Neuroprotection of selenite against ischemic brain injury through negatively regulating early activation of ASK1/JNK cascade via activation of PI3K/AKT pathway

Wang, Qing; Zhang, Quanguang; Wu, Dong-Na; Yin, Xiaohui; ZHANG, Guang-yi

doi:10.1111/j.1745-7254.2006.00469.x

Cited by 8 publications

(10 citation statements)

References 30 publications

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“…As expected, renal ischemia/reperfusion injury induced the activation of the ASK1/p38 cascade. Others have shown that selenite can block apoptosis induced by oxidative stress, which is related to blocking ASK1 activity and further stimulating the activation of the PI3K/AKT pathway, 21,30 in agreement with our current study. Importantly, we found that renal ischemia/reperfusion injury simultaneously promoted caspase 3 and cleaved PARP activation.…”

Section: Discussionsupporting

confidence: 94%

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Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Wang

Ji²,

Zheng³

et al. 2009

Redox Report

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Previous studies have reported that selenite, a known antioxidant, protects brain against ischemia/reperfusion injury, which is mediated by oxidative stress. The aim of this study was to investigate whether selenite can protect kidney against ischemic injury by reducing activation of the apoptosis signal regulating kinase 1 (ASK1)/mitogen-activated protein kinase kinase 3 (MKK3)/p38 mitogen-activated protein kinase signaling pathway. The activation and expression of ASK1, MKK3, p38, caspase 3 and cleaved PARP were analyzed by Western blot. Apoptosis of renal tubular epithelial cells was assessed by the terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling method. Malondialdehyde (MDA) levels were measured by the thiobarbituric acid reaction. Blood serum creatinine and blood urea nitrogen level were measured with an Olympus automatic multi-analyzer. We found that selenite attenuated significantly ASK1, MKK3, and p38 phosphorylation at 3 h after renal ischemia. Furthermore, selenite decreased significantly renal epithelial tubular cell apoptosis. In addition, selenite reduced the MDA level. These findings suggest that the protective action of selenite on ischemia renal injury is associated closely with reducing activation of the ASK1-MKK3-p38 signal pathway.

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Section: Discussionsupporting

confidence: 94%

“…brain. 21,30 Our present results indicate that renal ischemia/reperfusion leads to increases in MDA, serum creatinine and BUN. Selenite decreased significantly the increases in these parameters compared to those of the ischemia/reperfusion group.…”

Section: Discussionmentioning

confidence: 83%

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Wang

Ji²,

Zheng³

et al. 2009

Redox Report

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“…Recent studies have demonstrated that Akt and ASK1 are physically associated [34]. The activated ASK1/JNK3 signaling cascade mediates apoptosis, causing neuronal damage [26]. Thus, we decided to investigate whether the neuroprotective action of sevoflurane was related to the cross-talk modulation of the Akt and JNK signaling pathways in cerebral ischemia.…”

Section: Discussionmentioning

confidence: 99%

“…One is at Ser-83, and the other is at Thr-845. The p-ASK1 site at Ser-83 induces decreased ASK1 activation, while the p-ASK1 site at Thr-845 is correlated with ASK1 activity [26]. Thus, we next examined the possible effect of sevoflurane, LY294002, and wortmannin on ASK1 (Thr-845) phosphorylation.…”

Section: Neuroprotective Effects Of Sevoflurane Against I/r-induced Nmentioning

confidence: 99%

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Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

Wen

Liu

et al. 2015

Mol Neurobiol

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In this study, we investigated the neuroprotective effect of sevoflurane against ischemic brain injury and its underlying molecular mechanisms. Transient global brain ischemia was induced by 4-vessel occlusion in adult male Sprague-Dawley rats. The rats were pretreated with sevoflurane alone or sevoflurane combined with LY294002/wortmannin (selective inhibitor of PI3K) before ischemia. Cresyl violet staining was used to examine the survival of hippocampal CA1 pyramidal neurons. Immunoblotting and immunoprecipitation were performed to measure the phosphorylation of Akt1, PRAS40, ASK1, and JNK3 and the expression of cleaved-caspase-3. The results demonstrated that a moderate dose of sevoflurane inhalation of 2% for 2 h had significant neuroprotective effects against ischemia/reperfusion induced hippocampal neuron death. Sevoflurane significantly increased Akt and PRAS40 phosphorylation and decreased the phosphorylation of ASK1 at 6 h after reperfusion and the phosphorylation of JNK3 at 3 days after reperfusion following 15 min of transient global brain ischemia. Conversely, LY294002 and wortmannin significantly inhibited the effects of sevoflurane. Taken together, the results suggest that sevoflurane could suppress ischemic brain injury by downregulating the activation of the ASK1/JNK3 cascade via increasing the phosphorylation of Akt1 during ischemia/reperfusion.

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PAR-1 antagonist SCH79797 ameliorates apoptosis following surgical brain injury through inhibition of ASK1-JNK in rats

Manaenko

Sun

Kim

et al. 2013

Neurobiology of Disease

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Neurosurgical procedures inevitably produce intraoperative hemorrhage. The subsequent entry of blood into the brain parenchyma results in the release of large amounts of thrombin, a known contributor to perihematomal edema formation and apoptosis after brain injury. The present study seeks to test 1) the effect of surgically induced brain injury (SBI) on thrombin activity, expression of thrombin’s receptor PAR-1, and PAR-1 mediated apoptosis; 2) the effect of thrombin inhibition by argatroban and PAR-1 inhibition by SCH79797 on the development of secondary brain injury in the SBI model on rats. A total of 88 Sprague-Dawley male rats were randomly divided into sham, vehicle-, argatroban-, or SCH79797-treated groups. SBI involved partial resection of the right frontal lobe under inhalation isoflurane anesthesia. Sham-operated animals received only craniotomy. Thrombin activity, brain water content, and neurological deficits were measured at 24 hours following SBI. Involvement of the Ask1/JNK pathway in PAR-1-induced post-SBI apoptosis was characterized by using Ask1 or JNK inhibitors. We observed that SBI increased thrombin activity, yet failed to demonstrate any effect on PAR-1 expression. Argatroban and SCH79797 reduced SBI-induced brain edema and neurological deficits in a dose-dependent manner. SBI-induced apoptosis seemed mediated by the PAR-1/Ask1/JNK pathways. Administration of SCH79797 ameliorated the apoptosis following SBI. Our finding indicate that PAR-1 antagonist protects against secondary brain injury after SBI by decreasing both brain edema and apoptosis by inactivating PAR-1/Ask1/JNK pathway. The anti-apoptotic effect of PAR-1 antagonists may provide a promising path for therapy following SBI.

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Neuroprotection of selenite against ischemic brain injury through negatively regulating early activation of ASK1/JNK cascade via activation of PI3K/AKT pathway

Cited by 8 publications

References 30 publications

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Protective effect of selenite on renal ischemia/reperfusion injury through inhibiting ASK1–MKK3–p38 signal pathway

Neuroprotection of Sevoflurane Against Ischemia/Reperfusion-Induced Brain Injury Through Inhibiting JNK3/Caspase-3 by Enhancing Akt Signaling Pathway

PAR-1 antagonist SCH79797 ameliorates apoptosis following surgical brain injury through inhibition of ASK1-JNK in rats

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