Aim Systematic evolution of ligands by exponential enrichment(SELEX)techniquewas employed to screen and identify nucleic acid aptamers that specifically bind to mouse atherosclerotic pathological tissues,aiming to pro-vide a research foundation for the development of molecular targets and diagnostic reagents for early atherosclerosis.Methods A single-stranded DNA(ssDNA)library with a capacity of 1015～1016 was constructed,which was then subjec-ted to binding-elution(negative selection)with normal mouse vascular tissue slices.The eluted library was subsequently bound to atherosclerotic tissue slices for binding-elution(positive selection).PCR was used to amplify the positive and negative screening products,and agarose gel electrophoresis was used to verify the amplified products.The ssDNA library after multiple rounds of selection was sequenced using T-A cloning and sequencing to obtain the primary structure of the nu-cleic acid aptamers,and the secondary structure was predicted using the Mfold online software.The selected nucleic acid aptamers were labeled with a FAM fluorescent group at the 5'-end and were bound to both positive and negative selection tissue slices,with fluorescence intensity observed under a fluorescence microscope.Image Pro Plus 6.0 was used to cal-culate the relative average fluorescence intensity to evaluate the binding specificity of nucleic acid aptamers.Results After 8 rounds of selection,agarose gel electrophoresis imaging showed PCR amplification products in the positive selection lanes,while no PCR amplification products were observed in the negative selection lanes,indicating the successful acquisi-tion of a nucleic acid aptamer library that specifically binds to atherosclerotic tissues.Five nucleic acid aptamers were i-dentified by T-A cloning and sequencing,and their predicted secondary structures all had stem-loop structures.Immuno-fluorescence staining verified that five nucleic acid aptamers had different degrees of binding with As blood vessels,and the quantitative results of the relative average fluorescence intensity showed that nucleic acid aptamer No.11 had the highest relative average fluorescence intensity value,which can be used as a candidate nucleic acid aptamer for subsequent re-search.Conclusion Specific nucleic acid aptamers that bind to atherosclerotic vesselswere successfully obtained,providing a research foundation for further screening of early molecular targets of Asand developing in vivo early diagnostic reagents.

Aim Systematic evolution of ligands by exponential enrichment(SELEX)techniquewas employed to screen and identify nucleic acid aptamers that specifically bind to mouse atherosclerotic pathological tissues,aiming to pro-vide a research foundation for the development of molecular targets and diagnostic reagents for early atherosclerosis.Methods A single-stranded DNA(ssDNA)library with a capacity of 1015～1016 was constructed,which was then subjec-ted to binding-elution(negative selection)with normal mouse vascular tissue slices.The eluted library was subsequently bound to atherosclerotic tissue slices for binding-elution(positive selection).PCR was used to amplify the positive and negative screening products,and agarose gel electrophoresis was used to verify the amplified products.The ssDNA library after multiple rounds of selection was sequenced using T-A cloning and sequencing to obtain the primary structure of the nu-cleic acid aptamers,and the secondary structure was predicted using the Mfold online software.The selected nucleic acid aptamers were labeled with a FAM fluorescent group at the 5'-end and were bound to both positive and negative selection tissue slices,with fluorescence intensity observed under a fluorescence microscope.Image Pro Plus 6.0 was used to cal-culate the relative average fluorescence intensity to evaluate the binding specificity of nucleic acid aptamers.Results After 8 rounds of selection,agarose gel electrophoresis imaging showed PCR amplification products in the positive selection lanes,while no PCR amplification products were observed in the negative selection lanes,indicating the successful acquisi-tion of a nucleic acid aptamer library that specifically binds to atherosclerotic tissues.Five nucleic acid aptamers were i-dentified by T-A cloning and sequencing,and their predicted secondary structures all had stem-loop structures.Immuno-fluorescence staining verified that five nucleic acid aptamers had different degrees of binding with As blood vessels,and the quantitative results of the relative average fluorescence intensity showed that nucleic acid aptamer No.11 had the highest relative average fluorescence intensity value,which can be used as a candidate nucleic acid aptamer for subsequent re-search.Conclusion Specific nucleic acid aptamers that bind to atherosclerotic vesselswere successfully obtained,providing a research foundation for further screening of early molecular targets of Asand developing in vivo early diagnostic reagents.

Mitophagy,a special form of selective autophagy,plays a significant role in the pathogenesis of atherosclerosis by regulating cellular lipid metabolism,inflammation,and oxidative stress.However,its regulatory mech-anism is complex and has not been fully elucidated.Notably,many drugs and herbal ingredients exhibit anti-atherosclerot-ic effects by modulating mitophagy in macrophages,vascular endothelial cells,and vascular smooth muscle cells,offering potential new avenues for the prevention and treatment of atherosclerosis.In this article,we review the role of mitophagy in regulating cellular functions and the progression of atherosclerosis,as well as summarize potential therapeutic drugs that may contribute to anti-atherosclerosis by modulating mitophagy.Our aim is to provide a new literature basis for further ex-ploration of the role of mitophagy in atherosclerosis.

Mitophagy,a special form of selective autophagy,plays a significant role in the pathogenesis of atherosclerosis by regulating cellular lipid metabolism,inflammation,and oxidative stress.However,its regulatory mech-anism is complex and has not been fully elucidated.Notably,many drugs and herbal ingredients exhibit anti-atherosclerot-ic effects by modulating mitophagy in macrophages,vascular endothelial cells,and vascular smooth muscle cells,offering potential new avenues for the prevention and treatment of atherosclerosis.In this article,we review the role of mitophagy in regulating cellular functions and the progression of atherosclerosis,as well as summarize potential therapeutic drugs that may contribute to anti-atherosclerosis by modulating mitophagy.Our aim is to provide a new literature basis for further ex-ploration of the role of mitophagy in atherosclerosis.

Atherosclerosis is the pathological basis of a variety of cardiovascular diseases,which are still the leading cause of human death worldwide.Ferroptosis is a kind of iron dependent non-apoptotic cell death mode,which is closely related to various physiological mechanisms.Recent studies have found that ferroptosis in macrophages plays an important role in the occurrence and development of atherosclerosis.Based on the imbalance of iron metabolism in macrophages,this paper reviews the correlation between ferroptosis in macrophages and atherosclerosis in terms of the interaction between ferroptosis in macrophages and lipid peroxidation,inflammation,oxidative stress,etc.,in order to provide new ideas for the study of the pathogenesis of atherosclerosis.

Objective: To investigate the effect of oxLDL on CD36 expression and cholesterol influx in THP-1 macrophage. Methods: THP1 macrophage were treated with 50mg/L oxLDL for 0,12,24,36,48 h respectively.Oil red O staining was used to observe the intracellular lipid droplets.\labeled Cholesterol influx was determined by FJ-2107P type liquid scintillator.CD36 mRNA and protein level were determined by reverse transcription-polymerase chain reaction(RT-PCR) and Western blotting respectively. Results:We found that oxLDL elevated CD36 in both protein and mRNA levels and increased cholesterol influx in a time-dependent manner.The levels of cholesterol influx were 23.5%、(27.8%、)39.7%、44.1% and 49.7% respectively. Conclusion: oxLDL may upregulate CD36 expression and increase cholesterol influx.

AIM: To determine the effect of promoting cellular cholesterol efflux on the apoptosis of foam cells derived from monocytes. METHODS: RAW264.7 cells were incubated with 50 mg/L ox-LDL as a foam cell mode. The apoptosis rate of RAW264.7 cells was assayed by flow cytometry. Cellular lipid droplet was assayed by oil red staining. The rate of cellular cholesterol efflux was assayed with [~3H] label cholesterol, and the content of cellular cholesterol were assayed by high performance liquid chromatography. RESULTS: After incubation with 50 mg/L ox-LDL for 48 h, the content of cellular cholesterol ester increased from (6.8?3.6) mg/g to (101.7?4.5) mg/g (P