Abstract:Aim Cell culture system with glass-like rigid substrates is currently used to detect cell biological behaviors. However, the impact of the stiffness of tissue-like soft substrates on stem cell morphology and differentiation is rarely considered in cell-based cardiac repair. This work aimed to access the effects of myocardium-like soft culture substrates on the specification of CD34⁺ as well as CD34－ subsets along endothelial lineage in comparison with conventional glass-like rigid substrates. Methods Elastic modulus (E, a material property that describes the stiffness or elasticity) of normal myocardium was measured using atomic force microscopy (elastic modulus≈15 kPa). Myocardium-like soft culture substrates were prepared using polyacrylamide gel with a similar stiffness to normal myocardium. Meanwhile, cell culture system with glass-like rigid substrates (elastic modulus >1 GPa) was used as the control. Mouse bone marrow-derived CD34⁺ and CD34－ cells were collected by density gradient centrifugation and magnetic activated cell sorting (MACS). The isolated cells were cultured both on myocardium-like soft matrix and glass rigid substrate (E>1 GPa). At day 7 of culture, the surface markers of endothelial lineage, cell morphology, and cytoskeleton were observed by laser scanning confocal microscopy. Results Regardless of the substrate stiffness, mouse bone marrow-derived CD34⁺ cell subsets exhibited higher percentage of double-positive cells for dil-labelled acetylated-low density lipoprotein (Dil-ac-LDL) uptake and FITC-labelled ulex europaeus agglutinin I lectin (FITC-UEA-1) binding, and higher expression of endothelial lineage markers, CD31, vWF, Flk-1, and VE-cadherin than CD34－ subsets. Moreover, in terms of the difference in cell specification efficacy between CD34⁺ subsets and CD34－ subsets, myocardium-like soft substrate showed a more potent induction capacity than conventional glass-like rigid substrate. It might partially result from more stressful F-actin fibers and more abundant focal adhesions of CD34⁺ cell subsets on myocardium-like soft substrates. Conclusions Myocardium-like soft substrate was capable of inducing potently cell specification of CD34⁺ subsets compared with glass-like rigid substrate. It speculated that tissue-like soft substrate might be a more optimal culture system for detecting the specification of stem cells in vitro.

Abstract:Aim To explore whether Wenyang Tongmai decoction can regulate JAK2/STAT3 signal transduction pathway and the expression of aquaporins(AQP) to protect myocardial ischemia-reperfusion tissue. Methods Thirty male SD rats were randomly divided into 5 groups, 6 in each group:sham operation group, ischemia-reperfusion group, low-dose treatment group, middle-dose treatment group, high-dose treatment group. After 14 days of intragastric administration, the model of myocardial ischemia-reperfusion injury was established by ligation of the left anterior descending coronary artery for 30 minutes and then releasing the ligated artery for 120 minutes. The serum levels of creatine kinase isoenzymes (CK-MB) and lactate dehydrogenase (LDH) were detected by automatic biochemical analyzer. The ST-segment elevation of the rats was counted in the electrocardiogram. Pathological changes in cardiac tissue were observed by HE staining. The expressions of AQP1 and AQP4 in myocardial tissue were detected by immunohistochemical staining. The protein expressions of JAK2, p-JAK2, STAT3, p-STAT3, AQP1 and AQP4 were detected by Western blot method. Results Compared with the sham group, the levels of CK-MB and LDH in the serum of the ischemia-reperfusion group were significantly increased (P＜0.01), and the ST-segments of the electrocardiogram were significantly elevated after ischemia for 30 minutes and reperfusion for 120 minutes(P＜0.01). HE staining showed that the myocardial cells in the ischemia-reperfusion group were severely damaged. The expressions of AQP1 and AQP4 in immunohistochemistry was significantly increased (P＜0.01). The results of Western blot showed that the expressions of JAK2, p-JAK2, STAT3, p-STAT3, AQP1 and AQP4 were significantly increased (P＜0.01). Compared with the ischemia-reperfusion group, the serum levels of CK-MB and LDH were significantly decreased in the treated rats (P＜0.01), and the ST-segments were decreased after 30 minutes ischemia and 120 minutes reperfusion (P＜0.01), myocardial cells’ damage was alleviated to varying degrees in HE staining, the protein expressions of AQP1 and AQP4 in immunohistochemistry were significantly reduced, the expressions of JAK2, p-JAK2, STAT3 and p-STAT3 were generally increased, especially the expressions of p-JAK2 and p-STAT3 (P＜0.01), AQP1 and AQP4 expression levels were reduced to varying degrees(P＜0.01). Conclusion The cardioprotective effect of Wenyang Tongmai decoction may be related to activation of JAK2/STAT3 signaling pathway and down-regulation of AQP1 and AQP4 expression.

Abstract:Aim To observe the effect of miR-206 on proliferation of vascular endothelial cell and its mechanism, and provide a new therapeutic target for clinical arteriosclerosis. Methods The arterial endothelial tissue on lesion site and normal endothelial tissue were collected from the patients who were diagnosed as diabetic lower limb atherosclerosis by first time in clinical pathology. The expression of miR-206 was detected by qPCR. Normal HUVEC cell lines, HUVEC transfected with miR-206-mimics and HUVEC transfected with miR-206-inhibitor were studied through fundamental experiment, and the transfection efficiency were observed. In the three groups, CCK8 was used to detect the proliferation status, transwell was used to evaluate the migration ability, flow cytometry was used to detect cell cycle and Western blot was used to observe expression of Cx43. Results The mRNA expression of miR-206 on lesion site of lower limb artery (shin peroneal artery) in the patients with diabetic arteriosclerosis was significantly increased compared with normal endothelial tissue(P<0.05); The expression of miR-206 significantly increased (P<0.05) after transfected with miR-206-mimics, while it was significantly reduced (P<0.05) after transfected with miR-206-inhibitor. Compared with normal HUVEC and HUVEC transfected with miR-206-inhibitor, the cell proliferation rate was significantly lower in HUVEC transfected with miR-206-mimics for 24 h (P<0.05). After HUVEC was transfected with miR-206-mimics, the cell migration capacity was significantly lower than normal HUVEC group (P<0.05), and the cell cycle was blocked during G2 phase; while the cell migration capacity was higher in HUVEC transfected with miR-206-inhibitor group than that of normal HUVEC group (P<0.05). Cx43 expression was significantly reduced in miR-206-mimics group but significantly increased in miR-206-inhibitor group. Conclusion miR-206 can inhibit the proliferation of vascular endothelial cells, block endothelial cells in G2 phase and suppress their migration, and it may affect proliferation of endothelial cells by regulating Cx43 expression.

Abstract:Aim To investigate the protective effect of crocetin on isoprenaline induced ischemia and hypoxia in rats, and to verify whether its mechanism is related to the C/EBP- β/PGC-1α/UCP3 signaling pathway. Methods The rat model of ischemia and hypoxia was established by subcutaneous injection of isoproterenol, different doses of Crocin(5,0, 100 mg/kg) were given intragastrically. The levels of serum LDH-1, CK-MB, MDA, TNF- α, NO, CI and myocardial infarct size, myocardial Akt, ERK1/2, C/EBP-β, PGC-1α, UCP3 protein and gene expression were compared in each experimental group Results Compared with the blank control group, the survival rate of the model group was significantly decreased(P<0.01), the levels of serum LDH-1, CK-MB, MDA, TNF-α, NO, CI and myocardial infarction area were significantly increased(P<0.01). The arrangement of myocardial fibers was disordered and the infiltration of inflammatory cells was obvious. The expression of Akt and ERK1/2 protein was significantly increased(P<0.05), the expression of C/EBP-β, UCP3 protein and mRNA was significantly increased(P<0.01), and the expression of PGC-1α protein and mRNA was significantly decreased(P<0.01). The levels of serum LDH-1, CK-MB, MDA, TNF-α and NO in the positive control group were significantly higher than those in the control group(P<0.01). The infarct size was significantly decreased(P<0.01), CI was significantly decreased(P<0.05), the myocardial fibers were arranged neatly and the infiltration of inflammatory cells was significantly reduced. The expression of Akt and ERK1/2 protein was significantly increased(P<0.01), the expression of C/EBP-β protein and mRNA was significantly decreased(P<0.01), and the expression of PGC-1α protein was extremely high(P<0.05). The expression of mRNA was significantly increased(P<0.01), the expression of UCP3 protein was not different(P>0.05), but the expression of mRNA was significantly increased(P<0.05), which was compared with that of the model control group. The middle and high doses of Crocin could significantly increase the survival rate of rats(P<0.05), significantly decrease the levels of serum LDH-1, CK-MB, MDA, TNF-α and NO(P<0.05), and significantly decrease the areas of CI and myocardial infarction(P<0.05). Reduce inflammatory infiltration and improve the integrity of cardiomyocytes; The expression of Akt and ERK1/2 protein was significantly increased(P<0.05), the expression of C/EBP-β protein and mRNA was significantly decreased(P<0.05), and the expression of PGC-1α, UCP3 protein and mRNA was significantly increased(P<0.05). The comprehensive effect of high dose group was better than that of high dose group. Conclusion Crocin has obvious protective effect on myocardial ischemia and hypoxia injury in rats, and its mechanism may be related to the regulation of C/EBP-β/PGC-1α/UCP3 signaling pathway.

Abstract:Aim To investigate the effect of oxidized low-density lipoprotein (ox-LDL) on the synthesis of hyaluronic acid (HA) in human aortic vascular smooth muscle cells (HAVSMC), and explore its molecular mechanism. Methods The T/G HAVSMC were cultured in vitro with different concentration of ox-LDL(0,5, 0,5, 100 mg/L), the CCK-8 method was used to measure the cell proliferation and grouping analysis was carried out. T/G HAVSMC were treated with ox-LDL at concentrations of 25 and 50 mg/L for 48 hours. Natural LDL (N-LDL) group (50 mg/L N-LDL) and control group were set up. HPLC was used to determine the HA content, real-time quantitative PCR was used to detect the mRNA level of hyaluronic acid synthetase 2 (HAS2) and hyaluronic acid synthase 3 (HAS3), Western blot was used to detect the protein level of lectin-like oxidized low density lipoprotein recepter-1 (LOX-1), low-density lipoprotein receptor-related protein-1 (LRP), scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX) and cluster of differentiation 36 (CD36). Results After 48 h intervention, ox-LDL had no significant cytotoxicity on T/G HAVSMC cells. After 25 and 50 mg/L ox-LDL intervention for 48 h, the content of HA were significantly higher than those in the N-LDL group and the control group(P<0.05), the mRNA expression levels of HAS2 and HAS3 were significantly higher than those in the N-LDL group and the control group(P<0.05), and there was no significant difference between the N-LDL group and the control group(P>0.05). The expression of LOX-1 in 25 mg/L ox-LDL group and 50 mg/L ox-LDL group was significantly higher than that in the N-LDL group and the control group(P<0.05), while the expression of LRP-1, SR-PSOX and CD36 showed no significant change(P>0.05). Conclusion ox-LDL could induce the synthesis of HA in human aortic smooth muscle cells, and its mechanism may be related to the combination of LOX-1.

Abstract:Aim To investigate the relationship between single nucleotide polymorphism (SNP) of GATA6 gene promoter region－493 (rs144923558) G/A and －172 (rs146748749) G/A 2 sites and acute myocardial infarction (AMI) and their associated risk factors. Methods A case-control study was performed to collect 328 AMI patients and 344 normal controls (NC). Data were analyzed by polymerase chain reaction-restriction fragment length polymorphism technique combined with sequence alignment after DNA sequencing. After the Hardy-Weinberg balance test, the χ² test was used for correlation analysis; Logistic regression was used to analyze the relationship between multiple risk factors and two SNP loci and AMI incidence; linkage disequilibrium and haploid analysis was performed using Haplovview 4.2 software and SHEsis website. Results Three genotypes were detected in the two SNP loci, including GG, GA and AA. The genotype distribution was consistent with Hardy-Weinberg equilibrium (P>0.05), and there was no significant difference between the AMI group and the NC group(P>0.05). Multivariate Logistic regression analysis:age, hypertension, smoking, LDLC and TG were independent risk factors for AMI (P<0.05), and HDLC was protective factors (P<0.05) .Logistic regression analysis in three different genetic models of dominant, recessive and additive suggests that the two SNP loci are not associated with the onset of AMI. Linkage disequilibrium and haplotype analysis indicated that the two SNP loci were in the same linkage disequilibrium region (D′=1.000, r²=1.000), and haplotypes GG and AA did not increase AMI susceptibility (P>0.05). Conclusions The GATA6 gene promoter－493 (rs144923558) G/A and －172 (rs146748749) G/A two SNPs are completely unbalanced, of which GG is the main haplotype. The two SNP loci and their haplotypes were not associated with the onset of AMI, but provided population genetics of the GATA6 gene promoter region polymorphism.

Abstract:Aim To investigate the expression levels of serum microRNA-124 (miR-124) and microRNA-182 (miR-182) in acute cerebral infarction (ACI) and the value in the combined diagnosis and prognosis of ACI. Methods 120 patients with ACI were enrolled as the observation group, and 80 healthy subjects were used as healthy controls.According to the brain infarct volume, patients of the observation group were divided into small infarction group(＜5 cm³), middle infarction group (≥5 cm³ and ≤10 cm³) and large infarction group (＞10 cm³). The relative expression levels of serum miR-124 and miR-182 were measured in all enrolled patients, and the value of combined diagnosis was analyzed by receiver operating characteristic curve (ROC curve). ACI patients were followed up for one year, and the prognosis of the combined positive and negative groups was analyzed. Results The relative expressions of serum miR-124 and miR-182 in ACI patients were (2.63±0.59) and (2.69±0.69), respectively, which were significantly higher than those in the control group((1.08±0.32) and (1.07±0.46))(P<0.05). The relative expression of miR-124 in the middle and large infarction group was significantly lower than that in the small infarction group (P<0.05). The relative expression of miR-182 in the middle and large infarction group was significantly higher than that in the small infarction group (P<0.05). Pearson correlation analysis showed that the relative expression of miR-124 was negatively correlated with brain infarct volume (r=－0.613, P<0.01), and the relative expression of miR-182 was positively correlated with brain infarct volume (r=0.761, P<0.01). When miR-124 was cut off by 1.34, the sensitivity of diagnosis of ACI was 73.33%, the specificity was 90.00%, the area under the curve was 0.775 (95%CI 0.715～0.834, P=0.030); when miR-182 was cut off by 1.45, the sensitivity of diagnosis of ACI was 66.67%, the specificity was 87.50%, the area under the curve was 0.675 (95%CI 0.602～0.749, P=0.038); the sensitivity of combined diagnosis was 88.33%, the specificity was 86.25%, and the area under the curve was 0.811 (95%CI 0.756～0.866, P=0.028). The area under the combined detection ROC was significantly higher than that of the single test (P<0.05). The follow-up prognosis found that the patients with positive diagnosis had significantly higher mortality at 8 months and 12 months after treatment than those with negative diagnosis (P<0.05). Conclusion miR-124 and miR-182 are highly expressed in the serum of patients with ACI. The combination of the two is of great value in the diagnosis and prognosis evaluation of ACI.

Abstract:Aim To study the Influence of albumin in vulnerable phase among ejection fraction retention heart failure and ejection fraction intermediate heart failure(HFpEF and HFmrEF)patients. Methods Continuously selected 151 patients which diagnosed in heart failure in China Medical University (including 85 HFpEF patients and 66 HFmrEF patients). 151 patients with non-heart failure were enrolled in the same period. The patient's clinical data were collected and followed up. Clinical outcomes were defined as all cause mortality and rehospitalization due to worsening HF. Compared baseline data between the two groups, and used univariate logistic regression analysis to determine risk factors for patients with heart failure. Evaluated influence of albumin in vulnerable phase through Cox regression analysis and Kaplan-Meier survival analysis. Results The albumin of HFpEF and HFmrEF patients was obviously higher than non-heart failure patients(t=－6.431,P<0.001). Logistic regression analysis OR 0.162(95%CI 0.098~0.268, P<0.001). Albumin may be the protective factor of HFpEF and HFmrEF. Cox regression analysis and Kaplan-Meier survival analysis showed that serum albumin was associated with vulnerable phase prognosis in patients with HFpEF and HFmrEF. Univariate COX analysis (HR=0.1,5%CI 0.188~0.655, P=0.001) and multivariate COX analysis (HR=0.9,5%CI 0.225~0.858, P=0.016) were significant. Kaplan-Meier analysis between higher albumin group and lower albumin group(log-rank:χ²=11.881,P=0.001)also showed significant difference. Conclusions Serum albumin may be a risk factor for patients with HFpEF and HFmrEF. The lower the serum albumin, the worse the prognosis of the vulnerable period.

Abstract:Aim To evaluate the value of serum Betatrophin in coronary artery disease of Kazak and Han nationality in Xinjiang. Methods Patients without diabetes mellitus after arteriography were selected as study subjects, including 108 Kazak and 115 Han. The degree of coronary artery lesion was evaluated by Gensini integral system. The patients were divided into two groups according to the Gensini score:the case group and the control group. There were 132 patients in the case group and 91 in the control group. Double antibody sandwich enzyme-linked immunosorbent assay (ELISA) was used to detect serum Betatrophin level; AB-ELISA method was used to determine serum ANGPTL3 content; ELISA method was used to detect serum lipoprotein lipase (LPL) content; triglyceride (TG), total cholesterol (TC), fasting blood glucose (FBG) was detected in two groups. Results Compared with the control group, the level of body mass index (BMI), TC, TG, low density lipoprotein cholesterol (LDLC) were increased in the coronary heart disease group (P<0.05) and the BMI, TC, TG, LDLC level in the Kazak coronary heart disease group were higher than that in the Han nationality coronary heart disease group (P<0.05); There was no significant difference in fasting insulin (FINS), FBG, homeostatic model assessment for insulin resistance (HOMA-IR), HOMA-β between the case group and the control group (P>0.05); The serum Betatrophin, angiopioetin-like protein 3 (ANGPTL3), LPL of Kazak patients with coronary artery disease was higher than that of Han patients with coronary artery disease (P<0.05); There was a positive correlation between Gensini score and TC, TG, LDLC, Betatrophin in Kazak coronary artery disease group (r=0.4,0.4,0.2,0.446,P＜0.05); There was a positive correlation between Gensini score and BMI, TC, TG, LDLC, Betatrophin in patients with coronary heart disease in Han nationality (r=0.8,0.5,0.6,0.7,0.393,P＜0.05). Linear regression analysis showed that TG and Kazak were the factors of increasing Betatrophin, regression analysis showed that BMI, LDLC, Betatrophin was the factor influencing coronary artery lesion in Han nationality, and LDLC, Betatrophin, ANGPTL3, LPL was the factor influencing coronary artery disease in Kazak nationality. Conclusion The increase of Betatrophin level may aggravate coronary artery lesion of Kazak and Han nationality in Xinjiang; TG, Kazak may be the factor influencing Betatrophin serological level.

Abstract:Aim To investigate the expression of serum microRNA (miRNA) miR-181c and miR-128b in patients with cerebral infarction and its correlation with 90-day prognosis, and provide reference for the diagnosis and treatment of cerebral infarction. Methods 128 patients with cerebral infarction admitted to our hospital from January 2015 to June 2018 and 108 healthy subjects in the same period were selected as study subjects and control groups. The expression levels of miR-181c and miR-128b were compared between the two groups, and the correlation between miR-181c, miR-128b expression levels and disease severity, as well as risk factors associated with cerebral infarction were analyzed. According to the prognosis of 90 days follow-up, the good prognosis group and the poor prognosis group were classified, and the factors affecting the prognosis of 90 d were analyzed by single factor and logistic regression analysis to explore the independent influencing factors affecting the occurrence and prognosis of the disease. Results The smoking, hyperlipidemia, hypertension, diabetes and atrial fibrillation rate in the study group were significantly higher than those in the control group (P<0.05), and the expression levels of miR-181c and miR-128b in the study group were significantly higher than those in the control group (P<0.05). Logistic regression analysis showed that the diabetes and expression levels of miR-181c and miR-128b were independent risk factors for cerebral infarction (P<0.05); Spearman correlation analysis showed that the severity of acute cerebral infarction was positively correlated with serum miR-181c and miR-128b levels (r=0.867, P=0.005; r=0.885, P=0.002); The incidence of hypertension, diabetes, atrial fibrillation, NIHSS score at admission, and serum miR-181c and miR-128b levels were significantly higher in patients with poor prognosis than those with good prognosis (P<0.05). Conclusion Logistic regression analysis showed that NIHSS score and serum miR-181c and miR-128b levels were significantly correlated with the 90-day prognosis of patients with acute cerebral infarction.

Abstract:Aim To systematically evaluate the correlation between sleep duration and incidence risk of hypertension, and provide scientific basis for prevention and control of hypertension. Methods From Embase, Pubmed, CNKI, VIP and Wanfang database, screening the cross-sectional study of the correlation between sleep duration and hypertension from March 2012 to September 2018. Then the related data were evaluated and extracted. Publication bias was evaluated, and sensitivity and Meta-analyses were conducted with Stata12.0. Results A total of 17 studies were collected where 959 358 cases were included. The Meta-analysis showed that short sleep duration was associated with a higher risk of hypertension, the risk of hypertension increased by 55% when sleep duration<7 h (OR 1.55,95%CI 1.28～1.87, P<0.001). No evidence suggested any relation between higher risk of hypertension and the sleep duration>7 h (OR 1.2,5%CI 0.78～1.32, P>0.05). By subgroup analysis, it was found that different regional populations and different definitions of sleep duration were the major sources of heterogeneity. Funnel charts for Begg's and Eegg's tests showed that results were not exactly the same. Sensitivity analysis indicated these results of Meta-analysis were stable.Conclusion Short sleep duration in adults increases the incidence risk of hypertension, but long sleep duration is not associated with risk of hypertension.

Abstract:Atherosclerosis (As) is an important pathological basis for cardio-cerebrovascular diseases. In recent years, many studies have shown that epigenetic mechanisms also play an important role in the regulation of As. 5-hydroxymethyl cytosine (5hmC), known as the sixth base of human DNA, is an important epigenetic modification derived from the demethylation process of DNA mediated by the ten-eleven translocation (TET) protein family, and has been known to involve in various biological processes. Recent studies have shown that TET2 and its mediated hydroxymethylation are not only involved in the regulation of phenotypic transformation of vascular smooth muscle cells, but also closely related to the key factors of As such as endothelial function and inflammatory immune response. It is also found that TET2 and 5hmC are markedly absent in As plaque, and the level of deletion is positively correlated with the degree of injury. TET2 and hydroxymethylation may play an important protective role in the pathological process of As. This review will introduce the structure and function of TET2, the research overview of 5hmC and the breakthrough in detection techniques. It will focus on the role and mechanism of TET2 and its mediated hydroxymethylation modification in As, and provide new ideas and targets for the effective prevention and treatment of As.

Abstract:More and more studies have revealed that inflammation plays an important role in cardiovascular diseases, including hypertension and atherosclerosis et al. Caspase-1, caspase-4, caspase-5 and caspase-11 are named as inflammatory caspase, which cause the mature and secretion of inflammatory cytokines. Inflammatory caspase can induce and magnify inflammatory response that represents a new paradigm in innate immunity. In addition to mediating cleavage of the NLRP3 inflammasome-associated cytokines interleukin 1beta (IL-1β) and IL-18, inflammatory caspase modulate distinct forms of pyroptosis by shearing gasdermin D into N-terminal fragment that showed pore-forming activity, while pyroptosis of cells release a large number of inflammatory cytokines. This study will discuss the role of inflammatory caspase in cardiovascular diseases.

Abstract:With the in-depth study of atherosclerosis (As), promoting the stability of vulnerable plaque has become a new therapeutic concept for As. In the “inside-out” theory of As, the pathological changes of the intima are the initiating factors. However, recent studies have shown that the vasa vasorum (VV) plays a key role in the pathogenesis of As from the outside to the inside. In summary, treatment of As has changed from protecting the intima to regulating the outer membrane VV.

Abstract:Atherosclerosis (As) is the main cause of coronary heart disease, stroke and peripheral vascular disease. Nowadays, there are many theories to explain its pathogenesis, but none of them has clarified the specific pathogenesis. Anti-platelet aggregation, lipid-lowering, anticoagulation and thrombolysis are the main clinical drugs treatment at present, but they have little effect on the protection of vascular endothelium and have poor specificity. The traditional Chinese medicine salidroside (SAL) has significant anti-As effect in animal model experiments. A large number of mechanism studies have also confirmed that SAL can significantly reduce vascular endothelial cell injury, inhibit endothelial apoptosis, delay endothelial senescence, inhibit inflammation and stress response, prevent foam cell formation and the occurrence of apoptosis, prevent vascular smooth muscle cells from overproliferation, reduce blood viscosity, prevent thrombosis and stabilize plaque, thereby protecting the vascular system and inhibiting the occurrence and development of As. Therefore, SAL is expected to become an important treatment for preventing the entire process of As from occurrence, development to deterioration. This article summarizes the research progress of the mechanism of SAL intervening As in recent years, aiming to provide reference value for further research and clinical application.