RETRACTED: Effects of rehabilitation training on apoptosis of nerve cells and the recovery of neural and motor functions in rats with ischemic stroke through the PI3K/Akt and Nrf2/ARE signaling pathways

Jin, Xiaofei; Wang, Shan; Shen, Min; Wen, Xin; Han, Xin‐Rui; Wu, Jun-Chang; Tang, Gao-Zhuo; Wu, Dongmei; Lü, Jun; Zheng, Yuxin

doi:10.1016/j.brainresbull.2017.08.011

Cited by 26 publications

(11 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The PI3K/Akt pathway is a classical signal transduction pathway with various biological effects, and it exerts multiple roles in the regulation of cell growth, proliferation, differentiation and survival. The PI3K/Akt signaling pathway regulates apoptosis via regulating the expression of apoptosis-related molecules (Jin et al, 2017). The PI3K/Akt pathway plays an important role in epilepsy-induced neuronal damage, and activation of the PI3K/Akt pathway exhibits neuroprotective effects in epilepsy (Xue et al, 2011), which is consistent with our results.…”

Section: Discussionmentioning

confidence: 99%

The Neuroprotective Effect of Astaxanthin on Pilocarpine-Induced Status Epilepticus in Rats

Deng

Wang

et al. 2019

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Cognitive dysfunction is one of the serious complications induced by status epilepticus (SE), which has a significant negative impact on patients’ quality of life. Previous studies demonstrated that the pathophysiological changes after SE such as oxidative stress, inflammatory reaction contribute to neuronal damage. A recent study indicated that preventive astaxanthin (AST) alleviated epilepsy-induced oxidative stress and neuronal apoptosis in the brain. In the present study, rats were treated with vehicle or AST 1 h after SE onset and were injected once every other day for 2 weeks (total of seven times). The results showed that the cognitive function in SE rats was significantly impaired, and AST treatment improved cognitive function in the Morris water maze (MWM). Magnetic resonance imaging (MRI), hematoxylin-eosin (HE) staining and TdT-mediated dUTP Nick-End Labeling (TUNEL) staining showed obvious damage in the hippocampus of SE rats, and AST alleviated the damage. Subsequently, we evaluated the effect of AST on relative pathophysiology to elucidate the possible mechanisms. To evaluate the oxidative stress, the expression of malondialdehyde (MDA) and superoxide dismutase (SOD) in plasma were detected using commercially available kits. NADPH oxidase-4 (Nox-4), p22phox, NF-E2-related factor 2 (Nrf-2), heme oxygenase 1 (Ho-1) and sod1 in the parahippocampal cortex and hippocampus were detected using western blot and real-time polymerase chain reaction (RT-PCR). The levels of MDA in plasma and Nox-4 and p22phox in the brain increased in SE rats, and the levels of SOD in plasma and Nrf-2, Ho-1 and sod1 in the brain decreased. Treatment with AST alleviated these changes. We also detected the levels of inflammatory mediators like cyclooxygenase-2 (cox-2), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) and NF-κB phosphorylation p65 (p-p65)/p65 in the brain. The inflammatory reaction was significantly activated in the brain of SE rats, and AST alleviated neuroinflammation. We detected the levels of p-Akt, Akt, B-cell lymphoma-2 (Bcl-2), Bax, cleaved caspase-3, and caspase-3 in the parahippocampal cortex and hippocampus using western blot. The levels of p-Akt/Akt and Bcl-2 decreased in SE rats, Bax and cleaved caspase-3/caspase-3 increased, while AST alleviated these changes. The present study indicated that AST exerted an reobvious neuroprotective effect in pilocarpine-induced SE rats.

show abstract

Section: Discussionmentioning

confidence: 99%

The Neuroprotective Effect of Astaxanthin on Pilocarpine-Induced Status Epilepticus in Rats

Deng

Wang

et al. 2019

Front. Cell. Neurosci.

View full text Add to dashboard Cite

show abstract

“…The process of apoptosis involves the cascade amplification reaction process of irreversible limited hydrolytic substrate of caspases, with caspase-3 the most critical downstream apoptotic protease. It has been reported that the activation of PI3K/Akt leads to the phosphorylation of the proapoptotic protein Bcl-2-associated death promoter in nerve cells, the upregulation of the Inhibitior of apoptotis proteins levels, and the inhibition of the endogenous apoptotic pathway regulated by the Caspase cascade signal pathway, eventually exerting a cell protective effect (26). A study has demonstrated that 100 ng/ml Dex can induce apoptosis of inflammatory cells by activating the caspase cascade reaction of neutrophils and other inflammatory cells, whilst 1 ng/ml Dex has no significant effect on apoptosis of neutrophils (27), indicating that Dex has dose dependent effects on cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

et al. 2019

View full text Add to dashboard Cite

Obstructive jaundice (OJ) is a common disease in clinical surgery. The present study aimed to determine the effects of dexmedetomidine (Dex) on hepatocyte apoptosis in rats with OJ and also to explore the underlying mechanism. A total of 30 adult male Sprague Dawley rats were randomly divided into 3 groups: Sham group, bile duct ligation (BDL) group, and BDL+Dex group. The serum liver function index, expression levels of serum inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and the liver pathological changes were compared amongst groups. The serum liver function index and expression levels of inflammatory factors in the BDL group and BDL+Dex group were higher compared with the sham group. The serum liver function index and expression levels of inflammatory factors were lower in the BDL+Dex group compared with the BDL group. The severity of hepatic injury was diminished in the BDL+Dex group compared with the BDL group. Compared with the sham group, the hepatocyte apoptosis rate increased significantly in the BDL group and BDL+Dex group. The present findings suggested that Dex improved the liver function of rats with OJ, reduced the production of inflammatory factors and inhibited the apoptosis of hepatocytes. Dex demonstrated a protective effect on liver damage potentially via activation of the phosphoinositide 3-kinase/protein kinase B signaling pathway.

show abstract

“…Akt, found to be a PKC-related protein [11], is heavily involved in the regulation of apoptosis through a variety of downstream pathways [12][13][14]. Much evidence has implicated Akt for its neuroprotective role in cerebral ischemia, finding that Akt expression is associated with neuronal repairment, reduced oxidative stress, and decreased neuronal apoptosis [15][16][17][18]. Additionally, PKC has been studied for its role in ischemic tolerance and reperfusion injury [19,20].…”

Section: Of 13mentioning

confidence: 99%

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

et al. 2019

View full text Add to dashboard Cite

Phenothiazine treatment has been shown to reduce post-stroke ischemic injury, though the underlying mechanism remains unclear. This study sought to confirm the neuroprotective effects of phenothiazines and to explore the role of the NOX (nicotinamide adenine dinucleotide phosphate oxidase)/Akt/PKC (protein kinase C) pathway in cerebral apoptosis. Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) for 2 h and were randomly divided into 3 different cohorts: (1) saline, (2) 8 mg/kg chlorpromazine and promethazine (C+P), and (3) 8 mg/kg C+P as well as apocynin (NOX inhibitor). Brain infarct volumes were examined, and cell death/NOX activity was determined by assays. Western blotting was used to assess protein expression of kinase C-δ (PKC-δ), phosphorylated Akt (p-Akt), Bax, Bcl-XL, and uncleaved/cleaved caspase-3. Both C+P and C+P/NOX inhibitor administration yielded a significant reduction in infarct volumes and cell death, while the C+P/NOX inhibitor did not confer further reduction. In both treatment groups, anti-apoptotic Bcl-XL protein expression generally increased, while pro-apoptotic Bax and caspase-3 proteins generally decreased. PKC protein expression was decreased in both treatment groups, demonstrating a further decrease by C+P/NOX inhibitor at 6 and 24 h of reperfusion. The present study confirms C+P-mediated neuroprotection and suggests that the NOX/Akt/PKC pathway is a potential target for efficacious therapy following ischemic stroke.

show abstract

RETRACTED: Effects of rehabilitation training on apoptosis of nerve cells and the recovery of neural and motor functions in rats with ischemic stroke through the PI3K/Akt and Nrf2/ARE signaling pathways

Cited by 26 publications

References 31 publications

The Neuroprotective Effect of Astaxanthin on Pilocarpine-Induced Status Epilepticus in Rats

The Neuroprotective Effect of Astaxanthin on Pilocarpine-Induced Status Epilepticus in Rats

Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice

Reduced Apoptotic Injury by Phenothiazine in Ischemic Stroke through the NOX-Akt/PKC Pathway

Contact Info

Product

Resources

About