Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.4.2.30 (
PARP
)
13,611
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Salvianolic acid A
(
SAA
), one of the main derivatives of Salvia miltiorrhiza, has been shown to possess anti-inflammatory and anti-thrombotic activities. Its role in inhibiting tumor growth, however, remains elusive. The aim of this study was to investigate the effect of
SAA
on acute myeloid leukemia (AML). Here,
SAA
showed a dose-dependent cell viability inhibition and apoptosis induction in AML cells. At the molecular level,
SAA
increased the expression of Bak and decreased the expression of Bcl-xL, following by
PARP
cleavage and caspase-3 activation.
SAA
also markedly attenuated Akt phosphorylation in AML cells. In a xenograft mouse model,
SAA
significantly suppressed the growth of AML tumors in vivo. Furthermore,
SAA
exhibited a more profound pro-apoptotic effect on primary AML cells than on bone marrow mononuclear cells from patients with benign diseases. Therefore, the pro-apoptotic and anti-tumor properties of
SAA
suggested its promising therapeutic value for AML.
...
PMID:Salvianolic acid A, a novel PI3K/Akt inhibitor, induces cell apoptosis and suppresses tumor growth in acute myeloid leukemia. 2916 84
Treatment options are limited in patients with diffuse large B-cell lymphoma (DLBCL).
Salvianolic acid A
(
SAA
) is a water-soluble phenolic acid extracted from Salvia miltiorrhiza (Danshen) with anti-tumor properties. The anti-leukemic activity of
SAA
that has been shown in our recent finding prompts us to investigate the therapeutic effect and mechanism of action of
SAA
in DLBCL. Here, we find that
SAA
inhibits the viability of DLBCL cells by inducing cellular apoptosis, which is accompanied by upregulation of Bax and cleavage of
PARP
. Pre-incubation of
SAA
increases the phosphorylation of JNK, while decreases the phosphorylation of p38 and ERK in DLBCL cells. Importantly, pharmacological JNK inhibition partially mitigates the anti-survival effect of
SAA
, and inhibitions of p38 and ERK synergize with
SAA
. Furthermore,
SAA
suppresses DLBCL tumor growth in a xenograft mouse model in vivo. Therefore, our data suggests the therapeutic utility of
SAA
in the management of DLBCL.
...
PMID:Salvianolic acid A inhibits the growth of diffuse large B-cell lymphoma through MAPK pathways. 3327 89
