scholarly journals Neuroprotective Effect of 4T1 and Sertoli Cells Co-Transplantation in Animal Model of Brain Ischemia

2018 ◽  
Vol 3 (3) ◽  
pp. 133-139
Author(s):  
Sara Milanizadeh ◽  
Abbas Aliaghaei ◽  
Mohammad Reza Bigdeli
Keyword(s):  
Brain Edema ◽  
Blood Brain Barrier ◽  
Sertoli Cells ◽  
Neurotrophic Factors ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Brain Barrier Permeability

Aim: Introducing neurotrophic factors are among several new approaches to enhance neural resistance to the ischemic condition. Cancer cells such as 4T1 are one of the strongest cells with high viability in transplanted area. 4T1 cells are invasive breast carcinoma cells derived from spontaneous tumors in mouse Balb/C which their pathologic effects are limited to Balb/C species. Sertoli cells (SCs) can be a proper candidate for increasing transplanted cells survival. These cells not only suppress the immune system, but also secret growth factors. The aim of this study is to evaluate the possible neuroprotective effect of 4T1 transplantation on middle cerebral artery occlusion (MCAO) rat model alone and with SCs co-transplanted. Material and Methods: Rats were divided into five experimental groups: control, sham, SCs, 4T1 and 4T1+SCs treated groups. Cells were transplanted into the right striatum by using stereotaxic surgery. Ischemic surgery was done after five days. 24 hours after reperfusion, neurological severity score, infarct volume, brain edema, and blood-brain barrier permeability were assessed in different areas of the brain including cortex, striatum and piriform cortex-amygdala (Pir-Amy). Results: This study demonstrates that SCs and 4T1 transplantation ameliorate neurological deficits and reduce infarct volume, brain edema and blood-brain barrier permeability compared to the control group. Conclusion: Introducing cancer cell transplantation as a source of neurotrophic factors to enhance neural survival can be a new approach in cell therapy.

scholarly journals Dietary Virgin Olive Oil Reduces Blood Brain Barrier Permeability, Brain Edema, and Brain Injury in Rats Subjected to Ischemia-Reperfusion

2010 ◽  
Vol 10 ◽  
pp. 1180-1191 ◽  
Author(s):  
Fatemeh Mohagheghi ◽  
Mohammad Reza Bigdeli ◽  
Bahram Rasoulian ◽  
Ali Asghar Zeinanloo ◽  
Ali Khoshbaten
Keyword(s):  
Brain Edema ◽  
Blood Brain Barrier ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Virgin Olive Oil ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Recent studies suggest that dietary virgin olive oil (VOO) reduces hypoxia-reoxygenation injury in rat brain slices. We sought to extend these observations in anin vivostudy of rat cerebral ischemia-reperfusion injury. Four groups, each consisting of 18 Wistar rats, were studied. One group (control) received saline, while three treatment groups received oral VOO (0.25, 0.5, and 0.75 mL/kg/day, respectively). After 30 days, blood lipid profiles were determined, before a 60-min period of middle cerebral artery occlusion (MCAO). After 24-h reperfusion, neurological deficit scores, infarct volume, brain edema, and blood brain barrier permeability were each assessed in subgroups of six animals drawn from each main group. VOO reduced the LDL/HDL ratio in doses of 0.25, 0.5, and 0.75 mL/kg/day in comparison to the control group (p< 0.05), and offered cerebroprotection from ischemia-reperfusion. For controls vs. doses of 0.25 vs. 0.5 vs. 0.75 mL/kg/day, attenuated corrected infarct volumes were 207.82 ± 34.29 vs. 206.41 ± 26.23 vs. 124.21 ± 14.73 vs. 108.46 ± 31.63 mm3; brain water content of the infarcted hemisphere was 82 ±± 0.25 vs. 81.5 ± 0.56 vs. 80.5 ± 0.22 vs. 80.5 ± 0.34%; and blood brain barrier permeability of the infarcted hemisphere was 11.31 ± 2.67 vs. 9.21 ± 2.28 vs. 5.83 ± 1.6 vs. 4.43 ± 0.93 µg/g tissue (p< 0.05 for measures in doses 0.5 and 0.75 mL/kg/day vs. controls). Oral administration of VOO reduces infarct volume, brain edema, blood brain barrier permeability, and improves neurologic deficit scores after transient MCAO in rats.

RESVERATROL PREVENTS BRAIN EDEMA, BLOOD‐BRAIN BARRIER PERMEABILITY AND ALTERED AQUAPORIN PROFILE IN AUTISM ANIMAL MODEL

2021 ◽  
Author(s):  
Iohanna Deckmann ◽  
Júlio Santos‐Terra ◽  
Mellanie Fontes‐Dutra ◽  
Marília Körbes‐Rockenbach ◽  
Guilherme Bauer‐Negrini ◽  
...  
Keyword(s):  
Animal Model ◽  
Brain Edema ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Abstract T P84: Beneficial Stroke Outcomes Following Epicatechin Consumption in Young and Older Mice

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Christopher Leonardo ◽  
Sylvain Dore
Keyword(s):  
Blood Brain Barrier ◽  
Knockout Mice ◽  
Infarct Volume ◽  
Brain Barrier ◽  
Barrier Permeability ◽  
Blood Brain Barrier Permeability ◽  
Functional Deficits ◽  
Post Stroke ◽  
Brain Barrier Permeability ◽  
Nrf2 Knockout

Background: The consumption of flavanol containing foods, including (-)-epicatechin, has been linked to lower incidence of cardiovascular disease and stroke. We have previously demonstrated that epicatechin prophylaxis reduces stroke-induced anatomical and functional deficits in young, healthy mice; yet clinical stroke is primarily a disease of the elderly. Since neuroinflammation and vascular dysfunction are associated with aging, we aimed to test whether epicatechin is also protective in aging mice subjected to experimental stroke, and if so, whether this results from reduced glial cell activation and blood brain barrier permeability. Methods: Twelve-month-old wildtype and C57BL/6 Nrf2 knockout mice were administered 15mg/kg epicatechin, the minimum effective dose in young, healthy mice, prior to permanent distal middle cerebral artery occlusion. Mice were evaluated for functional recovery at one day post-stroke using the Adhesive Removal Test. Infarct volume, gliosis, and blood brain barrier permeability estimates were conducted seven days following stroke. Additionally, we compared anastomosis in wildtype and Nrf2 knockout mice and assessed hemorrhage frequency in studies using four- and 12-month-old mice. Results: Consistent with previous results in young mice, 12-month-old wildtype mice pretreated with epicatechin showed significant reductions in infarct volume and latency to remove adhesive tape relative to vehicle-treated controls, while Nrf2 knockout mice were not protected by epicatechin. Interestingly, epicatechin did not reduce Iba1 immunoreactivity or mouse IgG extravasation at seven days post-stroke. Similarly, there were no significant differences in anastomosis or spontaneous hemorrhage between wildtype and Nrf2 knockouts, indicating that cerebral vascular physiology is similar and gross vascular integrity was unaffected by treatment. Conclusion: Thus, although epicatechin prophylaxis reduces infarct volume and functional deficits, it does not exert sustained effects on gliosis or cerebrovascular integrity in aging mice.

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