triptolide/vefjadrep

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PG490 (triptolide) cooperates with tumor necrosis factor-alpha to induce apoptosis in tumor cells.

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Progress in the treatment of solid tumors has been slow and sporadic. The efficacy of conventional chemotherapy in solid tumors is limited because tumors frequently have mutations in the p53 gene. Also, chemotherapy only kills rapidly dividing cells. Members of the tumor necrosis factor (TNF)

[Effects of triptolide on cell proliferation and regulation of Ras-MAPKs pathway in synoviocytes induced by tumor necrosis factor].

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OBJECTIVE To investigate the effects of triptolide on proliferation and regulation of ras-MAPKs pathway in human fibroblast-like synoviocytes of rheumatoid arthritis (RA-HFLS) treated with tumor necrosis factor (TNF-alpha). METHODS RA-HFLS were cultured with TNF-alpha in the presence or absence of

Triptolide sensitizes human breast cancer cells to tumor necrosis factor‑α‑induced apoptosis by inhibiting activation of the nuclear factor‑κB pathway.

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Tumor necrosis factor‑α (TNF‑α) can act as either a tumor promoter, linking inflammation with carcinogenesis, or a tumor inhibitor, inducing cancer cell death. However, several types of cancer, including breast cancer, are resistant to TNF‑α therapy. Triptolide, a diterpene triepoxide, has been

Synergistic cytotoxicity and apoptosis induced in human cholangiocarcinoma cell lines by a combined treatment with tumor necrosis factor-alpha (TNF-alpha) and triptolide.

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Cholangiocarcinoma is known to be relatively resistant to chemotherapy. One alternative approach is to use a combination of an immunomodulating agent with an anticancer drug. Here we studied the synergistic actions of TNF-alpha and triptolide (a diterpene epoxide prepared from Tripterygium

[Effect of Triptolide on Cardiac Function in Arthritic Rats and Its Mechanism].

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To observe the changes of cardiac function in arthritic rats and the effect of triptolide on it.

Methods

Forty rats were divided in random into normal control (NC) group, model control (MC) group, leflunomide (LEF) group and triptolide (TP) group.

Triptolide sensitizes pancreatic cancer cells to TRAIL-induced activation of the death receptor pathway.

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The tumor necrosis factor related apoptosis-inducing ligand (TRAIL) causes cancer cell death, but many cancers, including pancreatic cancer, are resistant to TRAIL therapy. A combination of TRAIL and the diterpene triepoxide, triptolide, is effective in inducing pancreatic cancer cell death.

Effect of Triptolide on retinal ganglion cell survival in an optic nerve crush model.

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Optic nerve crush model could be used to investigate the mechanism of neuronal survival and axonal regeneration in central nervous system. Triptolide, a Chinese herb extract with anti-inflammatory and immunosuppressive activities, has shown neuron protective functions in nervous system. In this

Triptolide sensitizes TRAIL-induced apoptosis in prostate cancer cells via p53-mediated DR5 up-regulation.

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Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising agent for cancer therapy. However, a number of prostate cancer cells exhibit high resistance to TRAIL effect. In this study, we found that Triptolide, a Chinese medicine, significantly sensitizes prostate cancer cells to

Triptolide Reduces the Required Dose of Tacrolimus by Attenuating Inflammation, Enhancing Immunosuppression, and Increasing Donor Chimerism in a Heterotopic Hindlimb Transplantation Model.

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BACKGROUND Induction of tolerance and minimizing the toxicity of immunosuppression are two fundamental goals in vascularized composite allotransplantation. Accumulating data indicate that triptolide is an agent that may have the capacity to suppress inflammation and immunologic rejection. METHODS A

Triptolide and TRAIL combination enhances apoptosis in cholangiocarcinoma.

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BACKGROUND Cholangiocarcinoma originates from bile duct epithelial cells in the intrahepatic and extrahepatic biliary system. We recently observed that triptolide (a diterpenoid triepoxide) is effective in inducing apoptosis in pancreatic tumors. Death receptors 4 and 5 are overexpressed in several

Protection effect of triptolide to liver injury in rats with severe acute pancreatitis.

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BACKGROUND The high mortality of patients with severe acute pancreatitis (SAP) is due to multiorgan dysfunction. The mechanisms of SAP are still obscure. The aim of this study was to investigate the role of nuclear factor-kappa B (NF-kappaB) activation in rats with SAP associated with liver injury

Triptolide inhibits the progression of atherosclerosis in apolipoprotein E-/- mice.

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Atherosclerosis, the major cause of cardiovascular disease, is accompanied by a chronic inflammatory response during the disease. Triptolide (TPL) is an active natural compound that has been demonstrated to possess anti-inflammatory activities in various cell types. However, the effects of TPL on

Triptolide protects dopaminergic neurons from inflammation-mediated damage induced by lipopolysaccharide intranigral injection.

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Converging lines of evidence suggest that neuroinflammatory processes may account for the progressive death of dopaminergic neurons in Parkinson's disease (PD). Therefore, anti-inflammatory strategies have attracted much interest for their potential to prevent further deterioration of PD. Our

Antifibrotic effects of triptolide on hepatic stellate cells and dimethylnitrosamine-intoxicated rats.

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Triptolide (C₃₈H₄₂O₆N₂, TP, a diterpene triepoxide derived from Tripterygium wilfordii Hook F.), is a potent immunosuppresive and antiinflammatory agent. The present study investigated whether TP exerted antihepatofibrotic effects in vitro and in vivo. A cell line of rat hepatic stellate cells

Triptolide sensitizes resistant cholangiocarcinoma cells to TRAIL-induced apoptosis.

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BACKGROUND Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL/Apo2L) promotes apoptosis by binding to transmembrane receptors. It is known to induce apoptosis in a wide variety of cancer cells, but TRAIL-resistant cancers have also been documented. In this study, the relative resistance

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