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Patterson Bell posted an update 6 months, 3 weeks ago
Resveratrol improves cell apoptosis and tissue damage induced by high glucose, but the specific mechanism is unknown.
This is a basic research. We performed cell transfection, real-time fluorescence quantitative PCR (qPCR), flow cytometry, immunofluorescence, western blot, enzyme linked immunosorbent assay (ELISA) and cell viability assay to analyze cell viability, cell cycle, cellular oxidative stress, intracellular inflammatory factors and autophagy activities
. Meanwhile, dual luciferase reporter assay was conducted to explore the influence of miR-142-3p and sprouty-related EVH1 domain 2 (SPRED 2) on human glycated low-density lipoprotein (Gly-LDL)-induced vascular endothelial cell apoptosis, inflammatory factor secretion and oxidative stress.
Resveratrol inhibited the expression of miR-142-3p in human umbilical vein endothelial cells (HUVECs) induced by Gly-LDL in a dose-dependent manner, and the overexpression of miR-142-3p reverses the effect of resveratrol on the proliferation, apoptosis, secretion of inflammatory factors, oxidative stress, and autophagy. The dual-luciferase report analysis found a negative regulatory relationship between miR-142-3p and SPRED2. Inhibition of SPRED2 reversed the effects of resveratrol on Gly-LDL-induced HUVECs proliferation, apoptosis, inflammatory factor secretion and oxidative stress, and reversed the effects of resveratrol on Gly-LDL-induced HUVECs autophagy.
miR-142-3p promotes the development of diabetes by inhibiting SPRED2-mediated autophagy, including inducing cell apoptosis, aggravating cellular oxidative stress and secretion of inflammatory factors, and resveratrol improves this effect.
miR-142-3p promotes the development of diabetes by inhibiting SPRED2-mediated autophagy, including inducing cell apoptosis, aggravating cellular oxidative stress and secretion of inflammatory factors, and resveratrol improves this effect.Osteosarcoma is a malignancy that primarily affects children and young adults. The poor survival is largely attributed to acquisition of chemoresistance. Thus, the current study aimed to elucidate the role of ELK1/miR-134/PTBP1 signaling cascade in osteosarcoma chemoresistance. Doxorubicin (DXR)-resistant human osteosarcoma cells were initially self-established by continuous exposure of MG-63, U2OS and HOS cells to increasing DXR doses. Osteosarcoma chemoresistance in vitro was evaluated using CCK-8 assays and EdU staining. Aerobic glycolysis was evaluated by lactic acid production, glucose consumption, ATP levels, and Western blot analysis of GLUT3, HK2 and PDK1 proteins. The nude mice were injected with 5.0 mg/kg DXR following the subcutaneous transplantation of osteosarcomas. PTBP1 was upregulated in tumor tissues derived from non-responders to DXR treatment and correlated with patient poor survival. PTBP1 enhanced chemoresistance in cultured osteosarcoma cells in vitro and in vivo by increasing aerobic glycolysis. Additionally, miR-134 inhibited translation of PTBP1. ELK1 bound to miR-134 promoter and inhibited its expression. Overexpressed ELK1 enhanced chemoresistance and increased aerobic glycolysis by downregulating miR-134 and upregulating PTBP1 in DXR-resistant cells. Altogether, the key findings of the present study highlight ELK1/miR-134/PTBP1 signaling cascade as a novel molecular mechanism underlying the acquisition of osteosarcoma chemoresistance.The aim of our study was to examine the association between body mass index (BMI) and the risk of cardiovascular disease (CVD)-specific mortality among Chinese adults with hypertension by sex. This study included 212,394 adult hypertensive patients aged 20-85 years registered in the records of Minhang District during 2007-2018. Cox proportional hazards regression was performed to evaluate the association between BMI and CVD-specific mortality among Chinese adults with hypertension. There were 14,029 deaths over an average of 8.24 years (range, 0.19-11.96 years). The multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) across BMI categories ( less then 18.5 kg/m2, 18.5-24.9 kg/m2 , 25.0-29.9 kg/m2, and ≥ 30 kg/m2) for CVD-specific mortality were 1.37 (1.22-1.53), 1.00 (reference), 0.95 (0.90-1.01), and 1.21 (1.04-1.40) in males, and 1.44 (1.31-1.59), 1.00 (reference), 0.96 (0.91-1.01), and 1.04 (0.92-1.17) in females. A U-shaped relationship was observed between BMI and CVD-specific mortality (overall association P less then 0.001; non-linearity P less then 0.001). This association was attenuated in old age. This study revealed a U-shaped relationship between BMI and CVD-specific mortality among hypertensive men and women. https://www.selleckchem.com/products/resatorvid.html In older people, overweight and obesity are potential factors that reduce the risk of CVD death.The role of TRPM2-AS lncRNA in OvC has not been explored. This study aimed to investigate whether and how TRPM2-AS contributes to the progression of OvC. First, qRT-PCR was employed to measure the expression of TRPM2-AS, miR-138-5p and SDC3 in OvC samples. A xenograft formation assay was subsequently performed to detect the tumor growth in vivo. The cell viability, colony formation, cell migration, cell invasion and cell apoptosis were later evaluated using a series of experiments. The western blot assay was utilized to detect the SDC3 protein expression and cell-apoptosis markers. Luciferase reporter gene assay, RIP, and RNA pull-down assays were performed to identify the association between TRPM2-AS, miR-138-5p and SDC3. Findings indicated that the expression of TRPM2-AS and SDC3 was significantly upregulated in OvC tissues and cells, while miR-138-5p expression was significantly downregulated in OvC samples. Unlike miR-138-5p, TRPM2-AS and SDC3 were found to promote OvC development. It was also found that TRPM2-AS could sponge miR-138-5p to release SDC3, thus promoting OvC progression. Apart from that, we discovered that both sh-TRPM2-AS and cisplatin could enhance the apoptosis of OvC cells. Overall, our findings suggested that the TRPM2-AS/miR-138-5p/SDC3 axis was closely associated with OvC tumorigenesis and cisplatin resistance.Oxygen glucose deprivation (OGD)/re-oxygenation (OGDR) induces profound oxidative injury and neuronal cell death. It mimics ischemia-reperfusion neuronal injury. CPI-1189 is a novel tumor necrosis factor alpha-inhibiting compound with potential neuroprotective function. Here in SH-SY5Y neuronal cells and primary murine cortical neurons, CPI-1189 pretreatment potently inhibited OGDR-induced viability reduction and cell death. In OGDR-stimulated neuronal cells, p38 phosphorylation was blocked by CPI-1189. In addition, CPI-1189 alleviated OGDR-induced reactive oxygen species production, lipid peroxidation, and glutathione consumption. OGDR-induced neuronal cell apoptosis was also inhibited by CPI-1189 pretreatment. Furthermore, in SH-SY5Y cells and cortical neurons, CPI-1189 alleviated OGDR-induced programmed necrosis by inhibiting mitochondrial p53-cyclophilin D-adenine nucleotide translocase 1 association, mitochondrial depolarization, and lactate dehydrogenase release to the medium. In summary, CPI-1189 potently inhibited OGDR-induced oxidative injury and neuronal cell death.
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