Rosmarinic Acid as a Novel Agent in the Treatment of Autoimmune Disease

@inproceedings{Stansbury2012RosmarinicAA,
  title={Rosmarinic Acid as a Novel Agent in the Treatment of Autoimmune Disease},
  author={Jill Stansbury and Paul Richard Saunders and David Winston and Eugene R. Zampieron},
  year={2012}
}
Rosmarinic acid has been shown to selectively induce T cell apoptosis in aberrant lymphocytes, but not normal/quiescent T cells. Rosmarinic acid also reduces gamma interferon driven T cell responses and reduces interleukin production following T cell stimulation. Furthermore, rosmarinic acid affects signal transduction inside T cells by affecting specific tyrosine kinase enzymes inside the cell. By direct effects on T cells as well as other anti-inflammatory and antioxidant effects, rosmarinic… Expand

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References

SHOWING 1-10 OF 17 REFERENCES
Rosmarinic Acid Induces Apoptosis of Activated T Cells from Rheumatoid Arthritis Patients via Mitochondrial Pathway
TLDR
Results suggest that RosA induces apoptosis of activated T-cell subsets from RA patients via a mitochondrial pathway. Expand
Synergistic immunosuppressive effects of rosmarinic acid and rapamycin in vitro and in vivo1
TLDR
The combination of RosA and Rapa promotes immunosuppressive effects and prolong skin graft survival in vivo, and is evaluated in the mouse skin allograft model. Expand
Beneficial effects of rosmarinic acid on suppression of collagen induced arthritis.
TLDR
RosA suppressed synovitis in a murine collagen induced arthritis model; this effect may be beneficial for treatment of rheumatoid arthritis in clinical settings. Expand
Rosmarinic acid inhibits Ca2+-dependent pathways of T-cell antigen receptor-mediated signaling by inhibiting the PLC-gamma 1 and Itk activity.
TLDR
It is concluded that RosA inhibits TCR signaling leading to Ca(2+) mobilization and NF-AT activation by blocking membrane-proximal events, specifically, the tyrosine phosphorylation of inducible T cells kinase (Itk) and PLC-gamma 1. Expand
Rosmarinic Acid Induces p56lck-Dependent Apoptosis in Jurkat and Peripheral T Cells via Mitochondrial Pathway Independent from Fas/Fas Ligand Interaction 1
TLDR
Lck-dependent apoptotic activity may make RosA an attractive therapeutic tool for the treatment of diseases in which T cell apoptosis is beneficial, as observed in freshly isolated human PBMC. Expand
Prolonged survival of islet allografts in mice treated with rosmarinic acid and anti-CD154 antibody
TLDR
Treatment with both Ros A and MR1 has a synergistic effect in murine islet allotransplantation, and allograft survival was prolonged in the double-treated animals compared to animals that received only Ros A or MR1. Expand
Nonsteroidal Anti-inflammatory Drugs Suppress T-cell Activation by Inhibiting p38 MAPK Induction*
TLDR
The data identify COX-1 andCOX-2 as integral and sequential components of TCR signaling to p38 and contribute to elucidate the molecular basis of immunosuppression by NSAID. Expand
The structure-activity relationship of the series of non-peptide small antagonists for p56lck SH2 domain.
TLDR
Overall results revealed important structural requirements of the p56lck SH2 antagonists for in vitro T-cell inhibitory activity and in vitro protein binding activity. Expand
Rosmarinic acid inhibits TCR‐induced T cell activation and proliferation in an Lck‐dependent manner
TLDR
Large‐scale screening of plant extracts indicated that rosmarinic acid (RosA) in extracts of Prunella vulgaris consistently inhibits the interaction between Lck SH2 and a peptide containing its consensus binding sequence (pYEEI). Expand
Antioxidant and antimicrobial activities of rosemary extracts linked to their polyphenol composition
TLDR
The results suggested that the antimicrobial rosemary extract efficacy was associated with their specific phenolic composition, and Carnosic acid and rosmarinic acid may be the main bioactive antimicrobial compounds present in rosemary extracts. Expand
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