This review systematically summarizes the unique metabolic mechanisms of breast cancer,their interac-tions with the tumor microenvironment(TME),and the latest advances in targeted therapies.The interplay between metabolic reprogramming and the TME underpins malignant progression and therapeutic resistance.Breast cancer cells reshape energy supply through the Warburg effect,aberrant fatty acid synthesis,and amino acid metabolism,while immune cells,fibroblasts,and the acidic milieu within the TME promote immune evasion and drug resistance via metabolic coupling.Although traditional strategies targeting key metabolic enzymes remain valuable,they are often insufficient to overcome metabolic adaptability.In recent years,combined metabolic and immunotherapeutic approaches have emerged as promising strategies:by reducing lactate accumulation,restoring T-cell function,and reprogramming tumor-associated macrophages and cancer-associated fibroblasts,these therapies can remodel the immunosuppressive microenvironment and enhance immunotherapy efficacy.The application of metabolomics and single-cell sequencing further elucidates breast cancer heterogeneity,providing a basis for individualized precision treatment.Future challenges include deciphering resistance mechanisms,developing highly selective metabolic in-hibitors,and designing integrated multi-omics-based therapeutic regimens.

OBJECTIVE Tostudytheeffectofeffectivefractions(EFC)frommodifiedSimiaoWan (MSW)onthelevelofuricacidinhyperuricemicratsandinvestigatethemechanism.METHODS Two types of hyperurice mic models were established.A persistant hyperurice mic model was prepared by giving rats oxonic acid 200 mg·kg -1 and feeding the m with hypoxanthine.The models were ig given with modified Simiaowan (MSW)50 g·kg -1 or EFC 1 2.5,25 and 50 g·kg -1 consecutively for 5 d.The models were treated with MSW or EFC 50 g·kg -1 for 3 d.After the final treatment,the uric acid concen-trations in seru m and urine were determined by an auto matic bioche mistry analyzer.The activity of xan-thine oxidase (XOD )in the serum and liver was determined by enzymic colorimetric method.The activity of purine nucleoside phosphorylase (PNP)and uricase was detected by spectrophotometry. RESULTS Comparedwithnormalcontrolgroup,theserumlevelofuricacidinbothmodelgroupswas remarkably increased(P<0.01 ).Compared to model control group,MSW 50 g·kg -1 and EFC 12.5, 25 and 50 g·kg -1 significantly reduced the serum level of uric acid(P<0.05,P<0.01 ),but increased the activity of erythrocyte PNP(P<0.01 )in the oxonic acid potassium-induced hyperuricemia rats. MSW 50 g·kg -1 and EFC 50 g·kg -1 elevated the activity of liver uricase in the nicotinic acid-induced hyperuricemia rats(P<0.05).EFC 50 g·kg -1 also significantly decreased the serum XOD activity of hyperuricemicrats.CONCLUSION EFCsignificantlyinhibitstheserumlevelofuricacidinhyperurice-mic rats,which might involve down-regulation of protein levels of serum XOD to inhibit the production of uric acid and activation of uricase to pro mote the deco mposition of uric acid.

Chronic renal failure is clinical syndrome manifested as hypoactivity of renal function that can be caused by manifold diseases. CRF is difficult to be treated and has bad prognosis. In recent years, according TCM physiological and pathological mechanism, doctors have achieved good effects in preventing and delaying CRF in its early and middle stage by adopting the therapeutic principle of expelling toxin, strengthening body resistance, and promoting blood circulation to dissipating blood stasis.