The role of Hsa_circ_0001445 in oxidation Low Lipoprotein (ox-LDL) induced HUVEC inflammatory damage remains poorly characterized. The present study investigated the performance of the circRNA Hsa_circ_0001445 on ox-LDL-induced HUVEC inflammatory damage. ox-LDL was employed to treat HUVECs and the expression of Hsa_circ_0001445 in cells were detected by qRT-PCR. Then, the overexpression plasmid of circ_0001445 was transfected into HUVECs. The Cell Counting Kit-8 assay was performed to detect cell viability, and the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in treatment cells were measured using ELISAs. Furthermore, the oxidative stress kit was used to detect the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase in treatment cells. Flow cytometry assay was applied to measure cell apoptosis, and the expressions of apoptosis-related protein were measured by western blot. The luciferase reporter assay was applied to confirm the target binding between Hsa_circ_0001445 and micro-RNA-640 (miRNA-640). Next, miRNA-640 mimic was transfected into ox-LDL-induced HUVECs, and then cell proliferation, expression level of inflammatory factors, oxidative stress and apoptosis level in treatment cells were assessed, with the expression of related proteins measured. The results revealed that the expression of Hsa_circ_0001445 was obviously downregulated in ox-LDL-induced HUVECs. Overexpression of Hsa_circ_0001445 promoted cell proliferation, inhibited ox-LDL-induced HUVEC inflammatory response, downregulate the expression of TNF-α, IL-1β and IL-16, overexpression of Hsa_circ_0001445 inhibited cell apoptosis. miRNA-640 was confirmed as a direct target of Hsa_circ_0001445, and miRNA-640 mimic reversed the effects of Hsa_circ_0001445 overexpression on ox-LDL-induced HUVECs. Our findings concluded that Hsa_circ_0001445 inhibits ox-LDL-induced HUVEC inflammation, oxidative stress and apoptosis by regulating miRNA-640.

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Endothelial cell damage induced by oxidized low-density lipoprotein (ox-LDL) plays an important role in the pathogenesis of atherosclerosis (AS). We aimed to explore the effects of lysophosphatidic acid receptor 5 (LPAR5) on ox-LDL-induced damage of human umbilical vein endothelial cells (HUVECs). After HUVECs exposed to ox-LDL, LPAR5 expression was detected by RT-qPCR and western blotting. Then, LPAR5 was silenced and cell viability was determined with a CCK-8 assay. ELISA was employed to analyze the contents of inflammatory factors. The levels of oxidative stress markers were examined by kits. The expression of proteins related to endothelium function, including CD31, α-SMA, iNOS and eNOS, was evaluated with RT-qPCR and western blotting. Additionally, the effects of LPAR5 deletion on the NLRP3 inflammasome signaling in HUVECs under ox-LDL condition were assessed by determining NLRP3, caspase-1 and ASC expression. Afterward, NLRP3 agonist MSU was adopted for exploring the regulation of LPAR5 on NLRP3 inflammasome signaling in ox-LDL HUVECs injury. Results revealed that ox-LDL led to a significant upregulation in LPAR5 expression. NLRP3 knockdown enhanced cell viability, inhibited inflammation and oxidative stress in HUVECs after ox-LDL exposure. Besides, the expression of CD31 and eNOS was increased while that of α-SMA and iNOS was decreased after LPAR5 silencing. Moreover, interference with LPAR5 remarkably downregulated NLRP3, caspase-1 and ASC expression. Furthermore, MSU addition partially abrogated the inhibitory effects of LPAR5 deletion on the inflammation, oxidative stress and endothelium dysfunction of HUVECs. To conclude, we demonstrated that LPAR5 silencing alleviates ox-LDL-induced HUVECs injury by inhibiting NLRP3 inflammasome signaling.

Background and Hypothesis The rehabilitation effect of circuit resistance training in coronary heart disease (CHD) patients remains unclear. We perform this review to examine the rehabilitation effect of circuit resistance training in CHD patients and to provide a basis for the formulation of reasonable individual exercise prescriptions for CHD patients. Methods Randomized controlled trials (RCTs) were searched on PubMed, Web of Science, The Cochrane Library, Embase, Clinical Trials, and CNKI. About 1232 studies were identified. Nine RCTs were finally used for the present meta‐analysis to determine the rehabilitation effect of circuit resistance training in CHD patients, compared to aerobic training. Individuals enrolled for the studies were at a mean age of 60.5 years old and were all CHD patients. Following the PRISMA guidelines, we extracted basic information about the study and patient characteristics, as well as measurements (e.g., the peak oxygen uptake, the body mass index [BMI], the body fat percentage, the systolic blood pressure, the total cholesterol, and triglycerides). Subsequently, this meta‐analysis determined the overall effect by using standardized mean difference (SMD) and 95% confidence interval (CI). Results Compared with aerobic training, circuit resistance training significantly decrease the BMI and the body fat percentage. Conclusions As suggested from the present meta‐analysis of RCTs, circuit resistance training is effective in improving the BMI and the body fat percentage in CHD patients and may help delay the progression of CHD. CRT has the advantage of lower load in most cases with a similar effect.

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