Abstract:At present, with the development of new diagnostic technologies, the detection rate of aortic dissection has been increasing year by year, but its mortality rate still remains high. Cardiovascular disease is a chronic inflammatory disease, and vascular inflammation plays a major role in the progression of aortic dissection. Therefore, this article systematically describes the specific roles and mechanisms of inflammatory cells, inflammatory factors, and inflammasomes in the development of aortic dissection.

Abstract:In-stent restenosis(ISR) is a significant cause of long-term prognosis after percutaneous coronary intervention (PCI). The inflammatory response is a critical factor in its development. Unlike the chronic inflammatory process of traditional atherosclerosis, ISR may develop acute coronary events within even months or years, and the inflammatory mechanisms of ISR are more complex. Inflammatory factors regulate various mechanisms, including monocyte macrophage proliferation, endothelial cell damage and repair, foam cell formation, and smooth muscle cell proliferation and migration after PCI. The review briefly describes the classification and risk factors of ISR. It emphasizes the role of various inflammatory factors in ISR to provide new ideas for investigating the inflammatory mechanism of ISR and clinical intervention.

Abstract:Acute myocardial infarction is one of the more common clinical cardiovascular diseases,which is based on the occurrence and development of coronary atherosclerosis,and is caused by persistent myocardial ischemia and hypoxia due to thrombosis and plaque rupture,resulting in local myocardial necrosis. Inflammatory factors are involved in the formation and progression of coronary atherosclerotic plaque, and are closely related to the occurrence and development of acute myocardial infarction. This article reviews the research progress of related inflammatory factors in acute myocardial infarction.

Abstract:Aim To investigate the effect of lncRNA-BC200 on the inflammation and apoptosis of nerve cells induced by Aβ25-35 and its possible mechanism. Methods The nerve cells PC12 were divided into NC group (conventional cell culture) and 0,0, 40 μmol/L Aβ25-35 groups (cells were treated with 0,0, 40 μmol/L Aβ25-35 for 24 h), and then cell apoptosis was detected by flow cytometry. qRT-PCR method was used to detect the expression of lncRNA-BC200 in cells. The PC12 cells were divided into NC group (cells were routinely cultured), Aβ25-35 group (PC12 cells were intervened with 20 μmol/L Aβ25-35 for 24 h), si-NC+Aβ25-35 group (PC12 cells were transfected with si-NC and then intervened with 20 μmol/L Aβ25-35 for 24 h), si-lncRNA-BC200+Aβ25-35 group (PC12 cells were transfected with si-lncRNA-BC200 and then intervened with 20 μmol/L Aβ25-35 for 24 h) and TNF-α+si-lncRNA-BC200+Aβ25-35 group (PC12 cells were transfected with si-lncRNA-BC200 and then co-intervened with 20 μmol/L Aβ25-35 and 20 μg/L tumor necrosis factor (TNF-α) for 24 h). Flow cytometry was used to detect cell proliferation activity and apoptosis, ELISA was used to detect the expression of TNF-α, interleukin-6 (IL-6) and interferon-γ (IFN-γ) in the cell culture supernatant, and Western blot was used to detect the protein expression of cleaved-Caspase-3, p-p65 and p-IκBα in the cells. Results The apoptosis rate of PC12 cells and the expression of lncRNA-BC200 were higher in 0,0, 40 μmol/L Aβ25-35 groups than NC group. The protein expression of cleaved-Caspase-3, p-p65 and p-IκBα and the levels of TNF-α, IL-6 and IFN-γ in Aβ25-35 group cells were all higher than NC group. The apoptotic rate of PC12 cells, the protein expression of cleaved-Caspase-3, p-p65 and p-IκBα, and the levels of TNF-α, IL-6 and IFN-γ were all lower in the si-lncRNA-BC200+Aβ25-35 group than Aβ25-35 group. The apoptotic rate of PC12 cells, the protein expression of cleaved-Caspase-3, p-p65 and p-IκBα, and the levels of TNF-α, IL-6 and IFN-γ in the TNF-α+si-lncRNA-BC200+Aβ25-35 group were all higher than the si-lncRNA-BC200+Aβ25-35 group. Conclusion Knockdown of lncRNA-BC200 may inhibit Aβ25-35-induced neuronal cell PC12 secretion of inflammatory factors and apoptosis by inhibiting the activation of NF-κB signaling pathway.

Abstract:Atherosclerosis is the basis of many important adverse vascular events, which seriously threatens human health. In recent years, more and more attention has been paid to the role of inflammatory and immune regulatory factors in the occurrence and development of atherosclerosis. It has been noted that the risk of cardiovascular disease in patients with autoimmune diseases is significantly higher than that in ordinary people. It is speculated that there may be a relationship between autoimmune diseases and the pathogenesis of cardiovascular disease cross. Therefore, this paper reviews the mechanism of autoimmune diseases and As by searching the relevant literature at home and abroad, in order to provide new ideas for the prevention and treatment of autoimmune diseases complicated with cardiovascular disease.

Abstract:Atherosclerosis is considered as a chronic inflammatory disease that involves multiple cell types and factors. The outside layer of the vessels plays a vital role during pathological development. Under pathological conditions such as obesity and inflammation, perivascular adipose tissue (PVAT) will release adipokines and inflammatory factors through adipocyte phenotype transformation and regulate various inflammatory cells. PVAT regulates the immune response of blood vessels in an “outside-inside” manner and further regulates atherosclerosis. Intervention of PVAT may be a new strategy for prevention and treatment of atherosclerosis.

Abstract:Aim To investigate the effect of miR-140-3p on hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury and its mechanism. Methods In vitro cardiomyocyte H/R model was constructed, and H9c2 cells were transfected with miR-140-3p mimics and chemokine receptor 4 (CXCR4) overexpression plasmids. Cell viability was detected by methyl thiazolyl tetrazolium method. Cell apoptosis was detected by flow cytometry. Reverse transcription polymerase chain reaction and Western blot were used to detect miR-140-3p, CXCR4, and the activation of Janus protein tyrosine kinase 2 (JAK2)/signal transducers and activators of transcription 3 (STAT3) pathway and the expressions of apoptosis-related proteins in cells. The targeting relationship between miR-140-3p and CXCR4 was verified by dual-luciferase reporter gene experiment. The activity of lactate dehydrogenase (LDH) and the levels of inflammatory factors and reactive oxygen species (ROS) were detected with corresponding kits. Results In vitro H/R could inhibit the expression of miR-140-3p, up-regulate the expression of CXCR4 and the phosphorylation of JAK2/STAT3 pathway, induce the apoptosis of H9c2 cells and inhibit the proliferation of H9c2 cells, promote the release of inflammatory factors and ROS, and up-regulate the activity of LDH. miR-140-3p could inhibit the expression of CXCR4 by targeting CXCR4 3′UTR, thereby inhibiting the phosphorylation activation of JAK2/STAT3 pathway, inhibiting the release of inflammatory factors and ROS, down-regulating the activity of LDH, promoting the proliferation of H9c2 cells and inhibiting their apoptosis. Conclusion miR-140-3p may inhibit the JAK2/STAT3 pathway through targeted inhibition of CXCR4, thereby attenuating ischemia/reperfusion-induced cardiomyocyte injury.

Abstract:Aim To investigate the effect of coiled-coil domain containing protein 80 (CCDC80) on the expression of inflammatory factors in THP-1 macrophage-derived foam cells and related molecular mechanisms. Methods THP-1 cells were treated with phorbol ester (160 nmol/L) to induce the cells to differentiate into macrophages, and then treated with oxidized low density lipoprotein (50 mg/L) to form foam cell, performing conventional cell culture in vitro. The expression of interleukin-1β(IL-1β), interleukin-6(IL-6), tumor necrosis factor-α(TNF-α) and monocyte chemoattractant protein-1(MCP-1) was detected by ELISA, the expression of Toll like report 4(TLR4), lipoprotein lipase(LPL) and nuclear factor-κB(NF-κB) was detected by real-time PCR and Western blot. Foam cells were treated with TLR4 siRNA and LPL siRNA, and the effects of CCDC80 on the expression of TLR4, LPL, NF-κB and p-NF-κB in foam cells were detected by fluorescence quantitative PCR and Western blot. Results CCDC80 significantly increased THP-1 macrophage-derived foam cell inflammatory factor secretion and p-NF-κB expression. After TLR4 siRNA treated foam cells, the expression of TLR4, LPL and p-NF-κB reduced significantly. After LPL siRNA treated foam cells, the expression of LPL and p-NF-κB decreased significantly. Conclusion CCDC80 promotes the activation of NF-κB signaling pathway through the TLR4/LPL pathway, thereby increasing the secretion of IL-1β, IL-6, TNF-α and MCP-1.

Abstract:Aim To explore the expression and clinical significance of a novel long noncoding RNA n342721 (lncRNA n342721) in the serum of patients with acute myocardial infarction (AMI). Methods The expression of lncRNA in serum of 5 patients with AMI and 5 cases without coronary heart disease (non-CHD) was detected by using Human Transcriptome Array 2.0, and 6 up-regulated lncRNAs with different expression levels were screened out. Further verification and screening were carried out in serum of 20 patients with AMI and 20 cases with non-CHD and Jurkat T cells in vitro, and the most different lncRNA n342721 was selected for the study. In order to explore the clinical value of lncRNA n342721, the serum lncRNA n342721 expression and clinical data of 60 patients with AMI and 60 cases with non-CHD were analyzed. Furthermore, lncRNA n342721 was overexpressed and silenced at T cell level, then the changes of inflammatory cytokines such as interleukin-6 (IL-6), IL-10 and tumor necrosis factor α (TNF-α), and cholesterol transport related indexes such as liver X receptor β (LXR-β), ATP binding cassette transporter A1 (ABCA1) and ABCG1 were detected. Results Compared with non-CHD, 296 up-regulation and 74 down-regulation lncRNAs were detected among differentially expressed lncRNAs in the serum of AMI patients. Among the 6 selected lncRNAs, lncRNA n342721 was selected as the main research object, which had the greatest expression difference in serum and T cell levels. The results of quantitative real-time PCR showed that the expression of serum lncRNA n342721 in AMI group (n＝60) was significantly higher than that in non-CHD group (n＝60) (P＜0.05). Further logistic regression analysis showed that serum lncRNA n342721 was closely related to the occurrence of AMI. After construction of lncRNA n342721 overexpression lentivirus and transfection of T cells with small interfering RNA, it was found that, compared with the control group, the expressions of TNF-α and IL-6 increased in overexpression group (P＜0.05), the expressions of IL-10, LXR-β, ABCA1 and ABCG1 decreased (P＜0.05), the expressions of TNF-α and IL-6 decreased in silence group (P＜0.05), and the expressions of IL-10, LXR-β, ABCA1 and ABCG1 increased (P＜0.05). Conclusion As a new biomarker, serum lncRNA n342721 may promote the occurrence and development of AMI by promoting immune inflammatory response and inhibiting reverse cholesterol transport.

Abstract:Aim To study the effect of L-carnitine combined with CT10 regulator of kinase like protein (CrkL) on reducing myocardial cell injury induced by hypoxia/reoxygenation (H/R). Methods H9c2 cells were injured by H/R and treated with L-carnitine. CCK-8, flow cytometry, and Western blot were applied to determine cell proliferation, apoptosis, and nuclear associated antigen Ki67 (Ki-67), proliferating cell nuclear antigen (PCNA),Bü cell lymphoma/lewkmia-2 (Bcl-2), Bcl-2 associated X protein (Bax), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), nuclear factor-κB (NF-κB), and CrkL levels, respectively. Cells H9c2 were transfected with pcDNA-CrkL, and treated with H/R or treated with H/R and L-carritine. The above methods were used to detect cell proliferation and apoptosis.Results Compared with the control group, the viability , Ki-67, PCNA, Bcl-2, and CrkL protein expression of H9c2 cells were significantly decreased in the H/R group, and the apoptosis rate, Bax protein level, and the levels of inflammatory factors TNF-α, IL-1β, NF-κB were evidently increased (P＜0.05). Compared with the H/R group, L-carnitine obviously improved the H/R-induced H9c2 cell viability, Ki-67, PCNA, Bcl-2, and CrkL protein expression, and remarkably reduced the apoptosis rate, Bax protein level, and TNF-α, IL-1β, NF-κB levels (P＜0.05). CrkL overexpression dramatically enhanced H/R-induced H9c2 cell viability, Ki-67, PCNA, and Bcl-2 protein expression, while markedly reduced apoptosis rates, Bax protein levels, TNF-α, IL-1β, and NF-κB levels (P＜0.05). Compared with L-carnitine or CrkL overexpression alone, L-carnitine combined with CrkL overexpression clearly increased the viability of H9c2 cells, Ki-67, PCNA, and Bcl-2 protein expression, and distinctly reduced the apoptosis rate and Bax protein level, TNF-α, IL-1β, NF-κB levels (P＜0.05). Conclusion L-carnitine combined with CrkL promotes the proliferation of cardiomyocytes induced by H/R, reduces apoptosis and inflammatory response, and thus protects cardiomyocytes from damage.