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emodin/hypoxia

הקישור נשמר בלוח
מאמריםניסויים קלינייםפטנטים
עמוד 1 מ 26 תוצאות

Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
Congenital heart disease (CHD) is a catastrophic disease. Emodin possesses biological properties in protecting against some diseases. Our study investigated to explore the effects of emodin on hypoxia-stimulated cardiomyocytes, which mimicked CHD in

Emodin protects against oxidative stress and apoptosis in HK-2 renal tubular epithelial cells after hypoxia/reoxygenation.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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).
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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.

רק משתמשים רשומים יכולים לתרגם מאמרים
התחבר הרשם
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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