Survivin is involved in the anti-apoptotic effect of edaravone in PC12 cells

Liu, Xueyuan; Yao, Lingling; Chen, Yujuan; Tao, Bei-Bei; Yu, Yongchun; Bian, Wei-Hong; Yu, Jing; Wang, Yonggang

doi:10.1007/s11010-009-0037-1

Cited by 8 publications

(9 citation statements)

References 20 publications

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“…At present, most studies focus on tumors such as hepatocellular carcinoma and lung cancer [21–23]. Only a small number of studies on cerebral ischemia-reperfusion injury suggest that survivin protein can be expressed after brain ischemia-reperfusion injury [24, 25]. It can be seen from the results of this experiment that SCII can increase the number of survivin protein-positive cells in the anterior horn of spinal cord and increase the expression of survivin protein in spinal cord tissue, indicating that SCII can promote rat spinal cord neurons express survivin protein.…”

Section: Discussionmentioning

confidence: 99%

Effects of ginsenoside Rb1 on spinal cord ischemia-reperfusion injury in rats

Ye¹,

Li²,

Huang³

et al. 2019

J Orthop Surg Res

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Background The aim of this study was to evaluate the effects of different doses of ginsenoside Rb1 (GRb1) pretreatment on spinal cord ischemia-reperfusion (SCII) in rats and explore the potential mechanisms about the expression of survivin protein after the intervention. Methods A total of 90 healthy adult Sprague-Dawley (SD) rats were randomly divided into six groups: sham-operated ( n = 15), SCII model ( n = 15), and GRb1-treated groups ( n = 60). The GRb1-treated group was divided into four subgroups: 10 mg/kg, 20 mg/kg, 40 mg/kg, and 80 mg/kg ( n = 15). The corresponding dose of GRb1 was injected intraperitoneally 30 min before operation and every day after operation. Forty-eight hours after model establishment, the neurological function of hind limbs was measured with Basso, Beattie, and Bresnahan (BBB) scale. The superoxide dismutase (SOD) and malondialdehyde (MDA) levels in serum and spinal cord tissue were detected respectively. The expression of survivin protein was observed by immunofluorescence staining. HE and TUNEL staining were used to observe neural cell injury and apoptosis, respectively, in the spinal cord of rats with SCII. Results The intervention of different doses of GRb1 could increase SOD activity and decrease MDA content in serum and spinal cord tissue, increase survivin protein expression, and decrease neuronal apoptosis. It was dose-dependent, but there was no significant change between 40 mg/kg and 80 mg/kg. Conclusions GRb1 could reduce the cell apoptosis induced by SCII through inhibiting oxidative stress. It can also inhibit apoptosis by promoting the expression of Survivin protein. Ginsenoside Rb1 had a dose-dependent protective effect on SCII in the dose range of 10 mg/kg–40 mg/kg.

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Section: Discussionmentioning

confidence: 99%

Effects of ginsenoside Rb1 on spinal cord ischemia-reperfusion injury in rats

Ye¹,

Li²,

Huang³

et al. 2019

J Orthop Surg Res

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“…Intracellular calcium overloads significantly, generating a large amount of oxygen-free radical. Oxygen-free radicals are thought to be the main physiological and pathological basis of cerebral infarction ( 15 , 16 ). Ischemia reperfusion injury occurred after cerebral infarction.…”

Section: Discussionmentioning

confidence: 99%

“…Blood-brain barrier permeability for edaravone is ~60%. Its intravenous injection can effectively remove cytotoxic hydroxyl-free radicals and effectively inhibit the irreversible damage to nucleic acid, and protein damage mediated by peroxyl radical ( 16 – 18 ). Kimura et al ( 18 ) administered the auxiliary treatment of edaravone to 40 cases of patients with massive cerebral infarction and compared that treatment type with conventional symptomatic treatment.…”

Section: Discussionmentioning

confidence: 99%

Analysis of treatment effect of urinary kallidinogenase combined with edaravone on massive cerebral infarction

Jiang

Mou²

2016

Biomedical Reports

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The aim of the study was to investigate the clinical effect of urinary kallidinogenase combined with edaravone in the treatment of massive cerebral infarction. A total of 58 patients with massive cerebral infarction were admitted to hospital between January 2013 and January 2014. There were 34 male and 24 female patients. The patients were randomly divided into the observation and control groups (n=29 cases per group). The patients in the control group received edaravone treatment, while patients in the observation group were treated with urinary kallidinogenase and edaravone. The clinical effects of the two groups were then compared. The results showed that the National Institutes of Health Stroke Scale score and serum C-reactive protein level of the patients in the two groups were significantly decreased following treatment. The decreased degree in the observation group was significantly smaller than that in the control group. The difference was statistically significant [(11.03±3.75) vs. (16.58±7.43) scores, P<0.05; (9.88±4.82) vs. (11.98±4.69) mmol/l, P<0.05]. The serum levels of vascular endothelial growth factor were significantly increased in patients of the two groups after treatment. The increased degree in the observation group was significantly higher than that in the control group. The difference was statistically significant [(268.51±77.34) vs. (188.82±57.33) ng/l, P<0.05]. The total effective rate of the observation group was significantly higher than that of the control group and the difference was statistically significant (89.66 vs. 62.07%, P<0.05). In conclusion, urinary kallidinogenase combined with edaravone treatment has a certain clinical curative effect on massive cerebral infarction.

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“…Survivin is a member of the inhibitor of apoptotic protein family. ERK is a mitogen-activated protein kinase whose phosphorylation induces (1) upregulation of survivin 8 , and (2) increase of RBC adhesion to the endothelium 9 . Hence, our data, although obtained in a small cohort of patients, seem to indicate that in patients with RA, a mild alteration of intracellular redox state of RBC can occur.…”

Section: To the Editormentioning

confidence: 99%