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Sida 1 från 26 resultat
Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.
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Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study
[Hypoxia/reoxygenation and lipopolysaccharide induced nuclear factor-ΚB and hypoxia-inducible factor-1α signaling pathways in intestinal epithelial cell injury and the interventional effect of emodin].
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OBJECTIVE
To observe pathological process of intestinal epithelial cells subjected to ischemia, ischemia/reperfusion injury and inflammation simulated hypoxia/reoxygenation (H/R) and lipopolysaccharide (LPS) challenged human fetal normal colonic cell (FHC) line in vivo, and to observe the changes
Amelioration of hypoxia and LPS-induced intestinal epithelial barrier dysfunction by emodin through the suppression of the NF-κB and HIF-1α signaling pathways.
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Intestinal barrier dysfunction occurs in critical illnesses and involves the inflammatory and hypoxic injury of intestinal epithelial cells. Researchers are still defining the underlying mechanisms and evaluating therapeutic strategies for restoring intestinal barrier function. The anti-inflammatory
Emodin protects H9c2 cells against hypoxia-induced injury via regulation of miR-26a/survivin and the JAK1/STAT3 pathway.
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Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation.
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The aim of the present study was to determine the effects of emodin, a natural compound with antioxidant properties, on oxidative stress and apoptosis induced by hypoxia/reoxygenation (H/R) in HK-2 human renal tubular cells. In HK-2 cells subjected to H/R, it was observed that pre-treatment with
Emodin enhances cytotoxicity of chemotherapeutic drugs in prostate cancer cells: the mechanisms involve ROS-mediated suppression of multidrug resistance and hypoxia inducible factor-1.
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The intrinsic or acquired resistance to multiple drugs (MDR) of cancer cells remains one of the main obstacles for chemotherapy. Development of small molecule targeting to hypoxia inducible factor-1 (HIF-1) has been recently proposed as strategy for treatments of drug-resistant solid tumors. In the
Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells.
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Emodin (EMO) possesses extensive pharmacological activities, which has been proven to exert the protective impact in diverse nervous system diseases. Nonetheless, whether EMO emerges a neuro-protective activity in hypoxic-evoked ischemic brain injury is still further probed. The intention of the
Aloe-emodin suppresses hypoxia-induced retinal angiogenesis via inhibition of HIF-1α/VEGF pathway.
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Background: Aloe-emodin (AE) has been reported to possess the antiangiogenic effect on laser induced choroidal neovascularization. AE inhibits the vessel formation in the zebrafish embryos. However, it is still unclear whether AE can alleviate neovascularization. Here, we investigated the inhibitory
Emodin and rhein decrease levels of hypoxia-inducible factor-1α in human pancreatic cancer cells and attenuate cancer cachexia in athymic mice carrying these cells.
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The transcription factor hypoxia-inducible factor-1 (HIF-1) consists of oxygen-sensitive HIF-1α and constitutive HIF-1β. HIF-1α is undetectable in normal cells, but cancer cells frequently express HIF-1α to support their growth, angiogenesis, and high glycolysis (also known as the Warburg effect).
Exploration of effects of emodin in selected cancer cell lines: enhanced growth inhibition by ascorbic acid and regulation of LRP1 and AR under hypoxia-like conditions.
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This study explores the link between the antiproliferative activity of emodin through the generation of reactive oxygen species (ROS) in various cancer cell lines and the expression of the androgen receptor (AR) in the prostate cancer cell lines LNCaP (androgen-sensitive) and PC-3
Emodin attenuates radioresistance induced by hypoxia in HepG2 cells via the enhancement of PARP1 cleavage and inhibition of JMJD2B.
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Radioresistance in the tumor and radiotoxicity in the non‑tumorous liver significantly restrict efficient radiotherapy of hepatocellular carcinoma (HCC). It is therefore important to study the radioresistance mechanism and development of radiosensitization to optimize the effect of irradiation on
Emodin and [6]-gingerol lessen hypoxia-induced embryotoxicities in cultured mouse whole embryos via upregulation of hypoxia-inducible factor 1α and intracellular superoxide dismutases.
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Excess hypoxia during embryonic organogenesis leads to developmental abnormalities and postnatal deficits. To determine whether emodin and [6]-gingerol affects hypoxia-induced anomalies during embryonic organogenesis, we cultured embryonic day 8.5 mouse embryos under hypoxic conditions (5% O(2)) for
Emodin Decreases Hepatic Hypoxia-Inducible Factor-1[Formula: see text] by Inhibiting its Biosynthesis.
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Hypoxia-inducible factor-1 (HIF-1) is an [Formula: see text] dimeric transcription factor. Because HIF-1[Formula: see text] is instable with oxygen, HIF-1 is scarce in normal mammalian cells. However, HIF-1[Formula: see text] is expressed in pathological conditions such as cancer and obesity.
Emodin prevents ethanol-induced developmental anomalies in cultured mouse fetus through multiple activities.
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BACKGROUND
Maternal alcohol ingestion on pregnant period causes fetal alcohol syndrome including psychological and behavioral problems, and developmental abnormality. In this study, we investigated the effect of emodin, an active anthraquinone component found in the roots and bark of the genus
Emodin inhibits proinflammatory responses and inactivates histone deacetylase 1 in hypoxic rheumatoid synoviocytes.
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Chronic inflammation of rheumatoid arthritis (RA) is promoted by proinflammatory cytokines and closely linked to angiogenesis. In the present study, we investigated the anti-inflammatory effects of emodin (1,3,8-trihydroxy-6-methyl-anthraquinone) isolated from the root of Rheum palmatum L. in
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