trichosanthin/necroză

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Inhibition of Th1- and enhancement of Th2-initiating cytokines and chemokines in trichosanthin- treated macrophages.

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Trichosanthin (TCS), the major effective component from Chinese herb Trichosanthes Kirilowii Maxim, is also a potent allergen. Our previous work has shown that TCS can upregulate interleukin-4 (IL-4) and interleukin-13 (IL-13) while inhibit interferon-gamma (IFN-gamma) in mesenteric lymph node cells

Studies on the mechanisms of abortion induction by Trichosanthin.

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Radix trichosanthis, an abortifacient drug of mid-gestation, is extracted from the root tuber of Trichosanthes kirilowii Maxim, Cucurbitaceae. Its purified effective principle is a basic protein of molecular weight of approximately 18,000 and is named trichosanthin. By authorization it has been

Ectopic pregnancy treated with trichosanthin. Clinical analysis of 71 patients.

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Pathological studies on the aborted materials after the administration of trichosanthin at the end of mid-term gestation have revealed that there is an extensive coagulative necrosis of the trophoblastic tissue of the placental villi. In 1971, we first used trichosanthin successfully to treat

Roles of IL-4 and other factors in the trichosanthin-induced ovalbumin-specific IgE response.

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OBJECTIVE To study the mechanism of trichosanthin (TCS)-induced ovalbumin (OVA)-specific immunoglobulin E (IgE) response in vivo. METHODS To determine whether interleukin-4 (IL-4) was involved in TCS-induced IgE production, TCS and OVA co-immunized mice were treated with anti-IL-4 monoclonal

Trichosanthin-stimulated dendritic cells induce a type 2 helper T lymphocyte response through the OX40 ligand.

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BACKGROUND Trichosanthin (TCS) induces a type 2 helper T lymphocyte (T(H)2) immune response that leads to the production of TCS-specific immunoglobulin (Ig) E and a subsequent allergic reaction in vivo. However, events immediately following treatment with TCS are poorly understood. OBJECTIVE We

Immunolesioning of nerve growth factor p75 receptor-containing neurons in the rat brain by a novel immunotoxin: anti-p75-anti-mouse IgG-trichosanthin conjugates.

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In the present study, a comparison of potency between a commercially available immunotoxin, 192-immunoglobulin-SAP (192-IgG), and a novel immunotoxin produced in our laboratory, anti-p75-anti-mouse IgG-trichosanthin conjugates (p75-TCS), was conducted. Both of the immunotoxins were specific for

Neurological reactions in HIV-infected patients treated with trichosanthin.

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Trichosanthin is a ribosome-inactivating protein that is being studied as a possible treatment for patients infected with human immunodeficiency virus (HIV). We report the clinical and pathological features in two patients who experienced neurological reactions to trichosanthin. Both patients were

Possible mechanisms of trichosanthin-induced apoptosis of tumor cells.

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Trichosanthin (TCS) is a type I ribosome-inactivating protein that is isolated from the root tubers of the Chinese medicinal herb Trichosanthes kirilowii Maximowicz. TCS has been used as an abortifacient for 1,500 years in China because of its high toxicity on trophoblasts. Over the past 20 years,

Low concentrations of trichosanthin induce apoptosis and cell cycle arrest via c-Jun N-terminal protein kinase/mitogen-activated protein kinase activation.

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Trichosanthin (TCS) is a type I ribosome--inactivating protein, which inhibits cell viability in human epithelial type 2 (HEp-2) and AMC-HN-8 human laryngeal epidermoid carcinoma cells. Although TCS is a potential chemotherapeutic agent, its mechanism of action remains to be elucidated. In the

Trichosanthin enhances sensitivity of non-small cell lung cancer (NSCLC) TRAIL-resistance cells.

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Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) has a specific antitumour activity against many malignant tumours. However, more than half of lung cancer cells are resistant to TRAIL-relevant drugs. Trichosanthin (TCS) is a traditional Chinese medicine with strong inhibitive effects

Mechanism of the specific neuronal toxicity of a type I ribosome-inactivating protein, trichosanthin.

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The aim was to study the mechanism of neuronal toxicity, the cellular pathway, and the glial cell reactions induced by trichosanthin (TCS), a type I ribosome-inactivating protein (RIP). Ricin A chain (RTA) was included for comparison. TCS, RTA, and fluorescein isothiocyanate (FITC)-labeled TCS and

Different neuronal toxicity of single-chain ribosome-inactivating proteins on the rat retina.

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OBJECTIVE To investigate the neurotoxicity of two structurally similar single chains of ribosome-inactivating proteins (RIPs): trichosanthin (TCS) and ricin A chain (RTA). METHODS TCS, RTA and Ricinus communis agglutinin (RCA, a multi-chain RIP for comparison) were separately injected into rat eyes.

Different in vitro toxicities of structurally similar type I ribosome-inactivating proteins (RIPs).

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This study was aimed at investigating and comparing the cytotoxicities of two structurally similar type I RIPs, namely trichosanthin (TCS) and free ricin A chain (RTA). A type II RIP, namely Ricinus communis agglutinin (RCA), was also included for comparison. The three RIPs were added separately to

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