ObjectiveTo assess the level of health literacy and its influencing factors among middle school students aged 12‒18 years in Jing’an District, Shanghai, so as to provide a solid scientific foundation for further developing more targeted intervention measures. MethodsA stratified cluster random sampling method was used to randomly select 4 middle schools in Jing’an District, Shanghai from November to December 2023, and conducted a health literacy questionnaire survey on non-graduating middle and high school students, respectively. The2023 Survey on the Status of Health Literacy among Middle School Students in Jing’an District, Shanghai was adopted, which consisted of two parts: health literacy and basic information. Health literacy was divided into three dimensions: health knowledge and concept literacy, healthy lifestyle and behavior literacy, and health skill literacy. Three dimensions could be categorized into six types of health literacy issue: scientific health literacy, infectious disease prevention and control literacy, chronic disease prevention and control literacy, safety and first aid literacy, basic health literacy, and health information literacy. ResultsA total of 1 161 middle school students were enrolled into this study, including 571 males and 570 females. The overall health literacy level of middle school students was 33.51%, with 34.81% among middle school students and 31.69% among high school students, respectively. Results of logistic regression analysis showed that health knowledge acquisition and awareness, as well as application frequency of health knowledge, were the influencing factors for the overall health literacy level among middle school students (P<0.05). The degree of family attention to health maintenance, health knowledge acquisition and awareness, and application frequency of health knowledge were the main influencing factors for the three dimensions and literacy of six types of health issues among middle school students (P<0.05). ConclusionThe levels of different types of health literacy among middle school students in Jing’an District are uneven, with the highest being safety and first aid literacy and the lowest being basic health literacy. It is recommended to take targeted measures to comprehensively improve the health literacy level of middle school students.

Objective To investigate mitochondrial function mediated by phospholipase D1(PLD1)in the lungs of mice with bronchopulmonary dysplasia.Methods Wild-type(WT)and PLD1 knockout(PLD1-KO)newborn mice were assigned to four groups:normoxic+WT,normoxic+PLD1-KO,hyperoxic+WT,and hyperoxic+PLD1-KO,with nine mice in each group.Mice in the hyperoxia groups were exposed to hyperoxia(85％ O2)for 14 days.Mice in the normoxic groups were exposed to normoxic conditions(21％ O2)for 14 days.On the 14th day,the levels of oxidative stress,apoptosis,and fibrosis in lungs were evaluated using commercial kits for malondialdehyde(MDA)and superoxide dismutase(SOD),Western blot for BAX,BCL-2,and Cleaved Caspase-3,and immunohistochemistry for α-SMA and AIF.The following MLE-12 cell groups were prepared,normoxic+si-NC,hyperoxic+si-NC,normoxic+si-PLD1,and hyperoxic+si-PLD1.After transient transfection,the cells were exposed to normoxia or hyperoxia for 24 h.Mitochondrial reactive oxygen species(mtROS)and function were measured using MitoSOX Red and the hippocampus mitochondrial stress test.Results The levels of α-SMA and AIF staining,MDA,Cleaved Caspase 3,and BAX in lung tissue were significantly increased in the hyperoxic groups compared with the normoxic groups(P＜0.05),while SOD activity and BCL-2 levels were significantly decreased(P＜0.05).α-SMA and AIF staining,and the abundance of Cleaved Caspase-3 and BAX in lung tissue were lower in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05),while SOD activity and BCL-2 abundance were higher in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic groups was significantly lower than that in the normoxic groups(P＜0.05);however,the level of AIF was increased significantly in the cytoplasm of the hyperoxic groups compared with the normoxic groups(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic+si-PLD1 group was significantly increased compared with that in the hyperoxic+si-NC group(P＜0.05).The abundance of mtROS in hyperoxia MLE-12 cell groups was higher than that in the normoxia groups(P＜0.05),and the abundance of mtROS in the hyperoxia+si-PLD1 group was lower than that in the hyperoxia+si-NC group(P＜0.05).Compared with the normoxic+si-NC group,basic respiration,ATP production,maximum respiration,and spare respiratory capacity was significantly decreased in the hyperoxic+si-NC group(P＜0.05).Compared with the hyperoxic+si-NC group,the hyperoxic+si-PLD1 group had significantly increased basic respiration,ATP production,maximum respiration,and spare respiratory capacity(P＜0.05).Conclusions PLD1 is involved in hyperoxia-induced injury of mouse BPD and MLE-12 cells.Deletion of the PLD1 gene may alleviate hyperoxia-induced lung injury by inhibiting mitochondrial-dependent apoptosis.

Objective The present study was designed to explore the inhibitory effects of the ADC drug Disitamab Vedotin(RC-48)on breast cancer cells with different HER-2 expression levels by utilizing a tumor organoid culture system.Methods Within the framework of the tumor organoid culture system,the breast cancer cell lines MCF-7(characterized by low HER-2 expression,Luminal A subtype)and BT-474(exhibiting high HER-2 expression,HER-2 positive subtype)were cultured independently and in various mixed ratios.The histological characteristics,as well as the expression levels and distribution of HER-2 in MCF-7 and BT-474 organoids,were analyzed via immunohistochemistry and immunofluorescence techniques.MCF-7 and BT-474 organoids were separately treated with Vedotin(RC-48),Disitamab,and Monomethyl auristatin E(MMAE).Additionally,a drug sensitivity test of Disitamab Vedotin(RC-48)was carried out on mixed MCF-7 and BT-474 cell ratios and on patient-derived breast cancer organoids,with the assessment conducted using the 3D-Glo method.Results In the tumor organoid culture system,immunohistochemistry and immunofluorescence analyses demonstrated that HER-2 was predominantly localized in the cell membrane.Specifically,BT-474 organoids exhibited robust HER-2 expression,while MCF-7 organoids displayed relatively low expression levels.When compared with MCF-7 organoids,RC48-ADC exerted a more pronounced inhibitory effect on BT-474 organoids,with IC50 values of 109.7 μg/mL and 2.792 μg/mL,respectively.The co-culture model further confirmed the bystander effect of RC-48,revealing that the ratio of HER-2-positive to HER-2-negative cells significantly influenced drug efficacy.Additionally,treatment with RC-48 led to a reduction in HER-2 expression in breast cancer organoids with diverse HER-2 expression levels.Conclusions The tumor organoid model can accurately mirror drug sensitivity and bystander effects.Within this model,RC-48 effectively inhibited HER-2 highly-expressing breast cancer cells,augmented the killing effect through the bystander mechanism,and downregulated HER-2 expression,thereby suggesting its potential for targeting HER2-associated breast cancer.

Objective:To explore the mechanisms of oxaliplatin resistance mediated by TET2 methylation in the treatment of acute lymphoblastic leukemia (ALL) using bioinformatics methods.Methods:The data on drug-resistant and sensitive cell lines related to oxaliplatin treatment for ALL were download using the Genomics of Drug Sensitivity in Cancer (GDSC) database (updated in December 2023); the drug-resistant cell lines were screened based on half maximal inhibitory concentration ( IC50) > 10 μmol/L, and the difference in IC50 between drug-resistant and sensitive cell lines were analyzed using Mann-Whitney U test. The cancer driver mutation genes in drug-resistant cell lines were retrieved using the Cancer Cell Line Encyclopedia (CCLE) database (updated in December 2023). Using the protein-protein interaction (PPI) network functional enrichment analysis (STRING) database (updated in June 2024), PPI network analysis was performed on cancer driver mutation genes with biological functions. A confidence threshold of ≥ 0.7 (high confidence) and an average network node degree above 4 (high average) were selected to screen for cancer driver mutation genes with significant biological functions. Using the microRNA Data Integration Portal (mirDIP) database (updated in June 2024), the coexpression data of microRNA (miRNA) and mutant target genes were queried, miRNA-target gene pairs were screened according to the highest score threshold of 1% miRNA and interaction score > 0.9, and the regulatory effect of miRNA on mutant genes was analyzed. DNA methylation data were download from the Methylation in Human Cancer (MethHC) database (updated in June 2024) and the methylSig R software package was used to analyze the differentially methylated regions (DMR) of DNA methylation between drug-resistant and sensitive cell lines; genes with P < 0.05 and absolute difference > 0.2 were selected, and they were divided into high methylation gene group and low methylation gene group. Spearman correlation analysis and Spearman rank test were performed for the degree of methylation and gene expression, and the key genes with P < 0.01 were screened to reveal the relationship between methylation degree and gene expression. Results:As a result of searching the GDSC database, there were a total of 9 drug-resistant cell lines and 17 sensitive cell lines related to oxaliplatin treatment for ALL; after Z-score normalization of IC50 data between drug-resistant and sensitive cell lines, the average rank of drug-resistant cell lines was 21, and the average rank of sensitive cell lines was 8.5, with a statistically significant difference ( Z = -4.08, P < 0.01). Eight cancer driver mutation genes with significant biological functions that lead to drug resistance of the cell lines were screened using the CCLE database and STRING database. According to the mirDIP database, there were a total of 12 pairs of miRNA-target gene pairs with miRNA-target gene interaction scores >0.9. miRNA had strong regulatory effects on the expressions of NRAS and MAP2K1 target genes. In the MethHC database, the β values (numerical value of increased methylation level) of DMR for genes such as TP53, RXRG and SGIP in drug-resistant cell lines were 0.151, 0.165 and 0.149, respectively, compared to those in sensitive cell lines, the differences were statistically significant (all P < 0.01). The degree of methylation of SGIP gene was negatively correlated with the relative expression level of SGIP mRNA ( r = -0.71, P < 0.01), and SGIP gene underwent high methylation at promoter site 143886940. The cg08321569 locus in the TET2 gene domain of drug-resistant cell lines exhibited persistent high methylation, with a methylation level of β = 0.89. This locus was located 1.2 kb downstream of the transcription start point of exon 4, and the degree of TET2 methylation was negatively correlated with the relative expression level of TET2b mRNA ( r = -0.81, P < 0.01). Conclusions:TET2 methylation may be an important factor for oxaliplatin resistance in the treatment of ALL.

Objective To investigate mitochondrial function mediated by phospholipase D1(PLD1)in the lungs of mice with bronchopulmonary dysplasia.Methods Wild-type(WT)and PLD1 knockout(PLD1-KO)newborn mice were assigned to four groups:normoxic+WT,normoxic+PLD1-KO,hyperoxic+WT,and hyperoxic+PLD1-KO,with nine mice in each group.Mice in the hyperoxia groups were exposed to hyperoxia(85％ O2)for 14 days.Mice in the normoxic groups were exposed to normoxic conditions(21％ O2)for 14 days.On the 14th day,the levels of oxidative stress,apoptosis,and fibrosis in lungs were evaluated using commercial kits for malondialdehyde(MDA)and superoxide dismutase(SOD),Western blot for BAX,BCL-2,and Cleaved Caspase-3,and immunohistochemistry for α-SMA and AIF.The following MLE-12 cell groups were prepared,normoxic+si-NC,hyperoxic+si-NC,normoxic+si-PLD1,and hyperoxic+si-PLD1.After transient transfection,the cells were exposed to normoxia or hyperoxia for 24 h.Mitochondrial reactive oxygen species(mtROS)and function were measured using MitoSOX Red and the hippocampus mitochondrial stress test.Results The levels of α-SMA and AIF staining,MDA,Cleaved Caspase 3,and BAX in lung tissue were significantly increased in the hyperoxic groups compared with the normoxic groups(P＜0.05),while SOD activity and BCL-2 levels were significantly decreased(P＜0.05).α-SMA and AIF staining,and the abundance of Cleaved Caspase-3 and BAX in lung tissue were lower in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05),while SOD activity and BCL-2 abundance were higher in the hyperoxia+PLD1-KO group than in the hyperoxia+WT group(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic groups was significantly lower than that in the normoxic groups(P＜0.05);however,the level of AIF was increased significantly in the cytoplasm of the hyperoxic groups compared with the normoxic groups(P＜0.05).The level of AIF in MLE-12 cell mitochondria in the hyperoxic+si-PLD1 group was significantly increased compared with that in the hyperoxic+si-NC group(P＜0.05).The abundance of mtROS in hyperoxia MLE-12 cell groups was higher than that in the normoxia groups(P＜0.05),and the abundance of mtROS in the hyperoxia+si-PLD1 group was lower than that in the hyperoxia+si-NC group(P＜0.05).Compared with the normoxic+si-NC group,basic respiration,ATP production,maximum respiration,and spare respiratory capacity was significantly decreased in the hyperoxic+si-NC group(P＜0.05).Compared with the hyperoxic+si-NC group,the hyperoxic+si-PLD1 group had significantly increased basic respiration,ATP production,maximum respiration,and spare respiratory capacity(P＜0.05).Conclusions PLD1 is involved in hyperoxia-induced injury of mouse BPD and MLE-12 cells.Deletion of the PLD1 gene may alleviate hyperoxia-induced lung injury by inhibiting mitochondrial-dependent apoptosis.

Objective The present study was designed to explore the inhibitory effects of the ADC drug Disitamab Vedotin(RC-48)on breast cancer cells with different HER-2 expression levels by utilizing a tumor organoid culture system.Methods Within the framework of the tumor organoid culture system,the breast cancer cell lines MCF-7(characterized by low HER-2 expression,Luminal A subtype)and BT-474(exhibiting high HER-2 expression,HER-2 positive subtype)were cultured independently and in various mixed ratios.The histological characteristics,as well as the expression levels and distribution of HER-2 in MCF-7 and BT-474 organoids,were analyzed via immunohistochemistry and immunofluorescence techniques.MCF-7 and BT-474 organoids were separately treated with Vedotin(RC-48),Disitamab,and Monomethyl auristatin E(MMAE).Additionally,a drug sensitivity test of Disitamab Vedotin(RC-48)was carried out on mixed MCF-7 and BT-474 cell ratios and on patient-derived breast cancer organoids,with the assessment conducted using the 3D-Glo method.Results In the tumor organoid culture system,immunohistochemistry and immunofluorescence analyses demonstrated that HER-2 was predominantly localized in the cell membrane.Specifically,BT-474 organoids exhibited robust HER-2 expression,while MCF-7 organoids displayed relatively low expression levels.When compared with MCF-7 organoids,RC48-ADC exerted a more pronounced inhibitory effect on BT-474 organoids,with IC50 values of 109.7 μg/mL and 2.792 μg/mL,respectively.The co-culture model further confirmed the bystander effect of RC-48,revealing that the ratio of HER-2-positive to HER-2-negative cells significantly influenced drug efficacy.Additionally,treatment with RC-48 led to a reduction in HER-2 expression in breast cancer organoids with diverse HER-2 expression levels.Conclusions The tumor organoid model can accurately mirror drug sensitivity and bystander effects.Within this model,RC-48 effectively inhibited HER-2 highly-expressing breast cancer cells,augmented the killing effect through the bystander mechanism,and downregulated HER-2 expression,thereby suggesting its potential for targeting HER2-associated breast cancer.

Objective:To explore the mechanisms of oxaliplatin resistance mediated by TET2 methylation in the treatment of acute lymphoblastic leukemia (ALL) using bioinformatics methods.Methods:The data on drug-resistant and sensitive cell lines related to oxaliplatin treatment for ALL were download using the Genomics of Drug Sensitivity in Cancer (GDSC) database (updated in December 2023); the drug-resistant cell lines were screened based on half maximal inhibitory concentration ( IC50) > 10 μmol/L, and the difference in IC50 between drug-resistant and sensitive cell lines were analyzed using Mann-Whitney U test. The cancer driver mutation genes in drug-resistant cell lines were retrieved using the Cancer Cell Line Encyclopedia (CCLE) database (updated in December 2023). Using the protein-protein interaction (PPI) network functional enrichment analysis (STRING) database (updated in June 2024), PPI network analysis was performed on cancer driver mutation genes with biological functions. A confidence threshold of ≥ 0.7 (high confidence) and an average network node degree above 4 (high average) were selected to screen for cancer driver mutation genes with significant biological functions. Using the microRNA Data Integration Portal (mirDIP) database (updated in June 2024), the coexpression data of microRNA (miRNA) and mutant target genes were queried, miRNA-target gene pairs were screened according to the highest score threshold of 1% miRNA and interaction score > 0.9, and the regulatory effect of miRNA on mutant genes was analyzed. DNA methylation data were download from the Methylation in Human Cancer (MethHC) database (updated in June 2024) and the methylSig R software package was used to analyze the differentially methylated regions (DMR) of DNA methylation between drug-resistant and sensitive cell lines; genes with P < 0.05 and absolute difference > 0.2 were selected, and they were divided into high methylation gene group and low methylation gene group. Spearman correlation analysis and Spearman rank test were performed for the degree of methylation and gene expression, and the key genes with P < 0.01 were screened to reveal the relationship between methylation degree and gene expression. Results:As a result of searching the GDSC database, there were a total of 9 drug-resistant cell lines and 17 sensitive cell lines related to oxaliplatin treatment for ALL; after Z-score normalization of IC50 data between drug-resistant and sensitive cell lines, the average rank of drug-resistant cell lines was 21, and the average rank of sensitive cell lines was 8.5, with a statistically significant difference ( Z = -4.08, P < 0.01). Eight cancer driver mutation genes with significant biological functions that lead to drug resistance of the cell lines were screened using the CCLE database and STRING database. According to the mirDIP database, there were a total of 12 pairs of miRNA-target gene pairs with miRNA-target gene interaction scores >0.9. miRNA had strong regulatory effects on the expressions of NRAS and MAP2K1 target genes. In the MethHC database, the β values (numerical value of increased methylation level) of DMR for genes such as TP53, RXRG and SGIP in drug-resistant cell lines were 0.151, 0.165 and 0.149, respectively, compared to those in sensitive cell lines, the differences were statistically significant (all P < 0.01). The degree of methylation of SGIP gene was negatively correlated with the relative expression level of SGIP mRNA ( r = -0.71, P < 0.01), and SGIP gene underwent high methylation at promoter site 143886940. The cg08321569 locus in the TET2 gene domain of drug-resistant cell lines exhibited persistent high methylation, with a methylation level of β = 0.89. This locus was located 1.2 kb downstream of the transcription start point of exon 4, and the degree of TET2 methylation was negatively correlated with the relative expression level of TET2b mRNA ( r = -0.81, P < 0.01). Conclusions:TET2 methylation may be an important factor for oxaliplatin resistance in the treatment of ALL.

Objective:To analyze the status of respiratory pathogen detection and the clinical features in children with Mycoplasma pneumoniae pneumonia (MPP). Methods:A prospective, multicenter study was conducted to collect clinical data, including medical history, laboratory examinations and multiplex PCR tests of children diagnosed with MPP from 4 hospitals in China between November 15 th and December 20 th, 2023. The multiplex PCR results and clinical characteristics of MPP children in different regions were analyzed. The children were divided into severe and mild groups according to the severity of the disease. Patients in the severe group were further divided into Mycoplasma pneumoniae (MP) alone and Multi-pathogen co-detection groups based on whether other pathogens were detected besides MP, to analyze the influence of respiratory pathogen co-detection rate on the severity of the disease. Mann-Whitney rank sum test and Chi-square test were used to compare data between independent groups. Results:A total of 298 children, 136 males and 162 females, were enrolled in this study, including 204 children in the severe group with an onset age of 7.0 (6.0, 8.0) years, and 94 children in the mild group with an onset age of 6.5 (4.0, 7.8) years. The level of C-reactive protein, D-dimer, lactic dehydrogenase (LDH) were significantly higher (10.0 (5.0, 18.0) vs. 5.0 (5.0, 7.5) mg/L, 0.6 (0.4, 1.1) vs. 0.5 (0.3, 0.6) mg/L, 337 (286, 431) vs. 314 (271, 393) U/L, Z=2.02, 2.50, 3.05, all P<0.05), and the length of hospitalization was significantly longer in the severe group compared with those in mild group (6.0 (6.0, 7.0) vs. 5.0 (4.0, 6.0) d, Z=4.37, P<0.05). The time from onset to admission in severe MPP children was significantly shorter than that in mild MPP children (6.0 (5.0, 9.5) vs. 9.0 (7.0, 13.0) d, Z=2.23, P=0.026). All patients completed the multiplex PCR test, with 142 cases (47.7%) MPP children detected with 21 pathogens including adenovirus 25 cases (8.4%), human coronavirus 23 cases (7.7%), rhinovirus 21 cases (7.0%), Streptococcus pneumoniae 21 cases (7.0%), influenza A virus 18 cases (6.0%). The pathogens with the highest detection rates in Tianjin, Shanghai, Wenzhou and Chengdu were Staphylococcus aureus at 10.7% (8/75), adenovirus at 13.0% (10/77), adenovirus at 15.3% (9/59), and both rhinovirus and Haemophilus influenzae at 11.5% (10/87) each. The multi-pathogen co-detection rate in severe MPP children was significantly higher than that in mild MPP group (52.9% (108/204) vs. 36.2% (34/94), χ2=10.62, P=0.005). Among severe MPP children, there are 89 cases in the multi-pathogen co-detection group and 73 cases in the simple MPP group. The levels of LDH, D-dimer and neutrophil counts in the multi-pathogen co-detection group were significantly higher than those in the simple MPP group (348 (284, 422) vs. 307 (270, 358) U/L, 0.8 (0.5, 1.5) vs. 0.6 (0.4, 1.0) mg/L, 4.99 (3.66, 6.89)×10 9vs. 4.06 (2.91, 5.65)×10 9/L, Z=5.17, 4.99, 6.11, all P<0.05). Conclusions:The co-detection rate of respiratory pathogens, LDH and D-dimer in children with severe MPP were higher than those with mild MPP. Among severe MPP children the stress response of children in co-detection group was more serious than that of children with simple MPP.

Background::Limited information exists regarding the impact of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection on psoriasis patients. The objective of this study was to identify clinical factors associated with the prognosis of psoriasis following SARS-CoV-2 infection.Methods::A retrospective, multicenter study was conducted between March and May 2023. Univariable and multivariable logistic regression analyses were employed to identify factors associated with coronavirus disease 2019 (COVID-19)-related psoriasis outcomes. The study included 2371 psoriasis patients from 12 clinical centers, with 2049 of them having been infected with SARS-CoV-2.Results::Among the infected groups, lower exacerbation rates were observed in individuals treated with biologics compared to those receiving traditional systemic or nonsystemic treatments (22.3% [236/1058] vs. 39.8% [92/231] vs. 37.5% [140/373], P <0.001). Psoriasis progression with lesions (adjusted odds ratio [OR] = 8.197, 95% confidence interval [95% CI] = 5.685–11.820, compared to no lesions), hypertension (adjusted OR = 1.582, 95% CI = 1.068–2.343), traditional systemic (adjusted OR = 1.887, 95% CI= 1.263–2.818), and nonsystemic treatment (adjusted OR= 1.602, 95% CI= 1.117–2.297) were found to be associated with exacerbation of psoriasis after SARS-CoV-2 infection, but not biologics (adjusted OR = 0.931, 95% CI = 0.680–1.274, compared to no treatment), according to multivariable logistic regression analysis. Conclusions::A reduced risk of psoriasis exacerbation after SARS-CoV-2 infection was observed with biologics compared to traditional systemic and nonsystemic treatments. Significant risk factors for exacerbation after infection were identified as existing psoriatic lesions and hypertension.

OBJECTIVE To analyze and evaluate serious adverse drug reaction(SADR) and drug-drug interactions(DDIs) in the real-world, so as to obtain the clinical evidence of DDIs-related SADR, and to provide a reference for rational clinical use. METHODS The SADR reports reported to the National Adverse Drug Reaction Monitoring Center from January 2011 to December 2020 were collected, and Lexi-Interaction® software in UpToDate was used to analyze ≥2 drugs in SADR to evaluate whether there were potential DDIs. And the possible adverse drug reactions caused by DDIs were statistically analyzed. RESULTS Among the 360 cases of SADR, males were slightly more than females(50.83% vs 49.17%), the mean age was (65.27±14.71) years old, and 56.39% were ≥65 years old. Cardiovascular agents were the most common implicated pharmacological group, and the gastrointestinal system was the most frequently affected system, and aspirin was the most frequently reported drug. Among 150 cases of SADR with at least two suspected drugs, 64 cases had potential DDIs, while 42 cases had clinically significant DDIs, of which only 16 and 2 cases of SADR were caused by actual DDIs in category D and X, respectively. The majority of reports(71.43%) were caused by additive pharmacodynamic interactions. Aspirin was the most common drug in both potential DDIs and actual DDIs, while aspirin and clopidogrel was the most commonly involved drug pair in actual DDIs, with gastrointestinal bleeding being the most common SADR. CONCLUSION Attention should be paid to the influence of drug interactions on SADR, and prescription should be optimized, especially in the elderly population. According to the results of potential DDIs, therapeutic drugs should be rationally selected. Meanwhile, monitoring of cardiovascular drugs and key populations should be strengthened to ensure drug safety.