Metabolic associated fatty liver disease (MAFLD) is fundamentally driven by an imbalance in hepatic fatty-acid flux: the influx of fatty acids exceeds the liver’s capacity for disposal, resulting in excessive hepatic lipid accumulation, predominantly in the form of triglycerides (TGs). The occurrence and progression of MAFLD depend on disordered regulation across multiple metabolic steps, including fatty-acid uptake, de novo lipogenesis (DNL), fatty-acid oxidation (FAO), and very low-density lipoprotein (VLDL) export. Forkhead box protein O1 (FOXO1) is a key transcriptional regulator within the hepatic network coordinating glucose and lipid metabolism. Under metabolic stress and insulin resistance (IR), FOXO1 expression is frequently increased, whereas its inhibitory phosphorylation is reduced. These changes enhance FOXO1 nuclear localization and transcriptional activity, thereby reprogramming the expression of genes related to metabolism in the liver. Because hepatic lipid deposition is the central pathological feature of MAFLD, the functional status of FOXO1 directly influences hepatic lipid homeostasis. Growing evidence suggests that FOXO1 can exert bidirectional, environment-dependent effects on hepatic lipid accumulation; however, the molecular basis for this functional switch remains incompletely understood. This review systematically summarizes the biological functions and regulatory mechanisms of FOXO1 and its roles in hepatic lipid metabolism, with a particular focus on its crosstalk with insulin signaling. FOXO1 expression is shaped by RNA modifications and epigenetic regulation mediated by non-coding RNAs. Its transcriptional output is precisely governed by post-translational modifications—such as phosphorylation and acetylation—as well as by coordinated nucleocytoplasmic shuttling. Notably, these regulatory patterns vary markedly across nutritional states, degrees of insulin resistance, and stages of disease. In the fed state, insulin/IGF-1 signaling activates the PI3K-AKT pathway, promoting the inhibitory phosphorylation of FOXO1 and facilitating additional modifications, including acetylation, methylation, and ubiquitination. Together, these events drive FOXO1 export from the nucleus and dampen its transcriptional activity, suppressing gluconeogenesis and constraining lipogenic programs. Conversely, during fasting or when insulin signaling is weakened, FOXO1 inhibition is relieved. FOXO1 accumulates in the nucleus, binds to DNA, and regulates the transcription of downstream target genes. Mechanistically, FOXO1 can aggravate hepatic lipid accumulation by activating genes involved in TG synthesis while repressing FAO-related pathways, thereby favoring storage over oxidation. However, under specific conditions, FOXO1 may also alleviate the hepatic lipid burden by promoting TG hydrolysis and enhancing VLDL secretion, thereby reducing the net hepatic lipid load. In addition, lipotoxic signals mediated by ceramides and diacylglycerols (Cer/DAG) activate atypical protein kinase C (aPKC), further exacerbating the disruption of the AKT-FOXO1 axis. This vicious cycle ultimately produces a metabolic paradox in which increased hepatic glucose output coexists with persistent, insulin-independent lipogenesis, accelerating MAFLD progression. Importantly, FOXO1 regulation is not uniform: during early metabolic overload, insulin-mediated suppression may remain effective, whereas in advanced insulin resistance, the loss of AKT control permits sustained FOXO1 activity. Such stage-dependent dynamics may help explain why FOXO1 can either promote steatosis or, in certain contexts, support programs that facilitate lipid turnover. Accordingly, interventions should be liver-specific and tuned to the disease stage, aiming to curb maladaptive FOXO1 signaling while preserving its capacity to promote triglyceride hydrolysis and VLDL secretion when advantageous. Overall, this review offers an important perspective on MAFLD pathogenesis, emphasizing FOXO1 as a potential therapeutic target and providing a theoretical basis for developing liver-specific, disease-course-dependent precision interventions.

Aim To explore the underlying molecular mechanism of Alisol A 24-acetate(24A)in improving oxygen-glucose deprivation/reoxygenation(OGD/R)injury in brain microvascular endothelial cells(BMECs)and its correlation with miR-98-5p/transi-ent receptor potential melastatin-2(TRPM2).Meth-ods The ischemia-reperfusion injury in brain micro-vascular endothelial cells(BMECs)was established u-sing bEnd.3 cells subjected to 8 h of oxygen-glucose deprivation followed by 16 h of re-oxygenation.The cells were intervened by miR-98-5p mimics and/or 18.77 μmol·L-1 24A for 24 h and divided into the control group,OGD/R group,OGD/R+24A group,OGD/R+24A+miR-98-5p mimics group and OGD/R+miR-98-5p mimics group.The mRNA levels of miR-98-5p and TRPM2 were detected by qPCR.IL-1 β and TNF-α levels were detected by ELISA.The expression levels of TRPM2,p-AKT,p-GSK3 β,AKT,GSK3 β,Bcl-2,Bax,ZO-1,Occludin,Claudin-5 were detected by Western blot.Apoptosis and reactive oxygen species(ROS)levels were detected by flow cytometry.The targeting relationship between miR-98-5p and TRPM2 was verified using dual luciferase assay.Results Compared with the control group,the apoptosis of OGD/R group was obvious,Bcl-2/Bax decreased,ZO-1,Occludin,Claudin-5 decreased,IL-1 β,TNF-α and ROS increased,miR-98-5p,p-AKT/AKT,p-GSK3β/GSK3β decreased but TRPM2 increased.But com-pared with the OGD/R group,except the control group,the other three groups showed the opposite trend in the above aspects;compared with the OGD/R+24A group,OGD/R+24A+miR-98-5p mimics group showed decreased apoptosis,decreased degradation of ZO-1,Occludin and Claudin-5,and decreased inflam-mation and ROS.miR-98-5p,p-AKT/AKT,p-GSK3β/GSK3β increased and TRPM2 decreased.However,compared with the OGD/R+24A+miR-98-5p mimics group,the OGD/R+miR-98-5p mimics group reversed this trend.Dual luciferase confirmed that miR-98-5p targeted regulation of TRPM2.Conclusion 24A in-hibits the expression of TRPM2 in BMECs through miR-98-5p,regulates AKT/GSK3β signal pathway,re-duces OGD/R inflammation and oxidative stress-medi-ated apoptosis,prevents the degradation of ZO-1,Oc-cludin and Claudin-5,and improves BBB permeability.

Objective:To investigate the prognostic factors for esophageal cancer after radical resection and the application value of machine learning prediction model.Methods:The retrospective cohort study was conducted. The clinicopatholigical data of 406 esophageal cancer patients who were admitted to Qilu Hospital of Shandong University from January 2018 to March 2022 were collected. There were 357 males and 49 females, aged (64±8)years. All patients underwent radical resection of esophageal cancer. The 406 patients were randomly divided into a training set of 285 cases and a validation set of 121 cases at a 7∶3 ratio based on a random number table. The training set was used to construct prediction model, and the validation set was used to validate prediction model. Patients were divided into high-risk group and low-risk group based on risk scores. Observation indicators: (1) follow-up of patients and analysis of influencing factors for prognosis; (2) construction and validation of machine learning prediction models. Comparison of measurement data with normal distribution between groups was conducted using the independent sample t test. Comparison of measurement data with skewed distribution between groups was conducted using the Mann-Whitney U test. Comparison of count data between groups was conducted using the chi-square test. Comparison of ordinal data between groups was conducted using the rank sum test. The Kaplan-Meier method was used to calculate survival rate and plot survival curve, and the Log-rank test was used for survival analysis. The Cox proportional hazard regression model was used for univariate and multivariate analyses. Independent influencing factors were included, and data processing, machine learning model construction, and visualization were performed using R packages including random survival forest (RSF), gradient boosting machine (GBM), least absolute shrinkage and selection operator Cox regression (LASSO-Cox), Cox proportional hazards model boosting (CoxBoost), survival support vector machine (survivalsvm), extreme gradient boosting (XGBoost), supervised principal component analysis (SuperPC), and Cox partial least squares regression (plsRcox). Receiver operating characteristic (ROC) curves were drawn, and sensitivity, specificity, and area under the curve (AUC) were calculated. The Delong test was used to assess the differences in AUC among different models in the training set, and the time-dependent ROC was used to compare the predictive performance of different models. Calibration curves were used to evaluate model accuracy, and decision curve analysis (DCA) was used to evaluate overall net benefit. Results:(1) Follow-up of patients and analysis of influencing factors for prognosis. All 406 patients were followed up postoperatively for 28(range, 6-36)months, with 1- and 3-year overall survival rate of 86.5% and 40.9%, respectively. The 285 patients in the training set were followed up postoperatively for 30(range, 6-36)months, with 1- and 3-year overall survival rate of 85.1% and 35.5%, respectively. The 121 patients in the validation set were followed up postoperatively for 25(range, 6-36)months, with 1- and 3-year overall survival rate of 87.0% and 43.2%, respectively. There was no significant difference in postoperative overall survival rate between the training set and the validation set ( χ2=3.20, P>0.05). Results of multivariate analysis showed that left thoracic surgical approach, preopera-tive neutrophil count, vascular invasion, perineural invasion, pathological T2-4 stage, pathological N2-3 stage, and postoperative pneumonia were independent risk factors affecting postoperative survival of 285 patients in the training set ( hazard ratio=1.466, 1.037, 1.482, 1.549, 5.268, 7.727, 22.202, 2.539, 2.686, 1.425, 95% confidence interval as 1.026-2.096, 1.003-1.073, 1.008-2.179, 1.105-2.170, 1.201-23.099, 1.833-32.576, 4.734-104.128, 1.577-4.087, 1.631-4.422, 1.018-1.994, P<0.05). (2) Construction and validation of machine learning prediction models. Independent risk factors affecting postoperative survival were included to construct RSF, GBM, LASSO-Cox, CoxBoost, survivalsvm, XGBoost, SuperPC, and plsRcox machine learning prediction models. Results of Delong test showed that there were significant differences in the AUC of RSF and GBM from the other six models ( P<0.05). Results of time-dependent ROC curve showed that all 8 machine learning predic-tion models had good discriminative ability in the training cohort, among which the RSF machine learning prediction model had the best predictive performance. Results of calibration curve showed that the RSF machine learning prediction model fitted well for predicting postoperative 1-, 2-, and 3-year overall survival in the training cohort, with high consistency with actual results. Results of decision curve analysis showed that within a threshold range of 0-0.80, the RSF machine learning prediction model provided a better overall net benefit. Further analysis showed that in the validation set, the AUC of RSF machine learning prediction model for postoperative 1-, 2-, and 3-year survival prediction were 0.786 (95% confidence interval as 0.609-0.962), 0.774 (95% confidence interval as 0.676-0.873), and 0.750 (95% confidence interval as 0.652-0.848), respectively. Results of calibration curve showed that the RSF machine learning prediction model fitted well for predicting postopera-tive 1-, 2-, and 3-year overall survival in the validation set, with high consistency with actual results. In the training set, the optimal cutoff value of the RSF machine learning prediction model risk score was 11.7. Patients with risk score ≥11.7 were classified as the high-risk group, and those with risk score <11.7 as the low-risk group. The median survival times of the two groups were 18.0 months and >36.0 months, respectively, showing a significant difference between them ( χ2=73.30, P<0.05). In the validation set, the optimal cutoff value of the RSF machine learning prediction model risk score was 11.7. Patients with risk score ≥11.7 were classified as the high-risk group, and those with risk score<11.7 as the low-risk group. The median survival times of the two groups were 17.0 months and>36.0 months for the high-risk and low-risk groups, respectively, showing a significant difference between them ( χ2=35.20, P<0.05). Conclusions:Left thoracic surgical approach, preoperative neutrophil count, vascular invasion, perineural invasion, pathological T2-4 stage, pathological N2-3 stage, and postoperative pneumonia are independent risk factors affecting survival of esophageal cancer patients after radical resection. The RSF machine learning prediction model constructed based on these factors can effectively distinguish the survival prognosis of high-risk and low-risk patients.

Cancer-associated fibroblasts(CAFs)and tumor-asso-ciated macrophages(TAMs)play crucial roles in the tumor microenvironment,and their interaction exerts a significant influ-ence on tumorigenesis and development.With the rapid develop-ment of research techniques,we have acquired novel understand-ings of the cell communication between TAMs and CAFs at the single-cell level.The cell communication between the two is of-ten related to the polarization of TAMs and remodeling of the mi-croenvironmental matrix by CAFs,thereby mediating mechanisms such as immunosuppression or tumor invasion and metastasis.Specific subsets of CAFs and TAMs have also been discovered to play a role in suppressing tumor progression.Nutrient metabo-lites may also participate in the interaction between CAFs and TAMs and have the potential to become new therapeutic targets for tumors.This review explores the research progress in the cell communication between TAMs and CAFs,expounds on the com-plexity of their interaction,and is expected to provide new per-spectives for the treatment and prevention of cancer and tumors.

Objective Based on the national drug sampling inspection program,this study aims to comprehensively and systematically evaluate the quality of Xuanmai Ganjie preparations,analyze existing quality issues,and provide references and suggestions for quality control of this variety.Methods A total of 237 batches of Xuanmai Ganjie preparations were tested using legal standards,and methods were established for detecting adulteration of Ophiopogon japonicus with counterfeit varieties,paclobutrazol residue levels,and determining the content of platycodin D in Xuanmai Ganjie preparations.These methods were applied to the quality control and evaluation of Xuanmai Ganjie preparations.Results Through statutory inspection,one batch of Xuanmai Ganjie granules was found non-compliant.Specific batches were identified to contain the following irregularities:adulteration of Ophiopogon japonicus with counterfeit varieties,paclobutrazol residue levels exceeding proposed limits,and platycodin D content below the established threshold.Conclusion The overall quality of Xuanmai Ganjie granules was average,while the overall quality of Xuanmai Ganjie capsules and lozenges was relatively good.Manufacturing enterprises should strengthen their sense of primary responsibility and enhance control over the entire drug production process.

Aim To investigate the mechanism by which Aiweixin oral liquid(AWX)alleviates myocar-dial ischemia-reperfusion injury in rats through the reg-ulation of mitochondrial fusion and fission.Methods Seventy-two healthy male Sprague-Dawley rats were randomly assigned to six groups(n=12)using a ran-dom number table:sham surgery group,model group,low-dose AWX(1 mL·kg-1)group,medium-dose AWX(2 mL·kg-1)group,high-dose AWX(4 mL·kg-1)group,and positive control drug trimetazidine(10 mg·kg-1)group.A myocardial ischemia-reper-fusion injury(MIRI)model was established by ligating the left anterior descending coronary artery of the rat heart,followed by 30 minutes of ischemia and 90 mi-nutes of reperfusion.In the sham surgery group,only a suture was placed without ligation.The rats in the treatment groups were pre-gavaged with AWX starting 10 days prior to the modeling procedure.Lead Ⅱ elec-trocardiograms were recorded before and after reperfu-sion in each group to observe the changes in electrocar-diographic parameters.The myocardial infarct size in each group was assessed using TTC staining.The his-topathological changes in myocardial tissue were exam-ined under a light microscope using hematoxylin and eosin(HE)staining.The serum levels of adenosine triphosphate(ATP)and cardiac troponin I(cTnI)were measured using enzyme-linked immunosorbent as-say(ELISA).Superoxide dismutase(SOD)activity and the levels of malondialdehyde(MDA)and lactate dehydrogenase(LDH)were determined using bio-chemical assay kits.The protein expression levels of dynamin-related protein 1(dynamin-relatedprotein 1,DRP1),mitochondrial fission factor(mitochondrial fis-sion factor,MFF),mitochondrial fission protein 1(mi-tochondrial fission protein 1,FIS1),mitofusin 1(mito-fusion-1,MFN1),and mitofusin 2(mitofusion-2,MFN2)were evaluated by Western blot analysis.Re-sults Compared with the sham group,the model group exhibited aggravated myocardial tissue pathological damage,an increased percentage of myocardial infarct size,decreased serum SOD activity and ATP levels,and significantly elevated levels of MDA,cTnI,and LDH activity.Additionally,the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1 was up-regulated,while the expression of fusion-related factors MFN1 and MFN2 was downregulated.Compared with the model group,Aiweixin oral liquid significantly alle-viated myocardial injury,reduced the percentage of my-ocardial infarct size,increased serum SOD activity and ATP levels,decreased MDA content and cTnI and LDH activity,downregulated the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1,and up-regulated the protein expression of fusion-related factors MFN1 and MFN2.Conclusion Aiweixin oral liquid alleviates myocardial ischemia-reperfusion injury in rats by regulating abnormal mitochondrial fusion and fis-sion.

Aim To explore the underlying molecular mechanism of Alisol A 24-acetate(24A)in improving oxygen-glucose deprivation/reoxygenation(OGD/R)injury in brain microvascular endothelial cells(BMECs)and its correlation with miR-98-5p/transi-ent receptor potential melastatin-2(TRPM2).Meth-ods The ischemia-reperfusion injury in brain micro-vascular endothelial cells(BMECs)was established u-sing bEnd.3 cells subjected to 8 h of oxygen-glucose deprivation followed by 16 h of re-oxygenation.The cells were intervened by miR-98-5p mimics and/or 18.77 μmol·L-1 24A for 24 h and divided into the control group,OGD/R group,OGD/R+24A group,OGD/R+24A+miR-98-5p mimics group and OGD/R+miR-98-5p mimics group.The mRNA levels of miR-98-5p and TRPM2 were detected by qPCR.IL-1 β and TNF-α levels were detected by ELISA.The expression levels of TRPM2,p-AKT,p-GSK3 β,AKT,GSK3 β,Bcl-2,Bax,ZO-1,Occludin,Claudin-5 were detected by Western blot.Apoptosis and reactive oxygen species(ROS)levels were detected by flow cytometry.The targeting relationship between miR-98-5p and TRPM2 was verified using dual luciferase assay.Results Compared with the control group,the apoptosis of OGD/R group was obvious,Bcl-2/Bax decreased,ZO-1,Occludin,Claudin-5 decreased,IL-1 β,TNF-α and ROS increased,miR-98-5p,p-AKT/AKT,p-GSK3β/GSK3β decreased but TRPM2 increased.But com-pared with the OGD/R group,except the control group,the other three groups showed the opposite trend in the above aspects;compared with the OGD/R+24A group,OGD/R+24A+miR-98-5p mimics group showed decreased apoptosis,decreased degradation of ZO-1,Occludin and Claudin-5,and decreased inflam-mation and ROS.miR-98-5p,p-AKT/AKT,p-GSK3β/GSK3β increased and TRPM2 decreased.However,compared with the OGD/R+24A+miR-98-5p mimics group,the OGD/R+miR-98-5p mimics group reversed this trend.Dual luciferase confirmed that miR-98-5p targeted regulation of TRPM2.Conclusion 24A in-hibits the expression of TRPM2 in BMECs through miR-98-5p,regulates AKT/GSK3β signal pathway,re-duces OGD/R inflammation and oxidative stress-medi-ated apoptosis,prevents the degradation of ZO-1,Oc-cludin and Claudin-5,and improves BBB permeability.

Aim To investigate the mechanism by which Aiweixin oral liquid(AWX)alleviates myocar-dial ischemia-reperfusion injury in rats through the reg-ulation of mitochondrial fusion and fission.Methods Seventy-two healthy male Sprague-Dawley rats were randomly assigned to six groups(n=12)using a ran-dom number table:sham surgery group,model group,low-dose AWX(1 mL·kg-1)group,medium-dose AWX(2 mL·kg-1)group,high-dose AWX(4 mL·kg-1)group,and positive control drug trimetazidine(10 mg·kg-1)group.A myocardial ischemia-reper-fusion injury(MIRI)model was established by ligating the left anterior descending coronary artery of the rat heart,followed by 30 minutes of ischemia and 90 mi-nutes of reperfusion.In the sham surgery group,only a suture was placed without ligation.The rats in the treatment groups were pre-gavaged with AWX starting 10 days prior to the modeling procedure.Lead Ⅱ elec-trocardiograms were recorded before and after reperfu-sion in each group to observe the changes in electrocar-diographic parameters.The myocardial infarct size in each group was assessed using TTC staining.The his-topathological changes in myocardial tissue were exam-ined under a light microscope using hematoxylin and eosin(HE)staining.The serum levels of adenosine triphosphate(ATP)and cardiac troponin I(cTnI)were measured using enzyme-linked immunosorbent as-say(ELISA).Superoxide dismutase(SOD)activity and the levels of malondialdehyde(MDA)and lactate dehydrogenase(LDH)were determined using bio-chemical assay kits.The protein expression levels of dynamin-related protein 1(dynamin-relatedprotein 1,DRP1),mitochondrial fission factor(mitochondrial fis-sion factor,MFF),mitochondrial fission protein 1(mi-tochondrial fission protein 1,FIS1),mitofusin 1(mito-fusion-1,MFN1),and mitofusin 2(mitofusion-2,MFN2)were evaluated by Western blot analysis.Re-sults Compared with the sham group,the model group exhibited aggravated myocardial tissue pathological damage,an increased percentage of myocardial infarct size,decreased serum SOD activity and ATP levels,and significantly elevated levels of MDA,cTnI,and LDH activity.Additionally,the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1 was up-regulated,while the expression of fusion-related factors MFN1 and MFN2 was downregulated.Compared with the model group,Aiweixin oral liquid significantly alle-viated myocardial injury,reduced the percentage of my-ocardial infarct size,increased serum SOD activity and ATP levels,decreased MDA content and cTnI and LDH activity,downregulated the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1,and up-regulated the protein expression of fusion-related factors MFN1 and MFN2.Conclusion Aiweixin oral liquid alleviates myocardial ischemia-reperfusion injury in rats by regulating abnormal mitochondrial fusion and fis-sion.

This article systematically reviews and verifies the medicinal materials of Dioscoreae Hypoglaucae Rhizoma（DHR）， Dioscoreae Spongiosae Rhizoma（DSR）， Smilacis Chinae Rhizoma（SCR） and Smilacis Glabrae Rhizoma（SGR） from the aspects of name， origin， producing area， quality， harvesting， processing and efficacy by consulting historical literature， in order to provide reference for the development and utilization of famous classical formulas containing the four medicinal materials. DHR， DSR， SCR and SGR have a long history of application as medicinal materials. However， due to their similar growth environment and medicinal properties， as well as their functions of promoting dampness， dispelling wind and removing numbness， there have been instances of homonymous foreign objects and homonymous synonyms throughout history， resulting in confusion of the origin. Therefore， it is necessary to conduct comparative analysis and systematic research for clarifying the historical development and changes of the four， in order to provide a basis for safe and effective medication. According to research， Bixie was first recorded in Shennong Bencaojing and has been historically known as Baizhi， Chijie， Zhumu， and other aliases. From ancient times to the mid-20th century， there has always been a situation where the rhizomes of Dioscorea plants and Smilax plants， and even the rhizomes of Heterosmilax plants， were mixed together to be used as medicinal herbs for Bixie. However， since the Tang dynasty， it has been clearly advocated that the rhizomes of Dioscorea plants have excellent quality and have been the mainstream throughout history. The 2020 edition of Chinese Pharmacopoeia categorized it into two types of medicinal herbs（DHR and DSR）. Among them， the origin of DHR is the dry rhizomes of Dioscorea hypoglauca， and the origins of DSR are the dry rhizomes of D. spongiosa and D. futschauensis. In ancient times， due to different types， the corresponding production areas of DHR and DSR were also different. Nowadays， They are mainly produced in the southern region of the Yangtze River. Since the Tang dynasty， the quality of Bixie has been characterized by its white color and soft nature. In modern times， it has been summarized that those with white color， large and thin pieces， powdery texture， tough and elastic texture， and neat and unbreakable are the best. The harvesting times of DHR and DSR are in spring or autumn， with the best quality harvested in autumn. The mainstream processing methods of them are slicing and then using the raw products or wine-processed products. SCR was first recorded in Mingyi Bielu and has been known as Jinganggen， Tielingjiao， Tieshuazi， and other aliases in history. The mainstream source is the dry rhizomes of Smilax china in the past dynasties， with the best quality being those that are tough and rich in powder. The harvesting time is from the late autumn to the following spring， and the main processing method throughout history has been slicing for raw use. SGR was first recorded under the item of Yuyuliang in Variorum of Shennong's Classic of Materia Medica. It was listed as an independent medicinal material from Bencao Gangmu. In history， there were such aliases as Cao Yuyuliang， Lengfantuan， Xianyiliang， Tubixie， etc. The main source of the past dynasties was dry rhizomes of S. glabra. In history， there have also been instances of multiple plants belonging to the same genus， and even cases of mixing the rhizomes of plants in the genus Heterosmilax. It is mainly produced in Guangdong， Hunan， Hubei， Zhejiang， Sichuan， Anhui and other regions， its quality has been summarized as large in size， powdery in texture， with few veins， and light brown in cross-section since modern times. The harvesting time is in spring or autumn， and the main processing method throughout history has been slicing for raw use. DHR， DSR， SCR and SGR all have the effects of promoting dampness， dispelling wind， relieving rheumatism and detoxifying. However， their detoxification abilities are ranked as follows：SGR>SCR>Bixie（DHR and DSR）. Especially for the treatment of limb spasms， arthralgia and myalgia， scrofula， and scabies caused by syphilis and mercury poisoning， SGR has a unique effect. Based on the research results， DHR is recommended to develop the famous classical formulas containing Bixie as the first choice for medicinal herbs. It should be harvested in autumn， sliced thinly while fresh， and processed according to the requirements of the famous classical formulas， without any requirements for raw use. Selecting the rhizomes of S. china， harvested in late autumn， and thinly sliced while fresh. If there are no special processing requirements in the formulas， use it raw. Selecting the rhizomes of S. glabra， it is harvested in autumn and thinly sliced while fresh. If there are no special processing requirements in the formulas， raw products can be used.

Cancer-associated fibroblasts(CAFs)and tumor-asso-ciated macrophages(TAMs)play crucial roles in the tumor microenvironment,and their interaction exerts a significant influ-ence on tumorigenesis and development.With the rapid develop-ment of research techniques,we have acquired novel understand-ings of the cell communication between TAMs and CAFs at the single-cell level.The cell communication between the two is of-ten related to the polarization of TAMs and remodeling of the mi-croenvironmental matrix by CAFs,thereby mediating mechanisms such as immunosuppression or tumor invasion and metastasis.Specific subsets of CAFs and TAMs have also been discovered to play a role in suppressing tumor progression.Nutrient metabo-lites may also participate in the interaction between CAFs and TAMs and have the potential to become new therapeutic targets for tumors.This review explores the research progress in the cell communication between TAMs and CAFs,expounds on the com-plexity of their interaction,and is expected to provide new per-spectives for the treatment and prevention of cancer and tumors.