Radiation-protective and platelet aggregation inhibitory effects of five traditional Chinese drugs and acetylsalicylic acid following high-dose γ-irradiation

Wang, Hong-Fu; Li, Xingdi; Yong-Ming, Chen; Yuan, Liang; Foye, William O.

doi:10.1016/0378-8741(91)90040-k

Cited by 8 publications

(1 citation statement)

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“…An irradiated endothelium indeed increases the synthesis of von Willebrand factor (vWF) [140–144] and platelet-activating factor [145] while reducing thrombomodulin [68, 146, 147] and prostacyclin production [108, 117, 148], as well as its fibrinolytic activity [149–151]. These changes promote platelet adhesion and aggregation and the development of platelet–fibrin thrombi [152–155]. Cytokines produced during endothelial activation (e.g., IL-6 and CCL2) further affect hemostasis by inducing the expression of tissue factor, tissue plasminogen activator, and vWF [156–158].…”

Section: Procoagulatory and Prothrombotic Phenotypementioning

confidence: 99%

Pathological effects of ionizing radiation: endothelial activation and dysfunction

Baselet

Sonveaux

Baatout

et al. 2018

Cell. Mol. Life Sci.

195

141

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The endothelium, a tissue that forms a single layer of cells lining various organs and cavities of the body, especially the heart and blood as well as lymphatic vessels, plays a complex role in vascular biology. It contributes to key aspects of vascular homeostasis and is also involved in pathophysiological processes, such as thrombosis, inflammation, and hypertension. Epidemiological data show that high doses of ionizing radiation lead to cardiovascular disease over time. The aim of this review is to summarize the current knowledge on endothelial cell activation and dysfunction after ionizing radiation exposure as a central feature preceding the development of cardiovascular diseases.

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Section: Procoagulatory and Prothrombotic Phenotypementioning

confidence: 99%

Pathological effects of ionizing radiation: endothelial activation and dysfunction

Baselet

Sonveaux

Baatout

et al. 2018

Cell. Mol. Life Sci.

195

141

View full text Add to dashboard Cite

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Radioprotective Agents

Murray¹,

McBride²

2000

Kirk-Othmer Encyclopedia of Chemical Technology

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Developments in understanding agents having activity for the prevention and treatment of radiation injuries are discussed. Chemical radioprotectors have long been dominated by thiol compounds and their phosphorothioate derivatives. Advances have been made to understanding the fundamental mechanisms by which these agents protect against cell killing. The finding that thiols also protect against radiation‐induced mutations and transformation has generated considerable interest. Mutations may be expressed as undesirable late effects in radiotherapy. Such effects are reviewed herein, as is the enormous literature that has accumulated relating to preclinical and clinical studies of the effects of phosphorothioates in animals and humans. A number of nonthiol radioprotective agents, including protease inhibitors, vitamins, metalloelements, and calcium antagonists, are also discussed. There has been a virtual explosion of interest in biological, as opposed to chemical, modifiers of radiation injury. These biologics include cytokines such as interleukin 1 and granulocyte colony‐stimulating factor, eicosanoids such as prostaglandins and leukotrienes, and steroids/glucocorticoids such as dexamethasone and methylprednisolone. In addition, an array of immunomodulatory agents such as glucan and endotoxin have been described, which act by nonspecifically enhancing immunological and hemopoietic responses. Although some of these biologics act best when given prior to irradiation, many of them can modulate radiation injury when given after irradiation, presumably by affecting the recovery and repopulation of critical tissue elements. Biologics thus afford an opportunity for therapeutic intervention following accidental radiation exposure as well as in radiation therapy. Demonstrations of a potential therapeutic advantage from combining chemical radioprotectors, which decrease the extent of initial damage, with nonthiol biologics, which accelerate tissue recovery, provides an attractive approach to radioprotection which also minimizes toxicity.

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Radiosensitizers and Radioprotective Agents

Bump¹,

Hoffman²,

Foye

2003

Burger's Medicinal Chemistry and Drug Discovery

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Various approaches have been developed for diminishing the effects of radiation on normal tissues or enhancing tumor cell killing by ionizing radiation. An important potential use for these agents is to modify the outcome of radiation therapy. Potential radioprotectors or radiosensitizers are organized in this review according to mechanism of action. Most of the agents studied are believed to act by reacting with DNA radicals that are produced within milliseconds of exposure to ionizing radiation. According to this mechanism, protectors restore a single electron to electron‐deficient radicals, preventing degradation of the structure of DNA, whereas sensitizers, such as molecular oxygen or nitroimidazoles, form adducts with these radicals, resulting in damage fixation. WR2721 (Ethyol) is the best‐characterized chemical radioprotector. Preferential activation of WR2721 in certain normal tissues by removal of a phosphate group provides a rationale for selective protection of these tissues. Cytokines and biological modifiers represent an important emerging class of radioprotectors that may be particularly useful in modifying bone marrow injury. Nitroimidazoles have been the most widely studied chemical radiosensitizers. Although clinical results with nitroimidazoles have not been impressive, the potential for this approach has not been fully explored, given that the doses that can be administered have been limited by drug toxicity and supplemental strategies, such as concurrent depletion of endogenous protectors, have not been explored in the clinic. Modifiers of tumor oxygenation represent an important class of radiosensitizers that are currently generating considerable clinical interest. RSR13, a modifier of the oxygen affinity of hemoglobin, is highlighted as an example of the process of drug development for this type of agent.

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Radiation-protective and platelet aggregation inhibitory effects of five traditional Chinese drugs and acetylsalicylic acid following high-dose γ-irradiation

Cited by 8 publications

References 1 publication

Pathological effects of ionizing radiation: endothelial activation and dysfunction

Pathological effects of ionizing radiation: endothelial activation and dysfunction

Radioprotective Agents

Radiosensitizers and Radioprotective Agents

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