scholarly journals Dynamic Observation of the Effect of L-Theanine on Cerebral Ischemia-Reperfusion Injury Using Magnetic Resonance Imaging under Mathematical Model Analysis

2021 ◽  
Vol 2021 ◽  
pp. 1-7
Author(s):  
Hui Ye ◽  
Zaiming Liu ◽  
Long Zhou ◽  
Qiang Cai
Keyword(s):  
Mathematical Model ◽  
Cerebral Ischemia ◽  
Treatment Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Resonance Imaging ◽  
Partial Differential ◽  
Ischemia Group ◽  
Cerebral Ischemia Reperfusion Injury

This study was to use the partial differential mathematical model to analyze the magnetic resonance imaging (MRI) images of cerebral ischemia-reperfusion injury (CIRI) and to dynamically observe the role of L-theanine in CIRI based on this. 30 patients with cerebral ischemia in a hospital in a certain area were selected and divided into a cerebral ischemia group and a L-theanine treatment group. The two groups of patients were examined by MRI within 48 hours, and the relative apparent diffusion coefficient (rADC) of the cerebral ischemic part of the patients was determined. The partial differential mathematical model was used for data processing to obtain the function of cerebral ischemia time and infarct area, and the data of patients in the cerebral ischemia group and L-theanine treatment group were compared and analyzed. The results showed that the partial differential mathematical model could effectively analyze the linear relationship between the rADC value and time in the treatment of CIRI using L-theanine. The rADC values of the four points of interest in the L-theanine treatment group all increased with time, and there was a positive correlation between the variables X and Y. In observing the efficacy indicators of L-theanine, the L-theanine treatment group showed a significant advantage in the neurospecific enolase (NSE) content compared with the cerebral ischemia group ( P < 0.01 ), and the neurological function score of the L-theanine treatment group gradually decreased and showed a statistically obvious difference on the 7th day of treatment ( P < 0.05 ). In summary, it was verified in this study that the role of L-theanine in the treatment of CIRI was of a great and positive significance for the subsequent treatment of patients with cerebral ischemia, providing reliable theoretical basis and data basis for clinical treatment of CIRI.

Senescence marker protein 30 confers neuroprotection in oxygen-glucose deprivation/reoxygenation-injured neurons through modulation of Keap1/Nrf2 signaling: Role of SMP30 in OGD/R-induced neuronal injury

2020 ◽  
pp. 096032712095424
Author(s):  
Wenxiong Liu ◽  
Haikang Zhao ◽  
Yuqiang Su ◽  
Kefeng Wang ◽  
Jing Li ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Neuronal Survival ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Marker Protein ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Senescence marker protein 30 (SMP30) is a senescence marker molecule and identified as a calcium regulatory protein. Currently, SMP30 has emerged as a cytoprotective protein in a wide range of cell types. However, the role of SMP30 in regulating neuronal survival during cerebral ischemia/reperfusion injury remains unclear. In the present study, we aimed to investigate the biological function and regulatory mechanism of SMP30 on neuronal survival using a cellular model induced by oxygen-glucose deprivation/reoxygenation (OGD/R). The results showed that SMP30 expression was significantly decreased by OGD/R exposure in neurons. Functional experiments demonstrated that SMP30 overexpression significantly rescued the decreased cell viability and attenuated the apoptosis and reactive oxygen species generation in OGD/R-exposed neurons. By contrast, SMP30 knockdown exhibited the opposite effect. Mechanism research revealed that SMP30 overexpression contributed to the activation of nuclear factor erythroid 2-related factor (Nrf2)/antioxidant response element (ARE) signaling associated with downregulation of Kelch-like ECH-associated protein (Keap1). Keap1 overexpression or Nrf2 silencing significantly reversed SMP30-mediated neuroprotection against OGD/R-induced injury. Overall, these findings demonstrate that SMP30 overexpression protects neurons from OGD/R-induced apoptosis and oxidative stress by enhancing Nrf2/ARE antioxidant signaling via inhibition of Keap1. These data highlight the importance of the SMP30/Keap1/Nrf2/ARE signaling axis in regulating neuronal survival during cerebral ischemia/reperfusion injury.

scholarly journals Inhibiting of GRASP65 Phosphorylation by DL-3-N-Butylphthalide Protects against Cerebral Ischemia-Reperfusion Injury via ERK Signaling

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Bei-lei Zhu ◽  
Chen-long Xie ◽  
Ning-ning Hu ◽  
Xin-bo Zhu ◽  
Chun-feng Liu
Keyword(s):  
Cerebral Ischemia ◽  
Treatment Group ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Erk Signaling ◽  
Erk Pathway ◽  
Mice Model ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Background and Purpose. The aim of this study was to explore the role of DL-3-n-butylphthalide (NBP) in cerebral ischemia-reperfusion injury (CIRI) mice model. The involvement of extracellular signal-regulated kinase (ERK) signaling pathway was also investigated. Methods. All mice were divided into five groups: sham-operated group, CIRI group, NBP pretreatment group, NBP treatment group, and NBP pretreatment + treatment group. The CIRI mice model was established by the use of the Pulsinelli four-vessel occlusion method. Pretreatment mice received NBP (90 mg/kg/d) three times a day within four days before reperfusion by gavage. Treatment mice received NBP (90 mg/kg/d) three times a day within five days after reperfusion by gavage. We detected the infarction area, the neurological severity, and the superoxide dismutase and malondialdehyde levels. Furthermore, we observed the expressions of GRASP65, phosphorylation of GRASP65 (pGRASP65), ERK, and phosphorylation of ERK (pERK) by the use of Western blotting. Results. The result showed that the ERK pathway was activated in response to CIRI. NBP decreases the expressions of pERK and pGRASP65 following CIRI. Additionally, NBP could decrease MDA and increase SOD level in brain tissues. Decreased infarct volume was also observed in the NBP group. Thereby, NBP inhibited the activation of the ERK pathway induced by CIRI and reduced the GRASP65 phosphorylation. Conclusions. The current finding suggested that NBP protected the cerebrum from CIRI mediated by inhibiting the ERK signaling pathway and subsequently reducing GRASP65 phosphorylation.

scholarly journals Luoyutong Treatment Promotes Functional Recovery and Neuronal Plasticity after Cerebral Ischemia-Reperfusion Injury in Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Ning-qun Wang ◽  
Li-ye Wang ◽  
Hai-ping Zhao ◽  
Ping Liu ◽  
Rong-liang Wang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Treatment Group ◽  
Reperfusion Injury ◽  
Neural Plasticity ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Control Treatment ◽  
High Dose ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Luoyutong (LYT) capsule has been used to treat cerebrovascular diseases clinically in China and is now patented and approved by the State Food and Drug Administration. In this retrospective validation study we investigated the ability of LYT to protect against cerebral ischemia-reperfusion injury in rats. Cerebral ischemia-reperfusion injury was induced by middle cerebral artery occlusion followed by reperfusion. Capsule containing LYT (high dose and medium dose) as treatment group and Citicoline Sodium as positive control treatment group were administered daily to rats 30 min after reperfusion. Treatment was continued for either 3 days or 14 days. A saline solution was administered to control animals. Behavior tests were performed after 3 and 14 days of treatment. Our findings revealed that LYT treatment improved the neurological outcome, decreased cerebral infarction volume, and reduced apoptosis. Additionally, LYT improved neural plasticity, as the expression of synaptophysin, microtubule associated protein, and myelin basic protein was upregulated by LYT treatment, while neurofilament 200 expression was reduced. Moreover, levels of brain derived neurotrophic factor and basic fibroblast growth factor were increased. Our results suggest that LYT treatment may protect against ischemic injury and improve neural plasticity.

scholarly journals Induction of heme oxygenase‐1 attenuates cerebral ischemia/reperfusion injury: role of heme

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Giovanni Li Volti ◽  
Francesco La Delia ◽  
Agata Zappalà ◽  
Maria Francesca Serapide ◽  
Giovanni Puglisi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Heme Oxygenase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Heme Oxygenase 1 ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury
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