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Circular RNA hsa_circ_0006168 contributes to cell proliferation, migration and invasion in esophageal cancer by regulating miR-384/RBBP7 axis via activation of S6K/S6 pathway.

Esophageal cancer (EC) ranks as the sixth leading cause of cancer-related mortality worldwide. Circular RNAs (circRNAs) are involved in the pathogenesis of different cancers. However, the regulatory mechanism of circ_0006168 in EC progression is still unclear.

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Dexmedetomidine alleviates hepatic injury via the inhibition of oxidative stress and activation of the Nrf2/HO-1 signaling pathway.

Dexmedetomidine (Dex), frequently used as an effective sedative, was reported to play a critical role in the protection of multiple organs. However, its underlying mechanism of a putative protective effect on ischemia/reperfusion (I/R)-induced liver injury is still unclear. A hepatocyte injury model was established by treating WRL-68 cells with oxygen and glucose deprivation/reoxygenation (OGD/R). Enzyme Linked Immunosorbent Assay (ELISA) kits were used to determine the level of inflammatory factors (IL-6, IL-1β, and TNF-α), and oxidative stress indicators (ROS, MDA, GSH-Px, and SOD). MTT assay and flow cytometry analysis were used to determine the influence of Dex on cell viability and cell apoptosis. Expression of nuclear factor erythroid-derived 2- like 2 (Nrf2), HO-1, and apoptosis-related proteins (Bax, Bcl-2, caspase3, and caspase9) were detected by qRT-PCR and western blotting. Dex promoted cell viability and suppressed cell apoptosis in OGD/R-treated WRL-68 cells. Dex reduced TNF-α, IL-6, IL-1β, ROS, and MDA production, whereas it increased that of SOD and GSH-Px in OGD/R-treated WRL-68 cells. Moreover, Nrf2, HO-1, and Bcl-2 expression was upregulated, whereas, in contrast, transcripts for Bax, caspase3, and caspase9 were downregulated following Dex treatment under OGD/R. Knockdown of Nrf2 reversed the Dex effects on cell proliferation, apoptosis, and expression of TNF-α, IL-6, IL-1β, ROS, MDA, SOD, and GSH-Px. Dex protects WRL-68 cells against OGD/R-induced injury by inhibiting inflammation, oxidative stress, and cell apoptosis via the activation of Nrf2/HO-1 signaling pathway, suggesting that Dex may be a potential protector against hepatic injury.

1099 related Products with: Dexmedetomidine alleviates hepatic injury via the inhibition of oxidative stress and activation of the Nrf2/HO-1 signaling pathway.

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Chinese Medicine , Containing , and , Protects from Myocardial Ischemia Injury via Angiogenesis.

The Chinese patent medicine (SXXTN) is a clinical medication for coronary heart disease (CHD) and angina pectoris. This study aimed to investigate pharmacological effects of SXXTN and elucidate the role in angiogenesis on human umbilical vein endothelial cells (HUVECs) and acute myocardial ischemia (AMI) rats. We prepared SXXTN to treat the cells to reveal their effects on oxidative stress-damaged cell viability, as well as cell proliferation, migration, and tube formation processes. SXXTN was also used to treat coronary artery ligation-induced acute myocardial ischemia rats to confirm whether it had positive effect on myocardial issues by hematoxylin and eosin (HE), 2,3,5-triphenyltetrazolium chloride (TTC) staining and immunohistochemical staining. We measured the levels of peroxidative damage-related enzymes in cytoplasm and serum by biochemical kits and detected vascular endothelial growth factor (VEGF), angiotensin II (Ang II), thromboxane B2 (TXB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1) levels in cells and rats by enzyme-linked immunosorbent assay (ELISA) kits. The results showed that SXXTN protects HUVECs against oxidative stress damage and reversed the decrease of superoxide dismutase (SOD), glutathione (GSH) and increase of creatine kinase (CK), lactate dehydrogenase (LDH) caused by oxidative stress. SXXTN promoted angiogenesis through stimulating cell migration, tube formation, and activating VEGF/VEGFR2 and ERK1/2 pathways. Furthermore, SXXTN reduced infarct size and inhibited PGI2/TXA2 imbalance, preventing atherosclerosis plaque rupture leading to worsening coronary heart disease. Taken together, we report the first and evidence that SXXTN reduced oxidative stress-mediated damage and enhanced angiogenesis, which might be useful in treatment of myocardial infarction.

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Dexmedetomidine reduces the inflammation and apoptosis of doxorubicin-induced myocardial cells.

As the number of elderly patients increases, some patients with heart problems may also need surgery. The purpose of this study was to investigate whether dexmedetomidine (DEX), a common used anesthetic, was beneficial to the patients with heart problems. Myocardial cells induced by doxorubicin (DOX) was to simulate the myocardium injury in vitro. H9c2 cells were treated with DOX, DEX/DOX, Compound C and Compound C/DEX/DOX, respectively. The expression of p-AMPK, AMPK, p-GSK3β, GSK3β, Bcl2, Bax, Cleaved caspase3, Caspase3, TXNIP, NLRP3, ASC, Cleaved caspase-1 and Caspase-1 were analyzed by Western blot. CCK-8 assay and flow cytometry analysis were used to detect the cell viability and cell apoptosis. The levels of TNF-α, IL-1β and IL-18 were detected by ELISA assay and the levels of NO, ROS, LDH, SOD, MDA and taurine were detected by corresponding assay kits. As a result, DEX promoted the cell viability and inhibited the inflammation, oxidative stress and apoptosis. In addition, DEX suppressed the expression of taurine, TXNIP, NLRP3, ASC and cleaved caspase-1 and activated the expression of p-AMPK and p-GSK3β. However, those above changes could be reversed by Compound C. In conclusion, this study indicated that DEX could reduce the inflammation and apoptosis of DOX-induced myocardial cells through activating the AMPK-GSK3β signaling pathway. Because of the above effects of DEX, it may be beneficial for surgical patients with heart problems.

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Inhibition of miR-217 Protects Against Myocardial Ischemia-Reperfusion Injury Through Inactivating NF-κB and MAPK Pathways.

Recent studies have demonstrated that miRNAs play a vital role in regulating myocardial ischemia/reperfusion injury (MIRI). MiR-217 has been proven to be implicated in cardiac diseases such as chronic heart failure and cardiac myxoma. However, the role of miR-217 in MIRI is not clear.

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Long non-coding RNA Arid2-IR affects advanced glycation end products-induced human retinal endothelial cell injury by binding to Smad3.

Long non-coding RNAs (lncRNAs) have been reported to play significant roles in the pathogenesis of diabetic retinopathy (DR). The aim of the present study was to investigate the role of lncRNA Arid2-IR in advanced glycation end product (AGE)-induced human retinal endothelial cells (HRECs) injury.

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CGA restrains the apoptosis of Aβ-induced hippocampal neurons.

Chlorogenic acid (CGA) has anti-oxidant and anti-inflammatory effects, but the study on its role in Alzheimer's disease (AD) models remains rare. Here, the effects of CGA on β-amyloid protein (Aβ)-induced cell models were investigated, aiming to provide a direction for Aβ-induced AD. Hippocampal neurons were separated from newborn Sprague-Dawley (SD) rats and identified by immumofluorescence method. Hippocampal neurons were processed with Aβ after pre-treatment CGA. MTT assay was used for detecting viability of treated cells. The activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and lactate dehydrogenase (LDH) of treated hippocampal neurons were determined by corresponding kits. Flow cytometry analysis assessed the apoptosis and mitochondrial membrane potential (MMP) in hippocampal neurons after treatment. The expressions of proteins related to apoptosis and endoplasmic reticulum stress (ERS) were measured by western blot (WB) analysis. Immumofluorescence method showed that the Aβ induction models were successfully constructed. CGA increased the viability and decreased the apoptosis rate of Aβ-induced hippocampal neurons. Decreasing activities of LDH and MDA, and raised contents of SOD and GSH-Px were appeared in Aβ-induced cells that pre-treated with CGA. Moreover, CGA also enhanced MMP intensity of hippocampal neurons induced by Aβ. In WB analysis, CGA reversed the promoting effect of Aβ on the expressions of proteins related to pro-ERS and pro-apoptosis. CGA restrained the apoptosis of Aβ-induced hippocampal neurons improving the anti-oxidant capacity, mitochondrial injury and ERS state of cells, which may provide a direction for AD.

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Overexpression of miR‑30c‑5p reduces cellular cytotoxicity and inhibits the formation of kidney stones through ATG5.

MicroRNAs (miRNAs or miRs) are critical regulators in various diseases. In the current study, the role of miR‑30c‑5p in the formation of sodium oxalate‑induced kidney stones was investigated. For this purpose, human renal tubular epithelial cells (HK‑2 cells) were incubated with sodium oxalate at the concentrations of 100, 250, 500, 750 and 1,000 µM. Cell viability and the miR‑30c‑5p expression level were respectively measured by CCK‑8 assay and RT‑qPCR. After separately transfecting miR‑30c‑5p mimic and inhibitor into the HK‑2 cells, the cell apoptotic rate, the levels of mitochondrial membrane potential (MMP) and ROS were determined by flow cytometry. The levels of oxidative stress indicators [lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT)] were determined using commercial kits. Crystal‑cell adhesion assay was performed to evaluate the crystal adhesion capacity in vitro. miR‑30c‑5p binding at autophagy related 5 (ATG5) was predicted by TargetScan7.2 and further verified by dual‑luciferase reporter assay. Rescue experiments were performed to confirm the molecular mechanisms underlying sodium oxalate‑induced kidney formation in HK‑2 cells. The results revealed that sodium oxalate decreased the viability of HK‑2 cells in a concentration‑dependent manner, and that miR‑30c‑5p expression was significantly downregulated by exposure to 750 µM sodium oxalate. In addition, the increase in cell apoptosis and crystal number, and the upregulated levels of LDH, MDA and ROS were reversed by the overexpression of miR‑30c‑5p. Moreover, the overexpression of miR‑30c‑5p upregulated the levels of SOD, CAT and MMP induced by sodium oxalate. ATG5 was directly regulated by miR‑30c‑5p, and the inhibition of cell cytotoxicity and crystal‑cell adhesion induced by miR‑30c‑5p mimic was blocked by ATG5. These data indicated that the overexpression of miR‑30c‑5p alleviated cell cytotoxicity and crystal‑cell adhesion induced by sodium oxalate through ATG5. Thus, the current study provides a better understanding of the role of miR‑30c‑5p in sodium oxalate‑induced kidney stones.

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[Advanced glycated albumin induces macrophage pyroptosis via upregulating nucleotide-binding oligomerization domain-like receptor protein 3].

The purpose of the present study was to investigate the effect of advanced glycated albumin (AGE-alb) on pyroptosis of macrophages and the underlying molecular mechanisms. RAW264.7 macrophages were treated with AGE-alb (1, 2, 4 and 6 g/L) and control albumin (C-alb, 4 g/L) for 24 h, or preincubated with MCC950 (1 μmol/L) for 1 h and then treated with AGE-alb (4 g/L) for 24 h. Cell viability and caspase-1 activity were measured by MTT and assay kits, respectively. Lactate dehydrogenase (LDH) activity and the levels of interleukin-1β (IL-1β) and IL-18 in media were detected. Cell death degree was evaluated by TUNEL and Hoechst 33342/PI staining. The protein levels of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), procaspase-1 and cleaved caspase-1 were assessed by Western blot. The results showed that AGE-alb treatment caused obvious decrease in cell viability and increases in LDH leakage and the percentages of TUNEL- or PI-positive cells in a concentration-dependent manner. Additionally, AGE-alb promoted IL-1β and IL-18 secretion, upregulated NLRP3 expression, and increased caspase-1 activity especially at the dose of 4 and 6 g/L. However, MCC950 (an NLRP3 inhibitor) pretreatment inhibited significantly the decrease in cell viability and the increases in LDH leakage and percentages of TUNEL- or PI-positive cells induced by AGE-alb. Furthermore, MCC950 attenuated obviously AGE-alb-induced IL-1β and IL-18 secretion and caspase-1 activation. These results indicate that AGE-alb may induce macrophage pyroptosis, and the mechanism is at least partially by activating NLRP3-caspase-1 pathway.

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MicroRNA-16-5p aggravates myocardial infarction injury by targeting expression of insulin receptor substrates 1 and mediating myocardial apoptosis and angiogenesis.

Myocardial infarction is a common cardiovascular disease. miR-16-5p was upregulated in heart and kidney hypoxia/reoxygenation (H/R) injuty. However, the role of miR-16-5p in myocardial infarction injury is still unclear.

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