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:3.4.22.62 (
caspase-9
)
7,507
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Occlusion of coronary artery causes cardiomyocyte dysfunction. Reperfusion relieves ischemia by providing cells with metabolites and oxygen, thereby preventing extensive tissue damage. Although reperfusion salvages the myocardium, it also initiates a series of events including myocardial apoptosis and necrosis. The common inducers of apoptosis include reactive oxygen species (ROS).
Caffeic acid phenethyl ester
(
CAPE
) is known as an antioxidative, anti-inflammatory effects, may protect myocardial ischemia-reperfusion (MI/R)-induced apoptosis. We have previously reported that
CAPE
reduced MI/R-induced necrosis. Therefore, this study was focused to investigate protective effect of
CAPE
on the distinct form of cell death; apoptosis in an in vivo rat model. To produce MI/R, a branch of the descending left coronary artery was occluded for 30 min followed by 2 h reperfusion. ECG changes, blood pressure (BP), and heart rate (HR) were measured before occlusion and continued both occlusion and reperfusion.
CAPE
(50 micromol/kg) was given 10 min before ischemia via jugular vein. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the terminal deoxynucleotidyl transferase (TdT)-mediated d UTP-biotin nick and labeling (TUNEL) method. Also, cysteine aspartate specific proteinase (caspase)-3 and
caspase-9
activities a universal effector of apoptosis, were determined. Trunk blood was extracted to determine the serum contents related to oxidant-antioxidant status. In hemodynamic parameters, there was no significant difference in HR or BP values among any group.
CAPE
administration had no a significant effect on hemodynamic parameters during ischemia or reperfusion. Control group revealed extensive TUNEL-positive cardiomyocytes especially in free wall of left ventricule, interventiculare septum and nearly apex zone. Intensity of TUNEL-positive cardiomyocytes reduced as a result of
CAPE
treatment compared to control group in the same sections. Result of the caspase activities was found to correlate with TUNEL evaluation.
CAPE
also, ameliorated antioxidant status. We propose that
CAPE
acts in the heart as a potent scavenger of free radicals to prevent the apoptotic effect of I/R. Further studies are needed to elucidate the mechanisms of apoptotic death machinery.
...
PMID:Protective effect of caffeic acid phenethyl ester (CAPE) on myocardial ischemia-reperfusion-induced apoptotic cell death. 1572 9
The development of advanced cervical cancer therapies is a particularly urgent need due to the strong side effects and toxicities of current treatments.
Caffeic acid phenethyl ester
(
CAPE
) exhibits broad-spectrum antitumor activities and little toxicity or side effects. In our previous study, caffeic acid para-nitro phenethyl ester (
CAPE
-
p
NO
2
) significantly improved the effect of anti-platelet aggregation and attenuated myocardial ischemia. Based on this finding, we aimed to further explore the antitumor activity of
CAPE
-
p
NO
2
in cervical cancer cells and tumor xenografts. In addition, we assessed the biotransformation of
CAPE
-
p
NO
2
in cervical cancer cells. Our study demonstrated that both
CAPE
and
CAPE
-
p
NO
2
can inhibit cell proliferation via the induction of G2/M cell cycle arrest. More importantly,
CAPE
-
p
NO
2
dramatically induced cell apoptosis via significant down-regulation of pro-caspase-3, pro-
caspase-9
, Bcl-2, Cyclin B1 and Cdc2 and up-regulation of cleaved-caspase-3, Bax, CytoC and P21
Cip1
. Moreover,
CAPE
and
CAPE
-
p
NO
2
significantly suppressed the growth and angiogenesis of nude mice xenografts.
CAPE
and
CAPE
-
p
NO
2
were found to degrade into four and six metabolites, respectively. The metabolites of
CAPE
and
CAPE
-
p
NO
2
were different, and the major metabolic pathway may be phase II reactions. These results suggest that
CAPE
-
p
NO
2
induced cell apoptosis and cell cycle arrest via a strong regulatory effect on relevant apoptotic proteins. Therefore,
CAPE
-
p
NO
2
should be further studied as a potent anti-cancer agent.
...
PMID:Inhibited effects of CAPE-
p
NO
2
on cervical carcinoma
in vivo
and
in vitro
and its detected metabolites. 2921 21
