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RESULTS The data showed that expression of caspase 3, caspase 8, RIPK1, RIPK 3, and MLKL markedly increased in severely degenerated disc tissues. IL-1β promoted the cell death of NP cells, while NSA could reverse the effects of IL-1β. We found that NAS increased the antioxidant SOD1, SOD2, CAT, and GPX3 expression and suppressed oxidative stress in the disc. Moreover, MMP3, MMP10, IL-6, and TNF-α were significantly suppressed by the NSA. CONCLUSIONS These results suggest that NSA prevented NP degradation via inhibiting apoptosis and necroptosis of NP cells. Besides, the protective function of antagonizing cell death may owe to the inflammation and oxidative stress suppression.OBJECTIVE The aim of this study was to explore the relationships between ADAMTS-13 gene polymorphisms and hypertension-induced atrial fibrillation (AF). PATIENTS AND METHODS A total of 200 hypertensive patients without AF (hypertension group) and 200 hypertensive patients with AF (AF group) treated in our hospital were enrolled. Then, peripheral blood was drawn from these subjects enrolled, and the genomic deoxyribonucleic acids (DNAs) were extracted for analysis of ADAMTS-13 gene polymorphism. Next, Reverse Transcription-quantitative Polymerase Chain Reaction (RT-qPCR) was employed to determine the expression of ADAMTS-13 gene, and the correlations of ADAMTS-13 gene polymorphism with ADAMTS-13 gene expression and clinical indicators were analyzed. RESULTS Results revealed that there was a difference in the distribution of alleles of ADSMTS-13 rs3094374 (p=0.046) and rs34054981 (p=0.039) between AF group and hypertension group. The frequency of T allele of the locus rs3094374 and that of the locus rs34054981 MTS-13 gene was lower in patients carrying genotype TT in AF group. Furthermore, the ADAMTS-13 rs3094374 polymorphism was related to international normalized ratio (INR) (p=0.034), and the ADAMTS-13 rs28503257 polymorphism was correlated with the levels of brain natriuretic peptide (BNP) (p=0.047) and D-dimer (p=0.033). CONCLUSIONS ADAMTS-13 gene polymorphism is correlated with the susceptibility and procession of hypertension-induced AF.OBJECTIVE To explore the potential correlation between heat shock protein 60 (HSP60) gene polymorphisms and susceptibility to atherosclerosis. PATIENTS AND METHODS A total of 160 atherosclerosis patients treated in our hospital from February 2017 to February 2019 were randomly enrolled as case group, and 200 healthy adults receiving physical examination were selected as control group at the same period. Venous blood was drawn from all subjects to extract deoxyribonucleic acid (DNA). TaqMan probe technology was employed to genotype two loci rs2340690 and rs788016 of HSP60 gene in all 260 subjects. The correlations between HSP60 gene polymorphisms and the incidence rate and pathological grade of atherosclerosis were analyzed. RESULTS There were three genotypes (AA, AG, and GG) in HSP60 rs2340690 and three (GG, AG, and AA) in HSP60 rs788016. No significant differences in the frequency of each genotype were found between the two groups (p>0.05). HSP60 rs2340690 and HSP60 rs788016 had no significant associations with the incidence rate of atherosclerosis in the dominant, recessive, and additive genetic models. In the case of pathological grade IV, the proportion of atherosclerosis patients carrying GG genotype of HSP60 rs2340690 was higher than those carrying AA genotype and AG genotype of HSP60 rs2340690 (p less then 0.05). The probability in atherosclerosis patients carrying rs788016 A was higher than those carrying rs2340690 G (p less then 0.05). When atherosclerosis patients carried both genotype G of HSP60 rs2340690 and genotype A of HSP60 rs788016, the odds ratio (OR) was 1.721 (p=0.049). CONCLUSIONS The HSP60 gene polymorphisms are certainly correlated with the pathological grade and incidence rate of atherosclerosis.OBJECTIVE To study the influence of micro ribonucleic acid (miR)-26a on myocardial cell apoptosis in rats with acute myocardial infarction (AMI) through the glycogen synthase kinase 3 beta (GSK-3β) pathway. MATERIALS AND METHODS A total of 36 Sprague-Dawley rats were randomly divided into sham group (n=12), model group (n=12), and miR-26a mimics group (n=12). Only the heart was exposed, and normal saline was intraperitoneally injected postoperatively in sham group, and the model of AMI was prepared in model group. Besides, after modeling, miR-26a mimics were injected into the left ventricle in miR-26a mimics group. At 48 h after operation, sampling was performed. Then, the expressions of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax), as well as the protein expression of phosphorylated GSK-3β (p-GSK-3β) were detected via immunohistochemistry and Western blotting, respectively. Moreover, the expression level of miR-26a was measured via quantitative polymerase chain reaction (qPCR), and cell apothen 0.05). Additionally, the TUNEL-positive cells were considerably increased in both model group and miR-26a mimics group in comparison with that in sham group (p less then 0.05), and miR-26a mimics group had markedly fewer TUNEL-positive cells than model group (p less then 0.05). CONCLUSIONS MiR-26a activates the GSK-3β signaling pathway to inhibit myocardial cell apoptosis after AMI.OBJECTIVE Myocardial infarction (MI) is a serious cardiac disease due to its high incidence and mortality worldwide. Long noncoding RNAs (lncRNAs) have been found to play an essential role in the pathological progress of various cardiovascular diseases. ILF3-AS1 is a newly identified lncRNA, and many studies have demonstrated that ILF3-AS1 affects the development of various malignancies. However, the biological function of ILF3-AS1 and its underlying mechanism in MI are still unknown. In the present study, the function of ILF3-AS1 and the possible mechanisms against hypoxia-induced apoptosis in H9c2 cells were investigated. MATERIALS AND METHODS H9c2 cells were exposed to hypoxia (1% O2) to mimic the in vitro model of MI. The levels of lncRNA ILF3-AS1 and microRNA miR-212-3p were measured by real-time PCR (RT-PCR). Transfection was performed to upregulate the levels of ILF3-AS1 and miR-212-3p. Western blot assays were carried out to measure protein expression. BMS986165 The relationship between ILF3-AS1 and miR-212-3p was verified by Dual-Luciferase reporter assay.