Atherosclerosis is an inflammatory disease causing great morbidity and mortality in the Western world. To increase the anti-inflammatory action and decrease adverse effects of glucocorticoids (PLP), a nanomedicinal liposomal formulation of this drug (L-PLP) was developed and intravenously applied at a dose of 15 mg/kg PLP to a rabbit model of atherosclerosis. Since atherosclerosis is a systemic disease, emerging imaging modalities for assessing atherosclerotic

The chronic inflammatory environment of tumors is a target for novel antitumor therapeutic strategies. Besides cholesterol lowering effects, statins have been studied for their anti-inflammatory and immunomodulatory properties. These pleiotropic effects result mainly from the altered post-translational modification of GTP-binding proteins which regulate many intracellular pathways involved in cell growth and survival. Although pre-clinical studies

Liposomes are little vesicles composed of phospholipid bilayers, which can be loaded with drugs. It is known that such drug-loaded liposomes can accumulate in tumors. This way, it is possible to improve the effectiveness of many chemotherapeutics and to decrease the side effects. Recently we demonstrated that encapsulation of glucocorticoids in liposomes surprisingly enough induce a strong anti-tumor effect. A possible mechanism for this anti-tumor

Purpose. Our recent studies show specific localization of long-circulating liposomes (LCL) within the endosomal/lysosomal compartment of tumor-associated macrophages (TAM). Based on this finding, the present study aims to investigate whether clinically applied LCL formulations such as Doxil (LCLencapsulated doxorubicin), have alternative mechanisms of action additionally to direct drug-mediated cytotoxicity towards tumor cells. Methods. The antitumor

This study evaluates whether the inhibitory effects of prednisolone phosphate (PLP) encapsulated in longcirculating liposomes (LCL-PLP) on tumor growth and tumor angiogenesis described previously can be generalized to other types of glucocorticoids (GC) encapsulated in LCL (LCL-GC). Four types of synthetic GC, i.e. budesonide disodium phosphate (BUP), dexamethasone disodium phosphate (DXP), methylprednisolone disodium phosphate (MPLP), and PLP, were

Prednisolone disodium phosphate (PLP) encapsulated in long-circulating liposomes (LCL) (LCL-PLP) inhibited tumor growth by 80–90% after a single dose of 20 mg/kg, whereas PLP in the free form was completely ineffective at the same single dose. To generalize our findings with LCL-PLP, the antitumor activity and side effects of LCL containing synthetic glucocorticoids (LCL-GC) other than PLP were investigated. In addition to PLP, budesonide disodium

Glucocorticoids can inhibit solid tumor growth via downregulation of tumorassociated inflammation/angiogenesis. In this minireview we describe the possible mechanisms of glucocorticoid action in tumor growth inhibition. We also present an overview of the current status of tumor-targeted glucocorticoid delivery. It appears that long-circulating liposomes are the only targeting system currently being explored for this purpose.

Prednisolone phosphate (PLP) encapsulated in long-circulating liposomes (LCLs) (LCL-PLP) exerts antitumor activity through the inhibition of tumor angiogenesis. It is known that tumor-associated macrophages (TAMs) play a crucial role in tumor growth as they are actively involved in promoting and maintaining tumor angiogenesis. To gain more insight into the antiangiogenic mechanisms of LCL-PLP, this study aimed to investigate the role of TAM in the

Glucorticoids are potent drugs that have a multitude of pharmacological actions both at genomic and non-genomic levels. Many of the diseases in which glucorticoids are routinely administered are featured by angiogenesis and enhanced capillary permeability, permitting targeted delivery using long-circulating drug delivery systems. By encapsulation of glucorticoids in long-circulating liposomes, drug levels at the site of the pathology are markedly

Prednisolone phosphate (PLP) encapsulated in long-circulating liposomes can inhibit tumor growth after intravenous administration (i.v.). These antitumor effects of liposomal PLP are the result of the tumor-targeting property of the liposome formulation. The mechanism by which liposomal PLP inhibits tumor growth is unclear. We investigated the effects of liposome-encapsulated PLP versus free PLP on angiogenic protein production in tumor tissue in