation and survival of breast cancer cells. Similarly, the in vivo studies demonstrated that ICS I significantly suppressed tumor development and lung metastasis in the 4T1 mouse model. Tumor cells in vehicle group were arranged in a spoke-like pattern with obvious heterogeneity, and multinucleated tumor giant cells were seen. But, the tumor cells in the ICS I group were disorganized and necrotic lysis was seen in some areas. In ICS I-treated group, tumors' STAT3 phosphorylation level, IL-6, Cyclin D1, CDK4, bcl-2, and vimentin expression were downregulated, bax and cleaved caspase 3 expression were upregulated. In the lung tissue, we could find less metastasis of breast cancer cells and less lung injury in the ICS I group. Besides, the expression of metastasis-related genes MMP9 and vimentin was decreased in the lung tissue of ICS I group.CONCLUSIONS:These findings suggest that ICS I can inhibit breast cancer proliferation, apoptosis, invasion and metastasis probably via targeting IL-6/STAT3 pathway. Therefore, ICS I has the potential to become an innovative therapeutic candidate to breast cancer prevention and treatment.

Background The concentrations of linezolid, its optimal regimen and the associated side effects in elderly patients remain unclear.Methods In this multicentre, prospective study, elderly patients receiving linezolid at four tertiary hospitals in Beijing between May 2021 and December 2022 were included. Linezolid concentrations and haematological toxicity were monitored dynamically. Risk factors for linezolid overexposure and moderate-to-severe linezolid-induced thrombocytopenia (M/S LIT) were analysed, and a predictive model of M/S LIT was developed.Results A total of 860 linezolid concentrations were measured in 313 patients. The median trough concentrations of linezolid were 24.4 (15.3, 35.8) mg/L at 36-72 h and 26.1 (17.0, 38.1) mg/L at 5-10 days (P = 0.132). Severe linezolid exposure was independently associated with age, estimated glomerular filtration rate (eGFR) and the worst SOFA score (SOFA1), and we further recommended dose regimens for elderly patients based on these findings. The incidences of linezolid-induced thrombocytopenia(LIT) and M/S LIT were 73.5% and 47.6%, respectively. M/S LIT was independently correlated with treatment duration, average trough concentration (TDMa), baseline platelet count, eGFR and baseline SOFA score (SOFA0). The developed nomogram predicted M/S LIT with an area under the curve of 0.767 (95% CI 0.715-0.820), a sensitivity of 71.1% and a specificity of 73.2%.Conclusions Linezolid trough concentrations increased dramatically in the elderly, by about 10 mg/L in patients aged 65-80 years, followed by a further increase of 10 mg/L for every 10 years of age. Therapeutic drug monitoring is recommended in elderly patients receiving linezolid. The developed nomogram may predict M/S LIT and guide dosage adjustments of linezolid. Clinical trial registration number: ChiCTR2100045707Conclusions Linezolid trough concentrations increased dramatically in the elderly, by about 10 mg/L in patients aged 65-80 years, followed by a further increase of 10 mg/L for every 10 years of age. Therapeutic drug monitoring is recommended in elderly patients receiving linezolid. The developed nomogram may predict M/S LIT and guide dosage adjustments of linezolid. Clinical trial registration number: ChiCTR2100045707

BackgroundHealth-related quality of life (HRQoL) is a critical aspect of overall well-being for patients with lung cancer, particularly those with metastatic spinal cord compression (MSCC). However, there is currently a lack of universal evaluation of HRQoL in this specific patient population. The aim of this study was to develop a nomogram that can accurately predict HRQoL outcomes in patients with lung cancer-related MSCC.MethodsA total of 119 patients diagnosed with MSCC secondary to lung cancer were prospectively collected for analysis in the study. The least absolute shrinkage and selection operator (LASSO) regression analysis, along with 10-fold cross-validation, was employed to select the most significant variables for inclusion in the nomogram. Discriminative and calibration abilities were assessed using the concordance index (C-index), discrimination slope, calibration plots, and goodness-of-fit tests. Net reclassification index (NRI) and integrated discrimination improvement (IDI) analyses were conducted to compare the nomogram's performance with and without the consideration of comorbidities.ResultsFour variables were selected to construct the final nomogram, including the Eastern Cooperative Oncology Group (ECOG) score, targeted therapy, anxiety scale, and number of comorbidities. The C-index was 0.87, with a discrimination slope of 0.47, indicating a favorable discriminative ability. Calibration plots and goodness-of-fit tests revealed a high level of consistency between the predicted and observed probabilities of poor HRQoL. The NRI (0.404, 95% CI: 0.074-0.734, p = 0.016) and the IDI (0.035, 95% CI: 0.004-0.066, p = 0.027) confirmed the superior performance of the nomogram with the consideration of comorbidities.ConclusionsThis study develops a prediction nomogram that can assist clinicians in evaluating postoperative HRQoL in patients with lung cancer-related MSCC. This nomogram provides a valuable tool for risk stratification and personalized treatment planning in this specific patient population.

Gastric cancer (GC) is a prevalent malignant neoplasm that poses a serious threat to human health. Overexpression of Aurora A (AURKA) is frequently associated with the self-renewal and tumorigenicity of various cancers. Chebulagic acid (CA) has been examined as a potential tumor suppressor based on its ability against numerous tumor biological activities. However, the possible mechanisms of CA inhibition of the progression of GC by mediating the AURKA/β-catenin/Wnt signaling pathway have not been investigated. The present study investigated the level of AURKA expression in GC. We further examined the effect of CA on cell proliferation, migration, and apoptosis in the MKN1 and NUGC3 GC cell lines, and its efficacy in suppressing tumor growth was assessed in tumor bearing mice model. We demonstrated that AURKA was highly expressed in GC and associated with poor prognosis. We demonstrated that treatment with CA significantly inhibited the proliferation and migration of GC cells and induced apoptosis. Compared to the vehicle group, CA treatment severely diminished the volume and weight and the metastasis of tumors. CA also inhibited the expression of AURKA and the AURKA/β-catenin/Wnt signaling pathway in vitro and in vivo . Collectively, the present results demonstrated that high expression of AURKA may be an independent factor of poor prognosis in patients with GC, and CA significantly suppressed the tumor biological functions of GC and inhibited the AURKA/β-catenin/Wnt pathway.

OBJECTIVES:Jie Geng Tang (JGT) is an ancient traditional Chinese herbal decoction that exhibits various pharmacological activities, however, is poorly understood in the sensitivity of lung cancer to chemotherapy. Here, we explored the effect of JGT on sensitizing cisplatin (DDP)-resistant A549 cells (A549/DDP).METHODS:Cell viability was assessed using cell counting kit-8 assay. Flow cytometry was applied to detected cell apoptosis, mitochondrial membrane potential (MMP) and reactive oxygen species (ROS) levels. Western blotting and qRT-PCR were performed to determine protein and mRNA levels.KEY FINDINGS:The results demonstrated that DDP co-treatment with JGT significantly increased the cytotoxicity of A549/DDP cells and exhibited efficacy in suppressing the migration and proliferation. The rate of apoptosis was increased by co-treatment with DDP and JGT, along with a higher rate of Bax/Bcl-2, and increased loss of MMP. Furthermore, the combination promoted ROS accumulation and increased γ-H2AX levels. Moreover, Nrf2 levels were suppressed in a dose- and time-dependent manner, Nrf2 stability was reduced following treatment with JGT. Notably, the combination induced inhibition of the Nrf2/ARE pathway at the mRNA and protein levels.CONCLUSIONS:Collectively, these results indicate that co-treatment with JGT and DDP can be considered a combinational approach to treating DDP resistance.

Excess acetaminophen(APAP) can be converted by the cytochrome P450 system to the toxic metabolite N-acetyl-p-benzoquinoneimine(NAPQI), which consumes glutathione(GSH). When GSH is depleted, NAPQI covalently binds with proteins, inducing mitochondrial dysfunction and oxidative stress and thereby leading to hepatotoxicity. Schisandrin C(SinC) is a dibenzocyclooctadiene derivative isolated from Schisandra chinensis. Although there is some evidence showing that SinC has hepatoprotective activity, its protective effect and mechanism on APAP-induced liver injury remain unclear. In this paper, an acute liver injury mouse model was established by intraperitoneal injection of APAP at a dose of 400 mg·kg~(-1) to evaluate the effect of SinC administration on the APAP-induced liver injury and its mechanism through an animal experiment. At the same time, a potential candidate drug was provi-ded for traditional Chinese medicine(TCM) prevention and treatment of overdose APAP-induced liver injury. In the APAP-induced liver injury mouse model, we found that SinC can relieve hepatic histopathological lesions and significantly reduce the activities of alanine aminotransferase(ALT), aspartate aminotransferase(AST) and alkaline phosphatase(ALP). It was also capable of increasing the content of GSH and superoxide dismutase(SOD) and decreasing the levels of total bilirubin(TBIL), direct bilirubin(DBIL), malondialdehyde(MDA), interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α). Further analysis showed that SinC decreased the content of CYP2 E1 in liver tissues at protein and mRNA levels and increased nuclear factor erythroid 2-related factor 2(Nrf2) and the expression of its downstream targets(including HO-1, NQO1 and GCLC). Taken together, the above results indicate that SinC can alleviate APAP-induced liver injury by reducing the expression of CYP2 E1, suppressing apoptosis, improving inflammatory response and activating the Nrf2 signaling pathway to inhibit oxidative stress.

目的 研究五味子油联合莪术油防治肝纤维化的作用及机制.方法 采用蛋氨酸和胆碱缺乏及铁添加氨基酸饲料喂养小鼠构建非酒精脂肪肝炎伴肝纤维化模型,将112只C57BL/6小鼠分为对照组、模型组、扶正化瘀胶囊(585 mg/kg)组、五味子油单独给药组、莪术油单独给药组以及五味子油联合莪术油给药组;造模成功后,对照组和模型组ig 0.5％羧甲基纤维素钠溶液,各给药组ig相应药物,连续6周;采用酶标仪测定小鼠血清中丙氨酸转氨酶(alanine aminotransferase,ALT)和天冬氨酸转氨酶(aspartate aminotransferase,AST)活性;采用苏木素-伊红(HE)染色法观察各组小鼠肝组织病理变化;采用ELISA法检测小鼠血清中转化生长因子-β1(transforming growth factor-β1,TGF-β1)、肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和肝组织中羟脯氨酸(hydroxyproline,Hyp)含量;采用qRT-PCR法检测小鼠肝组织中Ⅰ型胶原(CollagenⅠ)、TGF-βl和Smad3的mRNA表达情况.人肝星形LX-2细胞给予药物预处理,再加入TGF-β1因子,采用Western blotting法检测细胞Collagen Ⅰ和α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)蛋白表达情况.结果 体内实验结果显示,与模型组相比,各给药组血清中ALT和AST活性均显著降低(P＜0.05、0.01、0.001),其中五味子油与莪术油联合给药高剂量组抑制小鼠ALT活性更为显著;肝脏颜色、光泽和质地都有明显改善,肝组织中脂肪空泡化改善、炎性细胞浸润减少;肝组织Hyp和血清TGF-β1、TNF-α含量均显著降低(P＜0.05、0.01、0.001),其中联合给药高剂量组改善小鼠肝组织Hyp含量更为显著;肝组织Collagen Ⅰ、TGF-β1和Smad3 mRNA表达水平显著降低(P＜0.05、0.01、0.001).体外实验结果显示,五味子油与莪术油联合给药组能下调TGF-β1诱导的LX-2细胞Collagen Ⅰ和α-SMA蛋白表达.结论 五味子油和莪术油均具有抗肝纤维化作用,且五味子油与莪术油联用的抗肝纤维化效应明显强于各药物的单独使用.

Objective To explore the transitive regularity of holistic constituents from the crude slices of the medicinal raw materials (MCS) to the formula granules (FG), fufang decoction (FD), and finally, the concentrated pills (CP) of Liuwei Dihuang Fufang (六味地黄复方, LWDHF). Methods Samples for MCS, FG, FD, and CP of LWDHF were obtained, and a fingerprint database was established using high-performance liquid chromatography (HPLC), by separating the samples in an XB-C18 column and analyzing the transitive regularity of components using the total quantum statistical moment (TQSM), including total quantum zero moment (AUCT), total quantum first moment (MRTT), total quantum second moment (VRTT), and its similarity approach. The AUCT, MRTT, and VRTT were calculated based on the representative HPLC chromatograms of FG, FD, and CP of LWDHF. Results AUCT of FG, FD, and CP of LWDHF was 71 804, 46 553, and 144 646 μV s, respectively; MRTT was 14.43, 14.54, and 18.85 min, respectively; and VRTT was 106.98, 112.84, and 269.12 min2, respectively. Comparing the similarity of FG/FD, FG/CP and FD/CP of LWDHF, the TQSM similarity values were 98.66%, 76.62%, and 75.37%, respectively, whereas the traditional similarity evaluation values were 98.68%, 85.43%, and 85.60%, respectively. Conclusion The results perform little distinction in the total composition between FG and FD, whereas some distinction existed between FD and CP. Experimental evidence, therefore indicates that FG could be used as the alternative of MCS in clinical applications.

Context Schisandra chinensis (Turcz.) Baill. (Magnoliaceae) essential oil (SCEO) composition is rich in lignans that are believed to perform protective effects in the liver.Objective This study investigates the effects of SCEO in the treatment of acetaminophen (APAP)-induced liver injury in mice.Materials and methods C57BL/6 mice (n = 56) were randomly divided into seven groups: normal; APAP (300 mg/kg); APAP plus bicyclol (200 mg/kg); APAP plus SCEO (0.25, 0.5, 1, 2 g/kg). Serum biochemical parameters for liver function, inflammatory factors, and antioxidant activities were determined. The protein expression levels of Nrf2, GCLC, GCLM, HO-1, p62, and LC3 were assessed by western blotting. Nrf2, GCLC, HO-1, p62, and LC3 mRNA were detected by real-time PCR.Results Compared to APAP overdose, SCEO (2 g/kg) pre-treatment reduced the serum levels of AST (79.4%), ALT (84.6%), TNF-α (57.3%), and IL-6 (53.0%). In addition, SCEO (2 g/kg) markedly suppressed cytochrome P450 2E1 (CYP2E1) (15.4%) and attenuated the exhaustion of GSH (43.6%) and SOD (16.8%), and the accumulation of MDA (22.6%) in the liver, to inhibit the occurrence of oxidative stress. Moreover, hepatic tissues from our experiment revealed that SCEO pre-treatment mitigated liver injury caused by oxidative stress by increasing Nrf2, HO-1, and GCL. Additionally, SCEO activated autophagy, which upregulated hepatic LC3-II and decreased p62 in APAP overdose mice (p < 0.05).Discussion and conclusions Our evidence demonstrated that SCEO protects hepatocytes from APAP-induced liver injury in vivo and the findings will provide a reliable theoretical basis for developing novel therapeutics.

LncRNA surfactant associated 1 (SFTA1P) exhibits low expression in non-small cell lung cancer (NSCLC) tissues as compared with that in adjacent tissues, and may play a suppressing role in NSCLC. However, the effect and mechanism of SFTA1P on the metastasis of lung adenocarcinoma (LUAD) remain undefined, which are thus investigated in this research. Herein, potential impacts of SFTA1P on LUAD were determined through the Cancer Genome Atlas (TCGA) database and Gene Expression Profiling Interactive Analysis (GEPIA). After knockdown/overexpression of SFTA1P, the metastatic ability of LUAD cells was evaluated by molecular biology experiments (cell counting kit-8 assay, scratch test, Transwell assay and Western blot). The effect of SFTA1P on Yes-associated protein (YAP) nuclear translocation was assessed by Western blot. Hypoxia-induced exosomes were extracted for LUAD metastasis analysis. The targeting relationship of SFTA1P/miR-4766-5p/large tumor suppressor kinase 1 (LATS1) was verified by dual-luciferase reporter assay and molecular biology experiments. Xenograft and lung metastasis models were constructed for in vivo validation. SFTA1P was lowly expressed in LUAD, which was associated with the poor prognosis of patients with LUAD. Up-regulated SFTA1P prevented the metastasis of LUAD cells and the nuclear translocation of YAP. Hypoxia-induced exosomes stimulated LUAD cell metastasis, but inhibited the SFTA1P and LATS1/YAP axes. MiR-4766-5p acted as an intermediate "bridge" for SFTA1P to regulate LATS1. SFTA1P repressed xenograft growth and LUAD cell metastasis. To sum up, SFTA1P activates hypoxic exosome-delivered miR-4766-5p through modulating LATS1/YAP pathway, thereby suppressing LUAD cell metastasis, which may serve as a suitable target for the LUAD therapy.

Increased medical application of psychotropic drugs raised attention concerning their toxicological effects. In fact, more than 160 psychotropic drugs including antidepressants and antipsychotics, have been shown to cause liver side effects, but the underlying mechanisms are still poorly understood. Here, we discovered that fluoxetine, a common antidepressant, was specifically sensed by NLRP3 inflammasome, whose subsequent activation resulted in the maturation of caspase-1 and IL-1β, as well as gasdermin D (GSDMD) cleavage, which could be completely abrogated by a selective NLRP3 inhibitor MCC950 or Nlrp3 knockout ( Nlrp3 −/− ). Mechanistically, mitochondrial damage and the subsequent mitochondrial reactive oxygen species (mtROS) accumulation were crucial upstream signaling events in fluoxetine-triggered NLRP3 inflammasome activation. In fluoxetine hepatotoxicity models, mice showed the alterations of aminotransferase levels, hepatic inflammation and hepatocyte death in an NLRP3-dependent manner, and MCC950 pretreatment could reverse these side effects of fluoxetine. Notably, we also found that multiple antidepressants, such as amitriptyline, paroxetine, and imipramine, and antipsychotics, such as asenapine, could specifically trigger the NLRP3 inflammasome activation. Collectively, our findings implicate multiple psychotropic drugs may act as danger signals sensed by the NLRP3 inflammasome and result in hepatic injury.

The accumulation of various genetic and epigenetic changes in colonic epithelial cells has been identified as one of the fundamental processes that drive the initiation and progression of colorectal cancer (CRC). This study aimed to explore functional genes regulated by DNA methylation and their potential utilization as biomarkers for the prediction of CRC prognoses. Methylation‐driven genes (MDGs) were explored by applying the integrative analysis tool (methylmix) to The Cancer Genome Atlas CRC project. The prognostic MDG panel was identified by combining the Cox regression model with the least absolute shrinkage and selection operator regularization. Gene set enrichment analysis was used to determine the pathways associated with the six‐MDG panel. Cluster of differentiation 40 (CD40) expression and methylation in CRC samples were validated by using additional datasets from the Gene Expression Omnibus. Methylation‐specific PCR and bisulfite sequencing were used to confirm DNA methylation in CRC cell lines. A prognostic MDG panel consisting of six gene members was identified: TMEM88, HOXB2, FGD1, TOGARAM1, ARHGDIB and CD40. The high‐risk phenotype classified by the six‐MDG panel was associated with cancer‐related biological processes, including invasion and metastasis, angiogenesis and the tumor immune microenvironment. The prognostic value of the six‐MDG panel was found to be independent of tumor node metastasis stage and, in combination with tumor node metastasis stage and age, could help improve survival prediction. In addition, the expression of CD40 was confirmed to be regulated by promoter region methylation in CRC samples and cell lines. The proposed six‐MDG panel represents a promising signature for estimating the prognosis of patients with CRC.

With the emergence of drug resistance in Western medicine, the repeated administration of clinical first-line drugs becomes more severe. There are many factors leading to multidrug resistance(MDR), so it is very difficult to solve the problem. Since traditional Chinese medicine(TCM) has been used in the field of MDR in recent years, the research on the transporter-associated drug resistance and intervention of TCM has gradually become a hot spot. Therefore, in order to further explore the relationships among drug resistance, transporters, and TCM intervention, we review the relevant research progress in recent years and comb the achievements and limitations of this research at present. In the end, we put forward the research direction of changing body's ADME through the host's transporters and gastrointestinal flora, which provides new ideas for future research.