taxol a/inflammation

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Taxol, a microtubule-stabilizing antineoplastic agent, induces expression of tumor necrosis factor alpha and interleukin-1 in macrophages.

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Taxol, a naturally occurring diterpene with antitumor activity, induces tubulin polymerization to generate abnormally stable and nonfunctional microtubules. Previously, we showed that taxol has lipopolysaccharide (LPS)-like effects on macrophages. As LPS is a potent inducer of macrophage cytokine

Granzyme A and thrombin differentially promote the release of interleukin-8 from alveolar epithelial A549 cells.

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Some of extracellular serine proteases with trypsin-like specificity of cleavage have been known to increase the release of inflammatory mediators from various cell types. For instance, two well-known trypsin-like serine proteases circulating in blood, granzyme A (GrA) and thrombin, have been found

Oxidant-induced intestinal barrier disruption and its prevention by growth factors in a human colonic cell line: role of the microtubule cytoskeleton.

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Reactive oxygen metabolites (ROM) are increased in the inflamed mucosa of inflammatory bowel disease (IBD) and may contribute to loss of intestinal barrier function in this disorder. Growth factors (GF) are protective. But the mechanisms of disruption and protection remain elusive. In the present

Effects of Electrical Stimulation on Peripheral Nerve Regeneration in a Silicone Rubber Conduit in Taxol-Treated Rats.

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Taxol, a type of antimitotic agent, could modulate local inflammatory conditions in peripheral nerves, which may impair their regeneration and recovery when injured. This study provided in vivo trials of silicone rubber chambers to bridge a long 10 mm sciatic nerve defect in taxol-treated rats. It

Cellular detachment and deformation induce IL-8 gene expression in human bronchial epithelial cells.

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Neutrophil elastase (NE) is known to be one of the most potent proteases capable of deforming and detaching human bronchial epithelial cells (BECs) and inducing IL-8 gene expression. However, mechanisms of NE-induced IL-8 gene expression are unclear, especially with respect to how they relate to

A3 adenosine receptor agonist prevents the development of paclitaxel-induced neuropathic pain by modulating spinal glial-restricted redox-dependent signaling pathways.

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Chemotherapy-induced peripheral neuropathy accompanied by chronic neuropathic pain is the major dose-limiting toxicity of several anticancer agents including the taxane paclitaxel (Taxol). A critical mechanism underlying paclitaxel-induced neuropathic pain is the increased production of

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