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piperlongumine/nekrose
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10 Ergebnisse
Two-stage nanoparticle delivery of piperlongumine and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) anti-cancer therapy.
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This study outlines a drug delivery mechanism that utilizes two independent vehicles, allowing for delivery of chemically and physically distinct agents. The mechanism was utilized to deliver a new anti-cancer combination therapy consisting of piperlongumine (PL) and TRAIL to treat PC3 prostate
Synthesis and evaluation of N-heteroaromatic ring-based analogs of piperlongumine as potent anticancer agents.
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Piperlongumine (PL) selectively targets a wide spectrum of cancer cells and induces their death by triggering various pathways, including apoptosis, necrosis and autophagy. However, the poor solubility is a serious concern for intensive study and clinical application. We synthesized its analogs 1-9
Piperlongumine and immune cytokine TRAIL synergize to promote tumor death.
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Malignant transformation results in increased levels of reactive oxygen species (ROS). Adaption to this toxic stress allows cancer cells to proliferate. Recently, piperlongumine (PL), a natural alkaloid, was identified to exhibit novel anticancer effects by targeting ROS signaling. PL induces
Novel candidate drugs in anti-tumor necrosis factor refractory Crohn's diseases: in silico study for drug repositioning
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Biologicals like anti-tumor necrosis factor (TNF) therapy for Crohn's disease (CD) are safe and effective but there is a significant rate of primary and secondary nonresponse in the patients. In this study, we applied a computational approach to discover novel drug therapies for anti-TNF refractory
Piperlongumine inhibits neuroinflammation via regulating NF-κB signaling pathways in lipopolysaccharide-stimulated BV2 microglia cells.
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Inflammatory processes in the central nervous system are feature among biological reactions to harmful stimuli such as pathogens and damaged cells. In resting conditions, microglia are involved in immune surveillance and brain homeostasis. However, the activation of abnormal microglia can be
Piperlongumine reduces ovalbumin‑induced asthma and airway inflammation by regulating nuclear factor‑κB activation.
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Asthma is a common chronic airway inflammatory disease, characterized by airway inflammation and remodeling. Piperlongumine (PL) has a number of physiological and pharmacological properties. However, the anti‑asthmatic effect of PL has not been reported to date. In the present study, ovalbumin (OVA)
Piperlongumine rapidly induces the death of human pancreatic cancer cells mainly through the induction of ferroptosis.
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Pancreatic cancer is one of the most lethal types of cancer with a mortality rate of almost 95%. Treatment with current chemotherapeutic drugs has limited success due to poor responses. Therefore, the development of novel drugs or effective combination therapies is urgently required. Piperlongumine
Piperlongumine attenuates collagen-induced arthritis via expansion of myeloid-derived suppressor cells and inhibition of the activation of fibroblast-like synoviocytes.
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Piperlonguminine (PL), a key compound from the Piper longum fruit, is known to exhibit anti‑tumor and anti‑inflammatory activities. However, little is known about its effects on collagen‑induced arthritis (CIA). Fibroblast‑like synoviocytes (FLS) have a pivotal role in the development of rheumatoid
The role of ferroptosis in digestive system cancer.
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Ferroptosis is a type of regulated cell death dependent on iron and reactive oxygen species. Ferroptosis is distinct from other cell death modalities, including apoptosis, autophagy and necrosis. Dysregulated ferroptosis has been implicated in a number of diseases, including neuropathy, ischemia
Nanotherapeutics interfere with cellular redox homeostasis for highly improved photodynamic therapy.
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Redox homeostasis inside malignant cells is a defense mechanism against the reactive oxygen species (ROS)-induced therapy means, but little importance has been paid to this innate barrier. The present study intends to make cancer cells more sensitive to the ROS-induced therapy by disturbing cellular
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