|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In addition, obviously higher ratio of Blc-2/Bax and decreased expression of cleaved caspase-3 in puerarin-treated SAH micecomparing with vehicle-treated SAH animals had been found.
|
30551525 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
We conducted a double-blind, prospective, randomized pilot study to evaluate the effect of 4 anesthetic agents on cerebrospinal fluid (CSF) and serum caspase-3 levels in aSAH patients.
|
31599811 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Administration of mitoquinone resulted in a decrease in expression of Keap1 (0.33×), Romo1 (reactive oxygen species modulator 1; 0.24×), Bax (B-cell lymphoma-2 associated X protein; 0.31×), Cleaved Caspase-3 (0.29×) and an increase in Nrf2 (2.13×), Bcl-xl (B-cell lymphoma-extra large; 1.67×), PINK1 (phosphatase and tensin-induced kinase 1; 1.67×), Parkin (1.49×), PHB2 (1.60×), and LC3II (1.67×) proteins compared with SAH+vehicle group.
|
30890112 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
The expression of pro-inflammatory and pro-apoptotic factors such as toll-like receptor 4 (TLR4), NF-κB (p-p65), tumor necrosis factor-α, p-p38 MAPK, p-p53, and caspase-3 were significantly increased after SAH.
|
30980845 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In addition, ANXA7 knockdown also significantly reduced glutamate release, which was consistent with a significant increase of Bcl-2 expression and decreases of Bax and cleaved caspase-3 expression.CONCLUSIONSANXA7 can induce neuronal apoptosis by affecting glutamate release in rats with SAH.
|
30717037 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Assessments in 24 h after SAH showed that treatment with 70 mg/kg Allicin in 30 min after SAH significantly restrained the expression of cleaved caspase-3, mitigated the severity of neuronal degeneration, decreased the proportion of apoptotic neurons and the elevated MDA levels, and increased the suppressed GSH and SOD levels.
|
30773476 |
2019 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, Hippocampal neuron apoptosis was induced by diabetes + SAH and expression levels of caspase-3, Bax and Bcl-2 were also increased.
|
29399092 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Meanwhile, the combination therapy attenuates apoptosis as shown by an increased Bcl-2 expression, decreased Bax expression and release of cytochrome c, and reduction of cleaved caspase-9 and caspase-3 at 24h after SAH.
|
29258835 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Our data show that early treatment with atorvastatin effectively ameliorates EBI after SAH through anti-apoptotic effects and the effects might be associated inhibition of caspase-3 and endoplasmic reticulum (ER) stress related proteins CHOP and GRP78.
|
29592873 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Increased levels of SOD2, Bax, and cleaved caspase-3 following SAH were reduced in the SAH + melatonin-treated group; reduced levels of Sirt3 and Bcl-2 following SAH were increased in the SAH + melatonin-treated group.
|
29872034 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Treatment with the p53 inhibitor, pifithrin‑α, suppressed p53 protein expression, increased IL‑6 mRNA expression, decreased microRNA‑22 expression, Bax protein expression and caspase‑3 activity, and induced Cyr61 expression in mice with SAH.
|
29336471 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
This finding was associated with an observed decrease in Bax/Bcl-2 ratio, cytochrome-c and PUMA expression, and the suppression of caspase-3 activation following SAH.
|
30036663 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Levels of caspase-3, bax and bcl-2, all showed a temporary rise after SAH in the hypothalamus, indicating the induction of apoptosis in this brain region.
|
29497296 |
2018 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, l-cysteine treatment significantly ameliorated brain edema, improved neurobehavioral function, and attenuated neuronal cell death in the PFC; these effects were associated with a decrease in the Bax/Bcl-2 ratio and the suppression of caspase-3 activation 48 h after SAH.
|
28512446 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Furthermore, GSK2606414 treatment increased p-Akt levels and the Bcl-2/Bax ratio as well as decreased cleaved caspase-3 expression and neuronal death, thereby improving neurological deficits at 72 h after SAH.
|
26887383 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Colocalization and correlating changes in expression of MSK1 and active caspase-3 at neurons and astrocytes indicated that MSK1 downregulation may contribute to SAH-induced apoptosis, validating that MSK1 may be involved in the pathophysiology of the brain cortex subsequent to SAH.
|
28927047 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
These findings suggest that TMP exerts an antiapoptosis property in the SAH rat model and this is probably mediated by the caspase-3 apoptotic pathway triggered by mitochondrial calcium overload.
|
28337226 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, AE1-329 significantly reduced the number of TUNEL-positive cells and active caspase-3 in cortex after SAH.
|
28239768 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
Moreover, low dose of LPS was used to verify whether it had nerve protection after SAH and the mechanism involving in MMP9 and caspase 3 was investigated.
|
27844284 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
Recombinant XIAP treatment also decreased the expression of cleaved caspase-3, caspase-8 and caspase-9, whereas there was no effect on the expression of p53, apoptosis-inducing factor or cytochrome c. These results show that XIAP acts as an endogenous neuroprotective and anti-apoptotic agent following SAH.
|
28327595 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
AlteredExpression
|
disease |
BEFREE |
The expression of PCMT1 and MST1 decreased, while the level of active caspase 3 increased in rats after SAH.
|
28534197 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
The results showed that NaHS treatment significantly improved brain edema and neurobehavioral function, and attenuated neuronal cell death in the prefrontal cortex, associated with a decrease in Bax/Bcl-2 ratio and suppression of caspase-3 activation at 48 h after SAH.
|
26822402 |
2017 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
BEFREE |
The results showed that PUR treatment significantly ameliorated brain edema, improved neurobehavioral function, and attenuated neuronal cell death in the prefrontal cortex (PFC), associated with a decrease in Bax/Bcl-2 ratio and suppression of caspase-3 activation at 48 h after SAH.PUR also promoted phospho-ERK levels.
|
28149272 |
2016 |
|
Subarachnoid Hemorrhage
|
0.600 |
Therapeutic
|
disease |
RGD |
A purine antimetabolite attenuates toll-like receptor-2, -4, and subarachnoid hemorrhage-induced brain apoptosis.
|
26163325 |
2015 |
|
Subarachnoid Hemorrhage
|
0.600 |
Biomarker
|
disease |
CTD_human |
Resveratrol prevents neuronal apoptosis in an early brain injury model.
|
24602480 |
2014 |