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parthenolide/necrosis
Il collegamento viene salvato negli appunti
Pagina 1 a partire dal 72 risultati
[Effect of parthenolide on serum expressions of interleukin-1beta and tumor necrosis factor-alpha in rabbits with knee osteoarthritis].
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OBJECTIVE
To observe the therapeutic effect of parthenolide (PTL) on rabbit knee arthritis (KOA) and its effects on serum expression of interleukin-1beta (IL-1beta) and contents of tumor necrosis factor-alpha (TNF-alpha).
METHODS
Eight rabbits were randomly selected from 40 healthy pure-bred New
[Parthenolide inhibits tumor necrosis factor-alpha induced catabolism of aggrecan in chondrocytes in osteoarthritis: in vitro experiment with cultured human chondrocytes].
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OBJECTIVE
To investigate the effect of parthenolide (PAR) on the tumor necrosis factor (TNF)-alpha induced aggrecan catabolism of chondrocytes in osteoarthritis (OA).
METHODS
Human chondrocytes were obtained from the condyles of femur of OA patients undergoing knee joint replacement during
Antitumor agent parthenolide reverses resistance of breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through sustained activation of c-Jun N-terminal kinase.
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The antitumor activity of the sesquiterpene lactone parthenolide, an active ingredient of medicinal plants, is believed to be due to the inhibition of DNA binding of transcription factors NF-kappaB and STAT-3, reduction in MAP kinase activity and the generation of reactive oxygen. In this report, we
Parthenolide Sensitizes Human Colorectal Cancer Cells to Tumor Necrosis Factor-related Apoptosis-inducing Ligand through Mitochondrial and Caspase Dependent Pathway.
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OBJECTIVE
Combination therapy utilizing tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in conjunction with other anticancer agents, is a promising strategy to overcome TRAIL resistance in malignant cells. Recently, parthenolide (PT) has proved to be a promising anticancer
Parthenolide and DMAPT exert cytotoxic effects on breast cancer stem-like cells by inducing oxidative stress, mitochondrial dysfunction and necrosis.
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Triple-negative breast cancers (TNBCs) are aggressive forms of breast carcinoma associated with a high rate of recidivism. In this paper, we report the production of mammospheres from three lines of TNBC cells and demonstrate that both parthenolide (PN) and its soluble analog
NF-kappaB inhibitor sesquiterpene parthenolide induces concurrently atypical apoptosis and cell necrosis: difficulties in identification of dead cells in such cultures.
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BACKGROUND
Apoptosis and necrosis ("accidental cell death") are distinct modes of cell death. The feature that often distinguishes apoptotic from necrotic cells is preservation of the plasma membrane integrity, reflected by ability of the former cells to exclude cationic dyes such as propidium
Thermosensitization by parthenolide in human lung adenocarcinoma A549 cells and p53- and hsp72-independent apoptosis induction via the nuclear factor-kappaB signal pathway.
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The thermo-enhancement effects of the sesquiterpene lactone parthenolide (PTL), which targets the transcription factor nuclear factor-kappaB (NF-kappaB), and hyperthermia at 40, 42 and 44 degrees C on the human lung adenocarcinoma A549 cell line were investigated in vitro. Thermotherapy using a
Parthenolide inhibits pro-inflammatory cytokine production and exhibits protective effects on progression of collagen-induced arthritis in a rat model.
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OBJECTIVE
Progressive destruction of synovial joint cartilage and bone occurs in pathological conditions such as rheumatoid arthritis (RA) because of the overproduction of pro-inflammatory cytokines and activation of nuclear factor kappa B (NF-κB). Through the screening of NF-κB inhibitors by a
Pathway-specific profiling identifies the NF-kappa B-dependent tumor necrosis factor alpha-regulated genes in epidermal keratinocytes.
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Identification of tumor necrosis factor alpha (TNF alpha) as the key agent in inflammatory disorders led to new therapies specifically targeting TNF alpha and avoiding many side effects of earlier anti-inflammatory drugs. However, because of the wide spectrum of systems affected by TNF alpha, drugs
Parthenolide reduces cisplatin-induced renal damage.
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Inflammatory events contribute to cisplatin-induced renal damage. Cisplatin promotes increased production of reactive oxygen species, which can activate nuclear factor-kappaB (NF-kappaB) that lead to increased expression of proinflammatory mediators which could intensify the cytotoxic effects of
Inhibition of DMXAA-induced tumor necrosis factor production in murine splenocyte cultures by NF-kappaB inhibitors.
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The induction of cytokine synthesis within tumor tissue is a key component of the antivascular action of 5,6-dimethylxanthenone-4-acetic acid (DMXAA) in murine tumors. We previously showed that DMXAA alone induced only low amounts of tumor necrosis factor (TNF) in cultured spleen cells, but the
Paclitaxel sensitivity of breast cancer cells with constitutively active NF-kappaB is enhanced by IkappaBalpha super-repressor and parthenolide.
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The transcription factor nuclear factor-kappaB (NF-kappaB) regulates genes important for tumor invasion, metastasis and chemoresistance. Normally, NF-kappaB remains sequestered in an inactive state by cytoplasmic inhibitor-of-kappaB (IkappaB) proteins. NF-kappaB translocates to nucleus and activates
Parthenolide reduces cell proliferation and prostaglandin E2 [corrected] in human endometriotic stromal cells and inhibits development of endometriosis in the murine model.
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OBJECTIVE
To evaluate the effects of parthenolide on human endometriotic cells and murine endometriotic lesions.
METHODS
Experimental study.
METHODS
University hospital and laboratory of animal science.
METHODS
Twenty women with ovarian endometrioma and 30 mice.
METHODS
Ectopic endometrial tissue
Potentiation of arsenic trioxide cytotoxicity by Parthenolide and buthionine sulfoximine in murine and human leukemic cells.
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OBJECTIVE
To possibly increase the in vitro cytotoxic activity of arsenic trioxide (ATO) by combining it with Parthenolide (PRT), a known NF-kappaB inhibitor and buthionine sulfoximine (BSO), an inhibitor of gamma-glutamylcysteine synthetase.
METHODS
Several cell lines representing various
Parthenolide Has Negative Effects on In Vitro Enhanced Osteogenic Phenotypes by Inflammatory Cytokine TNF-α via Inhibiting JNK Signaling
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Nuclear factor kappa B (NF-κB) regulates inflammatory gene expression and represents a likely target for novel disease treatment approaches, including skeletal disorders. Several plant-derived sesquiterpene lactones can inhibit the activation of NF-κB. Parthenolide (PTL) is an abundant sesquiterpene
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