Water-soluble dietary fibers have been shown to improve lipid profile and glucose metabolism in diabetes. The aim of this study was to review the effects of psyllium consumption on weight, body mass index, lipid profiles, and glucose metabolism in diabetic patients in randomized controlled trials. A comprehensive systematic search was performed in PubMed/MEDLINE, Web of Sciences, Cochrane, and Scopus by two independent researchers up to August 2019 without any time and language restrictions. The DerSimonian and Laird random-effects model method performed to calculate the pooled results. Inclusion criteria were randomized controlled trial design, adult subjects, and studies reporting the mean differences with the 95% confidence interval for outcome. Eight studies containing nine arms with 395 participants were identified and included in final analysis. Combined results found a significant reduction in triglycerides, low-density lipoprotein, fasting blood sugar, and hemoglobin A1c Abbreviations: BMI, body mass index; HDL, high-density lipoprotein; LDL-C, low-density lipoprotein cholesterol; TG/TAG, triglycerides.Hui Chen is the co-first author.

Atherosclerosis is a chronic lipid-induced inflammation of the vessel wall. Oxidized low-density lipoprotein was confirmed to drive the onset of atherogenesis. Zinc finger e-box–binding homeobox 1 antisense 1 (ZEB1-AS1) is a long noncoding RNA that is involved in human diseases, including atherosclerosis. In this study, the role of exosomes-mediated ZEB1-AS1 and its underlying mechanisms in atherosclerosis were explored in oxidized low-density lipoprotein (ox-LDL)-treated human umbilical vein endothelial cells (HUVECs). Exosomes were extracted from HUVECs. Quantitative real-time polymerase chain reaction was conducted to measure the expression of ZEB1-AS1, microRNA-590-5p (miR-590-5p), or erythroblastosis virus E26 oncogene homolog 1 (ETS1) in cells or exosomes. Cell proliferation and apoptosis were assessed by MTT assay and flow cytometry analysis, respectively. Western blot was performed to detect apoptosis-related factors, ETS1, and TGF-β/Smad pathway protein levels. The secretion of inflammatory factors in supernatant was detected by ELISA assay. Oxidative stress damage indicators were used to assess cellular damage. Relationship between miR-590-5p and ZEB1-AS1 or ETS1 was analyzed. Our data indicated that ox-LDL–induced exosomes-mediated ZEB1-AS1 in HUVECs. Ox-LDL treatment resulted in limited proliferation, proapoptosis, inflammation, and oxidative stress damage, whereas knockdown of ZEB1-AS1 could reverse these effects. Mechanically, ZEB1-AS1 sponged miR-590-5p to regulate ETS1 expression. MiR-590-5p knockdown inverted effects above of si-ZEB1-AS1 on HUVECs under ox-LDL exposure. Moreover, ETS1 reversed miR-590-5p–induced effects and activated the TGF-β/Smad pathway in ox-LDL–treated HUVECs. Taken together, our findings demonstrated that exosomes-mediated ZEB1-AS1 enhanced cell injuries by miR-590-5p/ETS1 axis through the TGF-β/Smad pathway in ox-LDL–induced HUVECs, suggesting that inhibiting ZEB1-AS1 might be an effective way for atherosclerosis treatment.

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Nowadays, there is limited prevention and treatment for myocardial fibrosis in diabetic cardiomyopathy (DCM). Our study aimed to depict the mechanism of the lncRNA TUG1/miR-145a-5p/ Cfl2 axis in DCM and to provide a molecular basis for the study of this disease. Male C57BL/6J mice were intraperitoneally injected with streptozotocin to establish DCM mouse models. The expression levels of lncRNA TUG1, miR-145a-5p, and Cfl2 in myocardial tissues of mice were tested by RT-qPCR or Western blot. Cardiac function was assessed by echocardiography. The contents of Ang-II, TNF-a, and IL-1b were measured using ELISA. The histopathological observation was performed by HE staining and Masson staining. The expression levels of myocardial fibrosis-related genes COL1A1, MMP2, and FN1 were determined by RT-qPCR. In addition, bioinformatics website, RIP assay, pull-down assay, and luciferase activity assay were conducted to verify the relationships of lncRNA TUG1, miR-145a-5p, and Cfl2. In the DCM mouse model, lncRNA TUG1 and Cfl2 expression levels were upregulated and miR-145a-5p expression was downregulated. Downregulation of lncRNA TUG1 improved cardiac function and myocardial fibrosis; decreased COL1A1, MMP2, and FN1 expression levels; as well as TNF-a, IL-1b, and Ang-II contents in myocardial tissues of DCM mice. Upregulation of miR-145a-5p showed the same trend as downregulation of lncRNA TUG1. In addition, upregulating miR-145a-5p reversed the promotion roles of lncRNA TUG1 on myocardial fibrosis in DCM mice, and upregulating Cfl2 compromised the improvement effect of downregulated lncRNA TUG1 on myocardial fibrosis in DCM mice. Mechanistically, there was a binding site between lncRNA TUG1 and miR-145a-5p, and miR-145a-5p had a targeting relationship with Cfl2. This study highlights that lncRNA TUG1 sponges miR-145a-5p to aggravate myocardial fibrosis in DCM mice by promoting Cfl2.

Chemotherapy resistance is one of the major challenges in the treatment of liver cancer (LC). The present study aimed to investigate the potential roles of Yes-associated protein (YAP), the core component of the Hippo signaling pathway, in chemoresistance of LC. YAP expression and its function in chemoresistance of LC cells were investigated. It was revealed that the expression levels and nuclear localization of YAP were increased in cisplatin (CDDP)-resistant LC (LC/CDDP) cells. The targeted inhibition of YAP using small interfering RNA or an inhibitor restored the CDDP sensitivity of LC cells. YAP overexpression was discovered to be essential for the increase of IL-6 and TGF-β expression levels in LC/CDDP cells. Furthermore, it was identified that increased mRNA stability was the primary reason for the upregulation of YAP expression in LC/CDDP cells, which was due to the downregulation of microRNA (miR)-375 expression in LC/CDDP cells. In conclusion, the findings of the present study suggested that the miR-375/YAP axis may regulate the expression levels of IL-6 and TGF-β, which may subsequently be involved in the CDDP resistance of LC cells. The current results indicated that the targeted inhibition of this axis and signaling pathway may be helpful in overcoming CDDP resistance.