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glycyrrhizin/atrofia
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 23 risultati
Glycyrrhizin suppresses inflammation and cell apoptosis by inhibition of HMGB1 via p38/p-JUK signaling pathway in attenuating intervertebral disc degeneration.
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Intervertebral disc degeneration (IDD) is associated with the nucleus pulposus (NP) cells inflammation and apoptosis. Previous studies have shown that glycyrrhizin (GL) is a valid inhibitor of the high-mobility group box-1 gene (HMGB1) which expressed much higher in an inflammatory condition.
[Effects of glycyrrhizin on dexamethasone-induced atrophy of the adrenal cortex--histopathological and enzyme histochemical studies].
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Stimulation of rat adrenocortical cells by glycyrrhizin with special reference to its inhibitory effect on dexamethasone-induced atrophy of the adrenal cortex.
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Glycyrrhizin (licorice)-induced hypokalemic myopathy. Report of 2 cases and review of the literature.
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Fifty-nine cases of glycyrrhizin (licorice)-induced hypokalemic myopathy (GIHM), 2 females treated in our departments (85 and 73 years old) and 57 cases reported in the literature were studied, and conditions leading to the onset, factors, clinical manifestations, laboratory assessments, muscle
Histopathologic and MRI findings in hypokalemic myopathy induced by glycyrrhizin.
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Histopathologic studies and magnetic resonance images of the leg muscles were conducted in two patients with glycyrrhizin-induced hypokalemic myopathy (GHM). Muscle biopsy showed myopathic changes and vacuolated fibers with light microscopy, and dilatation of the sarcoplasmic reticulum, various
Selective activation of extrathymic T cells in the liver by glycyrrhizin.
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Extrathymic pathways for T cell differentiation were recently demonstrated in the liver, intestine and omentum. In this study, glycyrrhizin (GL), a plant extract was investigated as to its effect on extrathymic T cells in the liver of mice. A new method using anti-LFA-1 mAb in conjunction with
Glycyrrhizin protects IGFBP-3 knockout mice from retinal damage.
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We previously reported that insulin-like growth factor binding protein 3 (IGFBP-3) knockout (KO) mice have neuronal and vascular damage to the retina. We also reported that glycyrrhizin, a high mobility growth factor binding protein 1 (HMGB1) inhibitor, is protective to the diabetic retina. In this
Glycyrrhizin inhibits osteoarthritis development through suppressing the PI3K/AKT/NF-κB signaling pathway in vivo and in vitro.
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Osteoarthritis (OA) is a serious and frequently occurring disease in the elderly, characterized by cartilage degeneration and proliferation of bone structure. Glycyrrhizin, a compound extracted from licorice, has been reported to have various important biological activities, such as antioxidant
In-vivo evidence that high mobility group box 1 exerts deleterious effects in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model and Parkinson's disease which can be attenuated by glycyrrhizin.
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High-mobility group box 1 (HMGB1) is a nuclear and cytosolic protein that is released during tissue damage from immune and non-immune cells - including microglia and neurons. HMGB1 can contribute to progression of numerous chronic inflammatory and autoimmune diseases which is mediated in part by
Hepatic protection by glycyrrhizin and inhibition of iNOS expression in concanavalin A-induced liver injury in mice.
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OBJECTIVE
In this study, the possible protective effect of glycyrrhizin (GL), an active compound derived from licorice root, was examined on T cell-mediated liver injury in mice.
METHODS
Mice were subjected to liver injury by intravenous injection of concanavalin A (Con A). They had been treated
Glycyrrhizin protects against sodium iodate-induced RPE and retinal injury though activation of AKT and Nrf2/HO-1 pathway.
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Glycyrrhizin is a bioactive triterpenoid saponin extracted from a traditional Chinese medicinal herb, glycyrrhiza, and has been reported to protect the organs such as liver and heart from injuries. However, there is no report about the effects of glycyrrhizin on atrophic age-related macular
Candesartan and glycyrrhizin ameliorate ischemic brain damage through downregulation of the TLR signaling cascade.
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Stroke is the second leading cause of death in industrialized countries and the most frequent cause of permanent disability in adults worldwide. The final outcome of stroke is determined not only by the volume of the ischemic core, but also by the extent of secondary brain damage inflicted to
Suspected Virus-Inducing Severe Acute Respiratory Distress Syndrome Treated by Multimodal Therapy Including Extracorporeal Membrane Oxygenation and Immune Modulation Therapy
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A 44-year-old man who had been feeling general fatigue was found in an unconscious state on the same day. He had no remarkable medical history. On arrival at the hospital, his Glasgow Coma Scale was E1V2M3; he had tachycardia and hypertension, was afebrile, and in a severe hypoxic state. His
Acute renal failure following hypokalemic rhabdomyolysis due to chronic glycyrrhizic acid administration.
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A 72-year-old man developed acute renal failure (ARF) following severe hypokalemic rhabdomyolysis. The hypokalemia was due to chronic glycyrrhizin (glycyrrhizic acid) administration. Although glycyrrhizin-induced hypokalemic rhabdomyolysis has been occasionally reported, the association of this type
Inhibition of HMGB1 protects the retina from ischemia-reperfusion, as well as reduces insulin resistance proteins.
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The role of inflammation in diabetic retinal amage is well accepted. While a number of cytokines and inflammatory mediators are responsible for these changes, upstream regulators are less well studied. Additionally, the role for these upstream mediators in retinal health is unclear. In this study,
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