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Drug: Dexamethasone

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Total 8 results found since Jan 2013.

Bim downregulation by activation of NF- κB p65, Akt, and ERK1/2 is associated with adriamycin and dexamethasone resistance in multiple myeloma cells
In this study, we examined the MDR mechanism in adriamycin- and dexamethasone-resistant cells. RPMI8226/ADM, ARH-77/ADM, RPMI8226/DEX, and ARH-77/DEX cells exhibited enhanced nuclear factor κB (NF-κB) p65, Akt, and extracellular signal-regulated kinase 1/2 (ERK1/2) activation. Combination treatment with NF-κB p65, phosphoinositide 3-kinase (PI3K), and mitogen-activated protein kinase 1/2 (MEK1/2) inhibitors resensitized to adriamycin and dexamethasone via increased Bim expression. A lthough treatment with MDR1 or Survivin siRNA did not overcome adriamycin and dexamethasone resistance in RPMI8226/ADM and RPMI8226/DEX cel...
Source: Clinical and Experimental Medicine - November 30, 2022 Category: Research Source Type: research

Serum/glucocorticoid ‐regulated kinase 1‐targeted transient receptor potential oxalate subtype 1 regulates bladder smooth muscle cell proliferation due to bladder outlet obstruction in mice via activated T cell nuclear factor transcription factor 2
In this study, SGK1 targeted TRPV1 to regulate the proliferation of MBSMCs mediated by BOO in mice through NFAT2 and then affected the process of b ladder remodeling after BOO. This finding may provide a strategy for BOO drug target screening.
Source: IUBMB Life - February 21, 2022 Category: Research Authors: Jiangshu He, Jin Yang, Lin Chen, Pinglin He, Xun Liu, Kai Wang, Taotao Dong, Jia Li, Xudong Ma, Amend Bastian, Stenzl Arnulf Tags: RESEARCH COMMUNICATION Source Type: research

SGK1 ‐targeted TRPV1 regulates bladder smooth muscle cell proliferation due to BOO in mice via NFAT2
ConclusionIn this study, SGK1 targeted TRPV1 to regulate the proliferation of MBSMCs mediated by BOO in mice through NFAT2 and then affected the process of bladder remodeling after BOO. This finding may provide a strategy for BOO drug target screening.This article is protected by copyright. All rights reserved.
Source: IUBMB Life - February 12, 2022 Category: Research Authors: Jiangshu He, Jin Yang, Lin Chen, Pinglin He, Xun Liu, Kai Wang, Taotao Dong, Jia Li, Xudong Ma, Amend Bastian, Stenzl Arnulf Tags: RESEARCH COMMUNICATION Source Type: research

Decrease of GSK3 β Ser-9 Phosphorylation Induced Osteoblast Apoptosis in Rat Osteoarthritis Model
AbstractNowadays, the cumulative intake of glucocorticoids has become the most common pathogenic factor for non-traumatic osteonecrosis of the femoral head (ONFH). Apoptosis of osteoblasts is considered as the main reason of ONFH at the molecular level. Glycogen synthase kinase 3 β (GSK3β) is an important regulator of cellular differentiation and apoptosis pathway, which can modulate the balance between osteoblasts and osteoclasts. Several studies have reported about its function in osteoporosis, but little is known about it in osteonecrosis. In our study, lipopolysacchari de and methylprednisolone were utilized to estab...
Source: Journal of Huazhong University of Science and Technology -- Medical Sciences -- - January 31, 2019 Category: Research Source Type: research

MAPK Signaling has Stage-dependent Osteogenic Effects on Human Adipose-derived Stem Cells in vitro.
CONCLUSIONS: It is likely that MAPK signaling plays a significant role in ASC osteogenesis, affecting differentiation in kinase- and stage-specific manners. PMID: 28398098 [PubMed - as supplied by publisher]
Source: Connective Tissue Research - April 13, 2017 Category: Research Tags: Connect Tissue Res Source Type: research

Suppression of cytokine production by glucocorticoids is mediated by MKP-1 in human lung epithelial cells
In conclusion, these data suggest that dexamethasone increases MKP-1 expression and th is results in the suppression of p38 MAPK signaling leading to the inhibition of cytokine production in human bronchial epithelial cells. These results point to the role of MKP-1 as an important factor in the therapeutic effects of glucocorticoids in the treatment of inflammatory lung diseases.
Source: Inflammation Research - March 14, 2017 Category: Research Source Type: research