Abstract
Introduction Protein kinases regulate the expression of many genes that are pivotal for inflammation. This review aims to summarise data on a group of small molecules capable to inhibit tyrosine kinases (TYKs), named tyrphostins. They are derivatives of benzylidenemalonitrile that decrease tyrosine phosphorylation, thereby affecting not a single mediator, but cell signalling transduction is affected. No single animal model fully represents the human disease, but these models provide valuable tools to understand particular pathways. In this review, we describe some of the recent investigations on tyrphostins as anti-inflammatory agents in vivo in animal models, and in vitro in cell culture systems. Conclusion It is anticipated that tyrphostins are suitable for the treatment of inflammation-related diseases. Future research is required to understand the mechanisms of their action to pave way for gaining pharmacological
Highlights
Protein kinases regulate the expression of many genes that are pivotal for inflammation
tyrosine kinase (TYK) are divided into receptor TYKs, including epidermal growth factor (EGF), platelet-derived growth factor (PDGF), fibroblast growth factor receptor (FGFR) and non-receptor TYKs, including Src, abelson murine leukaemia viral oncogene homolog (ABL), focal adhesion kinase (FAK) and Janus kinase (JAK)[2]
In a study performed by Chatterjee et al.[25], histological observations showed that tyrphostin AG126 (5 mg/kg) reduced the expression of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) levels in plasma and suppressed protease-activated receptor (PAR) activation and COX2 expression in ischemia-reperfusion in rat, ameliorating renal dysfunction and injury
Summary
Protein kinases regulate the expression of many genes that are pivotal for inflammation. This review aims to summarise data on a group of small molecules capable to inhibit tyrosine kinases (TYKs), named tyrphostins. They are derivatives of benzylidenemalonitrile that decrease tyrosine phosphorylation, thereby affecting not a single mediator, but cell signalling transduction is affected. TYKs catalyse the transfer of the terminal phosphate group of adenosine triphosphate (ATP) to the tyrosine residues on protein substrates, resulting in an activation of the substrate and further participating in the step of the signalling cascade[1]. Because protein tyrosine kinases (PTKs) are critical components of cellular signalling pathways, their catalytic activity should be tightly regulated. Over 20 drugs that target kinases have been introduced in clinical practice and many are currently in preclinical studies[3,4]
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