scholarly journals Electroacupuncture Inhibits Myelin Sheath Injury in the Internal Capsule After Focal Cerebral Infarction in Rats Through the Nogo-A/NgR Signaling Pathway

2021 ◽  
Vol 27 ◽  
Author(s):  
Wenqing Dong ◽  
Huachun Miao ◽  
Huaibin Li ◽  
Feng Wu
Keyword(s):  
Cerebral Infarction ◽  
Signaling Pathway ◽  
Myelin Sheath ◽  
Internal Capsule

scholarly journals Post-stroke upper limb spasticity incidence for different cerebral infarction site

Open Medicine ◽  
2018 ◽  
Vol 13 (1) ◽  
pp. 227-231 ◽  
Author(s):  
Yi Jin ◽  
Yuan Zhao
Keyword(s):  
Basal Ganglia ◽  
Cerebral Infarction ◽  
Incidence Rate ◽  
Upper Extremity ◽  
Upper Limb ◽  
Internal Capsule ◽  
Post Stroke ◽  
Total Incidence ◽  
Limb Spasticity

AbstractObjectiveThe purpose of this study was to evaluate the incidence rate of post-stroke upper limb spasticity and its correlation with cerebral infarction site.MethodsA total of 498 inpatient and outpatient cases are included in the present study. The post-stroke upper limb spasticity rate of different cerebral infarction site was calculated.ResultsA total of 498 patients with cerebral infarction are enrolled in this study. Of these patients, 91 have dropped out and 407 have completed the study. Of the completed cases, 172 are in the spasm group and 235 are in the non-spasm group. The total incidence of upper limb spasticity is 34.5%. The incidences of upper extremity spasms are 12.5%, 20%, 22.5%, 35%, 40%, and 42.5% in 2 weeks, 1 month, 2 months, 3 months, 6 months, and 12 months, respectively. The incidence of upper extremity spasms increases with time. The incidences of upper limb spasticity are 12.1%, 63.3%, 58.5%, 9.4% and 8.3% when cerebral infarction occurs in the cortical and subcortical mixed areas, basal ganglia and internal capsule, cerebralcortex, brainstem and cerebellum respectively. The incidence of upper limb spasticity varies in different infarction sites (P < 0.05).ConclusionThe post-stroke upper limb spasticity rates were different according to the different cerebral infarction site. Patients with the ganglia and internal capsule infarctions had the highest risk of developing post-stroke upper limb spasticity.

scholarly journals Octreotide ameliorates hypoxia/reoxygenation-induced cerebral infarction by inhibiting oxidative stress, inflammation and apoptosis, and via inhibition of TLR4/MyD88/NF-κB signaling pathway

2021 ◽  
Vol 20 (11) ◽  
pp. 2261-2266
Author(s):  
Yanbin Hou ◽  
Zhongze Lou ◽  
Yunxin Ji ◽  
Liemin Ruan ◽  
He Gao
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Signaling Pathway ◽  
Control Group ◽  
N2a Cells ◽  
Tnf Α ◽  
Octreotide Treatment ◽  
Vitro Model ◽  
Hypoxia Reoxygenation

Purpose: To explore the effects of octreotide (OCT) on oxidative stress, inflammation and apoptosis in hypoxia/reoxygenation (H/R)-induced cerebral infarction.Methods: The in vitro model of cerebral infarction was established by treating N2A cells with hypoxia for 4 h and reoxygenation for 24 h. The viability of N2A cells was determined by CCK-8 assay. The cells were divided into 3 groups: control group, H/R group, and H/R+OCT group. The cells in H/R+OCT group were pretreated with OCT (60 ng/mL) before H/R treatment. The oxidative stress of N2A cells were assessed by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA). Inflammation of N2A cells was evaluated by evaluating the levels of TNF-α, IL-1β, IL-6, and IL-8, while the apoptosis of N2A cells was assessed by flow cytometry. Western blot analysis was used to determine the expression of Bcl-2, Bax, TLR4, MyD88, and NF-κB.Results: Octreotide treatment significantly reduced the level of oxidative stress. The inflammation of N2A cells caused by hypoxia/reoxygenation was inhibited by treatment with octreotide. Apoptosis of N2A cells was also inhibited by octreotide treatment. Hypoxia/reoxygenation activated TLR4/MyD88/NF-κB signaling pathway, while octreotide inhibits the activation of this pathway.Conclusion: The results reveal that octreotide inhibits hypoxia/reoxygenation-induced oxidative stress,as well as the inflammation, and apoptosis of N2A cells by inhibiting TLR4/MyD88/NF-κB signaling pathway. Thus, these findings may provide new insights into the treatment of cerebral infarction.

Attenuation of kirenol inflammationinduced by ischemic/reperfusion cerebral infarction stroke via TLR4/ NLRP3 signaling pathway: An in vivo approach

2021 ◽  
Vol 17 (74) ◽  
pp. 268
Author(s):  
Qing Luo ◽  
Debo Yun ◽  
Yujiao Yang ◽  
Bin Shang ◽  
Heng Dong ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Signaling Pathway ◽  
Ischemic Reperfusion

Effect of acupuncture on neurovascular units after cerebral infarction in rats through PI3K/AKT signaling pathway

2020 ◽  
Vol 75 (4) ◽  
pp. 387-397
Author(s):  
Linlin Wei ◽  
Kexue Zeng ◽  
Juanjuan Gai ◽  
Feixiong Zhou ◽  
Zhenglin Wei ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Signaling Pathway ◽  
Sham Group ◽  
Escape Latency ◽  
Akt Signaling ◽  
Acupuncture Group ◽  
Akt Signaling Pathway ◽  
Model Group ◽  
Protein Expressions ◽  
The Times

OBJECTIVE: To study the effect of acupuncture on neurovascular units after cerebral infarction (CI) in rats through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/AKT) signaling pathway. METHODS: A total of 36 Sprague-Dawley rats were randomly divided into sham group (n = 12), model group (n = 12) and acupuncture group (n = 12). The external carotid artery was only exposed in model group, while the post-CI ischemia-reperfusion model was established using the suture method in the other 2 groups. After modeling, the rats in sham group and model group were fixed and sampled, while those in acupuncture group were treated with acupuncture intervention for 2 weeks and sampled. The neurological deficits of rats were evaluated using the Zea-Longa score, and the spatial learning and memory of rats were detected via water maze test. Moreover, the expressions of vascular endothelial growth factor (VEGF), growth associated protein-43 (GAP-43) and synuclein (SYN) in brain tissues were detected via immunohistochemistry, and the relative protein expressions of PI3K p85, PI3K p110 and p-AKT were detected via Western blotting. The messenger ribonucleic acid (mRNA) expressions of VEGF, GAP-43 and SYN were detected via quantitative polymerase chain reaction (qPCR). RESULTS: The Zea-Longa score was significantly increased in model group and acupuncture group compared with that in sham group (p < 0.05), while it significantly declined in acupuncture group compared with that in model group (p < 0.05). The escape latency was significantly prolonged and the times of crossing platform were significantly reduced in model group and acupuncture group compared with those in sham group (p < 0.05), while the escape latency was significantly shortened and the times of crossing platform were significantly increased in acupuncture group compared with those in model group (p < 0.05). The positive expressions of VEGF, GAP-43 and SYN were obviously increased in model group and acupuncture group compared with those in sham group (p < 0.05), while they were obviously increased in acupuncture group compared with those in model group (p < 0.05). Besides, model group and acupuncture group had significantly higher relative protein expressions of PI3K p85, PI3K p110 and p-AKT than sham group (p < 0.05), while acupuncture group also had significantly higher relative protein expressions of PI3K p85, PI3K p110 and p-AKT than model group (p < 0.05). The relative mRNA expressions of VEGF, GAP-43 and SYN were remarkably increased in model group and acupuncture group compared with those in sham group (p < 0.05), while they were remarkably increased in acupuncture group compared with those in model group (p < 0.05). CONCLUSION: Acupuncture promotes the repair of neurovascular units after CI in rats through activating the PI3K/AKT signaling pathway, thereby exerting a protective effect on neurovascular units.

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