Medication literacy directly impacts the safety of drug therapy and clinical outcomes.Patients with low medication literacy demonstrate poorer medication adherence,higher medication risks,and inferior disease control outcomes.Chronic disease patients face significant medication safety hazards due to multimorbidity and polypharmacy.Accurately assessing medication literacy can quantify individual medication capabilities and promote safe medication management.This paper reviews the structure,methods,applicable population,current applications,advantages,and limitations of medication literacy assessment tools for chronic disease patients,both domestically and internationally.The aim is to provide references for developing and applying medication literacy assessment tools for patients in China,offering a basis for scientifically evaluating medication literacy levels and formulating medication safety intervention strategies.

Medication literacy directly impacts the safety of drug therapy and clinical outcomes.Patients with low medication literacy demonstrate poorer medication adherence,higher medication risks,and inferior disease control outcomes.Chronic disease patients face significant medication safety hazards due to multimorbidity and polypharmacy.Accurately assessing medication literacy can quantify individual medication capabilities and promote safe medication management.This paper reviews the structure,methods,applicable population,current applications,advantages,and limitations of medication literacy assessment tools for chronic disease patients,both domestically and internationally.The aim is to provide references for developing and applying medication literacy assessment tools for patients in China,offering a basis for scientifically evaluating medication literacy levels and formulating medication safety intervention strategies.

Aim Toassesstheregulatoryeffectsofcar-damonin (CDN ) on toll-like receptor (TLR )-4/MyD88/NF-κB/iNOS signaling pathway in lipopolysac-charide (LPS )-stimulated RAW264. 7 macrophage cells.Methods LPS-stimulatedRAW264.7cells were divided into three groups:vehicle-treated group, LPS-treated group and LPS +CDN-treated group.Cell viability was assessed by CCK-8 assay.The concentra-tion of nitric oxide (NO)in cell culture medium was measured by Griess reagent.The mRNA levels of iN-OS,COX-2,MCP-1 ,TNF-α,IL-6 and IL-1βwere de-termined by reverse transcription real-time quantitative PCR(RT-qPCR).The protein levels of inducible nitric oxide synthase(iNOS),TLR4,myeloid differentiation factor 88(MyD88),nuclear factor κB(NF-κB)phos-phorylated (p )-p65 ,inhibitor κBα(IκBα),and p-IκBαweredeterminedbyWesternblot.Results 1~50 μmol·L-1 CDN had no cytotoxicity in RAW264. 7 cells.However,CDN inhibited the LPS-induced secre-tion of nitric oxide(NO)and mRNA expressions of iN-OS,COX-2,MCP-1 ,TNF-α,IL-6 and IL-1βin a dose-dependent manner.Moreover,50 μmol · L-1 CDN inhibited the LPS-induced up-regulation of iNOS, TLR4,MyD88,NF-κB p-p65,p-IκBαand down-reg-ulationofIκBα.Conclusion Cardamonininhibitsthe production of NO via a mechanism associated with the inhibition of TLR4/MyD88/NF-κB/iNOS pathway.

Apoptosis is a process of programmed cell death that is controlled by genes. Normally, there are three regulation pathways involved in the process of apoptosis, including the signaling of intracel-lular mitochondria, endoplasmic reticula and extracellular death receptors. Recent studies showed that NF-κB is a key regulator in the process of apoptosis. NF-κB plays a promotional and a inhibitory role as well in the regulation of apoptosis, closely related to the the inhibitor of apoptosis proteins family, the B cell lymphoma/ lewkmia-2 family, tumor necrosis factor receptor associated factors, c-Jun N-terminal kinase, tumor necrosis factor related apoptosis inducing ligand and Fas-associated death domain protein-like interleukin-1β. Thus, investigation of the mechanism regarding NF-κB in apoptosis regulation is of great importance for apoptosis-related drug development. The paper reviews the recent research progress in the function of NF-κB in apoptosis pathway regulation.

Aim To evaluate the effect and mecha-nism of vitexin in a mouse model of DSS-induced ulcer-ative colitis (UC).Methods C57BL/6 mice were randomly placed into three groups: normal control group,DSS group and DSS +Vitexin group.Mice coli-tis was induced by adding 4% dextran sulphate sodium (DSS)into the drinking water for seven days.Vitexin was administered once a day along with DSS treatment. Mice were monitored daily with body weight change and diarrhea symptoms.After sacrifice,colon was re-moved and fixed in 1 0% (W/V)buffered formalin for hematoxylin-eosin (H&E)staining.Histological dam-age was assessed as a combined score of inflammatory cell infiltration and mucosal damage.The remaining colon pieces were collected to measure the activity of myeloperoxidase (MPO)by ELISA method and to de-termine the mRNA expression of TNF-α,IL-6 and COX-2.Results None of the mice receiving vehicle alone exhibited body weight loss and mucosal disrup-tion at any point during the study.Vitexin treatment significantly ameliorated DSS-induced body weight loss and histological score.The activity of MPO and the mRNA expression of TNF-α,IL-6 and COX-2 were markedly inhibited by vitexin treatment.Conclusion Vitexin ameliorates DSS-induced colitis through sup-pressing leukocyte infiltration and pro-inflammatory mediators production.