scholarly journals Alleviation of Neuronal Cell Death and Memory Deficit with Chungkookjang Made with Bacillus amyloliquefaciens and Bacillus subtilis Potentially through Promoting Gut–Brain Axis in Artery-Occluded Gerbils

Foods ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2697
Author(s):  
Ting Zhang ◽  
Myeong-Seon Ryu ◽  
Xuangao Wu ◽  
Hee-Jong Yang ◽  
Su Ji Jeong ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cell Death ◽  
Ischemic Stroke ◽  
Normal Control ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Control Group ◽  
Β Cell ◽  
Post Stroke

Short-term fermented soybeans (chungkookjang) with specific Bacillus (B.) spp. have anti-obesity, antidiabetic, and anti-stroke functions. We examined the hypothesis that the long-term consumption of B. amyloliquefaciens SCGB 1 fermented (CKJ1) and B. subtilis SCDB 291 (CKJ291) chungkookjang can alleviate clinical symptoms and hyperglycemia after ischemic stroke by promoting the gut microbiota–brain axis. We examined this hypothesis in Mongolian male gerbils with stroke symptoms induced by carotid artery occlusion. The artery-occluded gerbils were divided into five groups: no supplementation (Control, Normal-control), 4% cooked soybeans (CSB), CKJ1, or CKJ291 in a high-fat diet for 3 weeks. The carotid arteries of gerbils in the Control, CSB, CKJ1, and CKJ291 groups were occluded for 8 min and they then continued on their assigned diets for an additional 3 weeks. Normal-control gerbils had no artery occlusion. The diets in all groups contained an identical macronutrient composition using starch, casein, soybean oil, and dietary fiber. The CSB, CKJ1, and CKJ291 groups exhibited less neuronal cell death than the Control group, while the CKJ1 group produced the most significant reduction among all groups, as much as 85% of the Normal-control group. CKJ1 and CKJ291 increased the blood flow and removal of blood clots, as determined by Doppler, more than the Control. They also showed more improvement in neurological disorders from ischemic stroke. Their improvement showed a similar tendency as neuronal cell death. CKJ1 treatment improved memory impairment, measured with Y maze and passive avoidance tests, similar to the Normal-control. The gerbils in the Control group had post-stroke hyperglycemia due to decreased insulin sensitivity and β-cell function and mass; the CKJ291, CSB, and CKJ1 treatments protected against glucose disturbance after artery occlusion and were similar to the Normal-control. CKJ1 and CKJ291 also reduced serum tumor necrosis factor-α concentrations and hippocampal interleukin-1β expression levels, compared to the Control. CKJ1 and CKJ291 increased the contents of Lactobacillus, Bacillus, and Akkermansia in the cecum feces, similar to the Normal-control. Picrust2 analysis showed that CKJ1 and CKJ291 increased the propionate and butyrate metabolism and the starch and glucose metabolism but reduced the lipopolysaccharide biosynthesis and fatty acid metabolism compared to the Control. In conclusion, daily CKJ1 and CKJ291 intake prevented neuronal cell death and memory dysfunction from the artery occlusion by increasing blood flow and β-cell survival and reducing post-stroke-hyperglycemia through modulating the gut microbiome composition and metabolites to influence the host metabolism, especially inflammation and insulin resistance, protecting against neuronal cell death and brain dysfunction. CKJ1 had better effects than CKJ291.

scholarly journals Protection against Neurological Symptoms by Consuming Corn Silk Water Extract in Artery-Occluded Gerbils with Reducing Oxidative Stress, Inflammation, and Post-Stroke Hyperglycemia through the Gut-Brain Axis

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 168
Author(s):  
Jin Ah Ryuk ◽  
Byoung Seob Ko ◽  
Na Rang Moon ◽  
Sunmin Park
Keyword(s):  
Ischemic Stroke ◽  
Neuronal Cell Death ◽  
Cell Mass ◽  
Water Extract ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Sham Control ◽  
Β Cell ◽  
Post Stroke ◽  
Corn Silk

Corn silk (Stigma maydis), rich in flavonoids, is traditionally used to treat edema, depression, and hyperglycemia and may alleviate ischemic stroke symptoms in Chinese medicine. This study examined whether corn silk water extract (CSW) could alleviate ischemic stroke symptoms and post-stroke hyperglycemia in Mongolian gerbils with transient cerebral ischemia and reperfusion (I/R). After being given 0.05% (I/R-LCSW) and 0.2% (I/R-HCSW), 0.02% aspirin (I/R-aspirin), and cellulose (I/R-control) in their 40 energy% fat diets for three weeks, the gerbils underwent an artery occlusion for eight minutes and reperfusion. They took the assigned diet for an additional three weeks. Sham-operated gerbils without artery occlusion had the same diet as Sham-control. CSW intake reduced neuronal cell death in gerbils with I/R and dose-dependently improved the neurological symptoms, including drooped eyes, crouched posture, flexor reflex, and walking patterns. CSW intake also alleviated the short-term memory and spontaneous alteration and grip strength compared to the I/R-control group. The protection against ischemic stroke symptoms was associated with the reduced tumor necrosis factor-α, interleukin-1β, superoxide, and lipid peroxide levels, promoting superoxide dismutase activity in the hippocampus in the CSW groups, compared to the I/R-control. The blood flow measured by Doppler was improved with CSW compared to the I/R-control. Furthermore, CSW intake prevented the post-stroke hyperglycemia related to decreasing pancreatic β-cell mass as much as the Sham-control, and it was related to protection against β-cell apoptosis, restoring the β-cell mass similar to the Sham-control. CSW intake elevated the relative abundance of Lactobacillus, Bifidobacterium, Allobaculum, and Akkermansia compared to the I/R-control. Picrust2 analysis showed that CSW increased the propionate and butyrate metabolism and the starch and glucose metabolism but reduced lipopolysaccharide biosynthesis compared to the I/R-control. In conclusion, CSW intake protects against neuronal cell death and post-hyperglycemia by reducing oxidative stress and inflammation and increasing blood flow and the β-cell mass. The alleviation was associated with promoting the gut-brain axis by changing the gut microbiome community.

Abstract 114: Neuroprotective Role of Brain Pericytes through PDGFRβ-Akt Signaling in Ischemic Stroke

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Koichi Arimura ◽  
Tetsuro Ago ◽  
Masahiro Kamouchi ◽  
Hiroshi Sugimori ◽  
Junya Kuroda ◽  
...  
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Infarct Volume ◽  
Neurovascular Unit ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Akt Signaling ◽  
Artery Occlusion ◽  
Brain Functions ◽  
Brain Pericytes

Brain pericytes are a constituent of the neurovascular unit and play various important roles in brain functions, such as regulation of capillary blood flow, maintenance of blood-brain barrier and angiogenesis. Previous reports have elucidated that PDGF-B prevents neuronal cell death during ischemic insults in adult rodent models; however, the detailed mechanisms by which PDGF-B signaling protects neurons from ischemic damage are not fully understood. In the present study, we investigated whether brain pericytes play neuroprotective roles in brain ischemia, using a permanent middle cerebral artery occlusion stroke model (MCAO) and cultured human brain pericytes. Immunohistochemistry revealed that the expression of PDGF receptorβ(PDGFRβ) was induced predominantly in pericytes in peri-infarct areas. PDGF-B induced marked phosphorylation of Akt in cultured pericytes. Consistently, Akt was markedly phosphorylated in the PDGFRβ-expressing pericytes in peri-infarct areas. PDGF-B upregulated the expression of neurotrophins, such as neuronal growth factor (NGF) and neurotrophin-3 (NT-3), through Akt activation in the cultured pericytes. We subjected PDGFRβheterozygous knockout (PDGFRβ+/-) mice to MCAO. Infarct volume, as assessed by MAP2 immunostaining, was significantly greater in PDGFRβ+/- than wild-type mice ( 48% increase at day 7, p < 0.01 , n=5). The number of TUNEL positive apoptotic cells was significantly greater in PDGFRβ+/- mice (54 % increase at day 4, p < 0.001 , n=6). Production of NGF and NT-3 at mRNA and protein levels in infarct areas was significantly decreased in PDGFRβ+/- mice (NGF: 28% decrease, p<0.05, NT-3: 22% decrease, p<0.05). Since it has been established that neurotrophin receptors are induced in peri-infarct areas, the decreases in neurotrophin production may increase apoptotic neuronal cell death in the PDGFRβ+/- mice. In conclusion, brain pericytes may have a direct neuroprotective role through secreting neurotrophins via PDGFRβ-Akt signaling, thereby decreasing infarct volume in ischemic stroke.

scholarly journals Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat

2016 ◽  
Vol 88 (suppl 1) ◽  
pp. 653-663 ◽  
Author(s):  
Dulce-Mariely Álvarez-Croda ◽  
Juan Santiago-García ◽  
Jesús S. Medel-Matus ◽  
Joel Martínez-Quiroz ◽  
Angel A. Puig-Lagunes ◽  
...  
Keyword(s):  
Cell Death ◽  
Status Epilepticus ◽  
Mrna Expression ◽  
Dorsal Hippocampus ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Control Group ◽  
Rat Pups ◽  
Fluoro Jade B ◽  
Developing Rat

The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteen-days-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohistochemical procedures; Fluoro-Jade B staining was carried out in parallel sections in order to detect neuronal cell death. IL-1β mRNA expression was increased 6 h following SE, but not at 24 h; however IL-1RI mRNA expression was unaffected when comparing with the control group. IL-1β and IL-1RI immunoreactivity was not detected in control animals. IL-1β and IL-1RI were expressed in the CA1 pyramidal layer, the dentate gyrus granular layer and the hilus 6 h after SE, whereas injured cells were detected 24 h following seizures. Early expression of IL-1β and IL-1RI in the hippocampus could be associated with SE-induced neuronal cell death mechanisms in the developing rat.

scholarly journals Cerebral Ischemia Causes Dysregulation of Synaptic Adhesion in Mouse Synaptosomes

2007 ◽  
Vol 28 (1) ◽  
pp. 99-110 ◽  
Author(s):  
Willard J Costain ◽  
Ingrid Rasquinha ◽  
Jagdeep K Sandhu ◽  
Peter Rippstein ◽  
Bogdan Zurakowski ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Adhesion Molecules ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Synaptic Proteins ◽  
Mrna Levels ◽  
Neuronal Nuclei ◽  
Protein Levels

Synaptic pathology is observed during hypoxic events in the central nervous system in the form of altered dendrite structure and conductance changes. These alterations are rapidly reversible, on the return of normoxia, but are thought to initiate subsequent neuronal cell death. To characterize the effects of hypoxia on regulators of synaptic stability, we examined the temporal expression of cell adhesion molecules (CAMs) in synaptosomes after transient middle cerebral artery occlusion (MCAO) in mice. We focused on events preceding the onset of ischemic neuronal cell death (< 48 h). Synaptosome preparations were enriched in synaptically localized proteins and were free of endoplasmic reticulum and nuclear contamination. Electron microscopy showed that the synaptosome preparation was enriched in spheres (≈650 nm in diameter) containing secretory vesicles and postsynaptic densities. Forebrain mRNA levels of synaptically located CAMs was unaffected at 3 h after MCAO. This is contrasted by the observation of consistent downregulation of synaptic CAMs at 20 h after MCAO. Examination of synaptosomal CAM protein content indicated that certain adhesion molecules were decreased as early as 3 h after MCAO. For comparison, synaptosomal Agrn protein levels were unaffected by cerebral ischemia. Furthermore, a marked increase in the levels of p-Ctnnb1 in ischemic synaptosomes was observed. p-Ctnnb1 was detected in hippocampal fiber tracts and in cornu ammonis 1 neuronal nuclei. These results indicate that ischemia induces a dysregulation of a subset of synaptic proteins that are important regulators of synaptic plasticity before the onset of ischemic neuronal cell death.

scholarly journals miR-455 inhibits neuronal cell death by targeting TRAF3 in cerebral ischemic stroke

2016 ◽  
Vol Volume 12 ◽  
pp. 3083-3092 ◽  
Author(s):  
Shengtao Yao ◽  
Bo Tang ◽  
Gang Li ◽  
Ruiming Fan ◽  
Fang Cao
Keyword(s):  
Cell Death ◽  
Ischemic Stroke ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic

scholarly journals Corrigendum

2016 ◽  
Vol 36 (2) ◽  
pp. 456-456
Keyword(s):  
Blood Flow ◽  
Cell Death ◽  
Cerebral Blood Flow ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Pyroptotic neuronal cell death mediated by the AIM2 inflammasome Adamczak SE, de Rivero Vaccari JP, Dale G, Brand FJ 3rd, Nonner D, Bullock MR, Dahl GP, Dietrich WD, Keane RW Journal of Cerebral Blood Flow & Metabolism 2014; 34: 621–629 .

scholarly journals PSD-93 mediates the crosstalk between neuron and microglia and facilitates acute ischemic stroke injury by binding to CX3CL1

2020 ◽  
Author(s):  
qingxiu zhang ◽  
Lei He ◽  
Mo Chen ◽  
Hui Yang ◽  
Xiaowei Cao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Amino Acid ◽  
Amino Acid Sequence ◽  
Acute Ischemic Stroke ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Amino Acid Sequences ◽  
Glutamate Excitotoxicity ◽  
Underlying Mechanisms

Abstract Background: Postsynaptic density 93 (PSD-93) mediates glutamate excitotoxicity induced by ischemic brain injury, which then induces microglial inflammatory response. However, the underlying mechanisms of how PSD-93 mediates the crosstalk between neurons and microglia in the postsynaptic dense region remain elusive. CX3 chemokine ligand 1 (CX3CL1) is a chemokine specifically expressed in neurons while its receptor CX3CR1 is highly expressed in microglia. In this study, we aimed to investigate the role of PSD-93 and CX3CL1 interaction in the crosstalk between neuron and microglia in acute ischemic stroke.Methods: Male C57BL/6 mice were used to establish middle cerebral artery occlusion model and co-immunoprecipitation and immunoblotting were used to detect the binding of PSD-93 and CX3CL1 at different time points following cerebral ischemic/reperfusion (I/R). ELISA was used to detect soluble CX3CL1. Yeast two-hybrid and co-immunoprecipitation were used to identify special amino acid sequences responsible for the interaction between PSD-93 and CX3CL1. Finally, a fusion small peptide Tat-CX3CL1 was designed to inhibit PSD-93 and CX3CL1 interaction.Results: The binding of PSD-93 and CX3CL1 peaked at 6 h after I/R. The binding sites were located in the 420-535 amino acid sequence of PSD-93 and 357-395 amino acid sequence of CX3CL1. Tat-CX3CL1 (357-395aa) could inhibit the interaction of PSD-93 and CX3CL1 and inhibited the pro-inflammatory cytokine IL-1β and TNF-α expression and provided neuroprotection following reperfusion.Conclusions: PSD-93 binds CX3CL1 to activate microglia and initiate neuroinflammation. Specific blockade of PSD-93-CX3CL1 interaction reduces I/R induced neuronal cell death, and provides a new therapeutic target for ischemic stroke.

scholarly journals The Efficacy of Cinnamomum burmanii Extract on the Protection of Neuronal Cell Death in Haloperidol Induced Male Wistar Rats

2018 ◽  
Vol 2 (4) ◽  
pp. 1-11
Author(s):  
Nita Parisa ◽  
MT Kamaluddin ◽  
Theodorus Theodorus
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Positive Control ◽  
Control Group ◽  
Cinnamon Extract ◽  
White Rats ◽  
Before And After ◽  
Mean Differences

Background Haloperidol is categorized as the first class antipsychotic drug. Long-term use of haloperidol may convey to increased Reactive Oxygen Species (ROS) that will yield oxidative damage which further leads to cell death. Several studies had identified the effects of cinnamon extract on cell death. This study aimed to determine the efficacy of cinnamon extract (Cinnamomum burmanii) on the protection of neuronal cell death in haloperidol-induced male Wistar white rats. Methods This study was experimental with pre and post-test design. Thirty male Wistar rats were divided into 5 groups, induced with haloperidol and followed by treatment. Caspase-3 and dopamine were assayed by ELISA sandwich method using ELISA kit. Mean difference of caspase expression and dopamine levels before and after induction were shown (p<0.05). Results There were mean differences of caspase-3 expression level in the positive control group, cinnamon extract of 100 and 200mg/kgBW before and after treatment (p<0.05). Whereas for dopamine levels, there were mean differences in positive control group, cinnamon extract of 50, 100 and 200mg/kgBW before and after treatment (p<0.05). With Post Hoc test, it was found that there were no mean differences of caspase-3 expression level between positive group with cinnamon extract group of 100 and 200mg/kgBW (p>0,05) and there were also no mean differences of positive group dopamine level with group of cinnamon extract of 100 and 200mg/kgBW (p>0.05). Conclussion Cinnamomum burmanii extract at dose of 100 and 200mg/kgBW were effective in the protection against neuronal cell death in haloperidol induced male Wistar white rats.

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