Evaluation of the Neuroprotective Effect of Pycnogenol in a Hypoxic-Ischemic Brain Injury Model in Newborn Rats

2021 ◽  
Author(s):  
Ruya Çolak ◽  
Aslı Celik ◽  
Gulden Diniz ◽  
Senem Alkan Özdemir ◽  
Osman Yilmaz ◽  
...  
Keyword(s):  
Brain Injury ◽  
Cell Injury ◽  
Neuroprotective Effect ◽  
Neuronal Cell ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Albino Rats ◽  
Protective Agent ◽  
Injury Model ◽  
Group B ◽  
Factor Α

Objective This study aimed to evaluate the efficacy of Pycnogenol (PYC) and its antioxidant and antiapoptotic effect in an experimental hypoxic-ischemic (HI) rat model. Study Design A total of 24 Wistar albino rats who were on the seventh postnatal day were divided into three groups with developed HI brain injury model under the sevoflurane anesthesia: 40 mg/kg PYC was given to Group A, saline was given to Group B, and the sham group was Group C. Neuronal apoptosis was investigated by terminal deoxynucleotidyl transferase dUTP nick end labeling and immunohistochemically stained manually with primer antibodies of tumor necrosis factor-α and interleukin-1β. Results The neuronal cell injury was statistically lower in the PYC treatment group. Conclusion This is the first study that investigates the role of PYC in the HI brain injury model. PYC reduces apoptosis and neuronal injury in the cerebral tissue of the rats. PYC may be a protective agent against hypoxic-ischemic encephalopathy. Key Points

scholarly journals Neuroprotective Effect of Grewia carpinifolia Extract against Vanadium Induced Behavioural Impairment

2016 ◽  
Vol 60 (4) ◽  
pp. 5-13 ◽  
Author(s):  
O. E. Adebiyi ◽  
J. O. Olopade ◽  
F. O. Olayemi
Keyword(s):  
Neuroprotective Effect ◽  
Ethanolic Extract ◽  
Control Group ◽  
Protective Agent ◽  
Central Nervous System Toxicity ◽  
Sodium Metavanadate ◽  
Latent Time ◽  
Group A ◽  
Vanadium Toxicity ◽  
Group B

Abstract Vanadium (V), a heavy metal, has been reported to induce central nervous system toxicity leading to various behavioural impairments. It is characterized by the production of reactive oxygen. The present study was designed to test the possibility of Grewia carpinifolia ethanolic extract in preventing behavioural alterations following acute vanadium toxicity in mice. Twenty five Swiss albino mice (25—27 g) were completely randomized into 5 groups (A—E) of 5 animals each. Group A received distilled water and served as a control; group B, received vitamin E (500 mg.kg−1 b. w. every 72 hours), a known antioxidant orally, along with a daily dose of sodium metavanadate intraperitoneally (i. p.) for 7 days; group C and group D received Grewia carpinifolia leaf extract at 100 and 200 mg.kg−1 b.w orally respectively, along with the sodium metavanadate i. p. for 7 days; while group E received sodium metavanadate i. p. only for 7 days. The behavioural and motor functions were analysed by the open field, negative geotaxis, and hanging wire tests; the daily body and brain weights were recorded. Grewia carpinifolia ethanolic extracts significantly reduced the number of grooming, stretched attend posture, and freezing time that were significantly increased in the vanadium only group and also enhanced the vestibular functions. In addition, the latent time spent on the hanging wire in groups simultaneously administered with the extract and V compared favourably (P > 0.05) with the control groups but a decrease in latent time was observed in the V only group. The results suggest that acute V toxicity results in various behavioural deficits and support a possible role of Grewia carpinifolia as a protective agent against acute vanadium-toxicity with a better result at 200 mg.kg−1 b. w.

scholarly journals Microparticles Impair Hypotensive Cerebrovasodilation and Cause Hippocampal Neuronal Cell Injury after Traumatic Brain Injury

2016 ◽  
Vol 33 (2) ◽  
pp. 168-174 ◽  
Author(s):  
Leif-Erik Bohman ◽  
John Riley ◽  
Tatyana N. Milovanova ◽  
Matthew R. Sanborn ◽  
Stephen R. Thom ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cell Injury ◽  
Neuronal Cell

scholarly journals Heat Acclimation Regulates the Autophagy-Lysosome Function to Protect Against Heat Stroke-Induced Brain Injury in Mice

2017 ◽  
Vol 41 (1) ◽  
pp. 101-114 ◽  
Author(s):  
Junfeng Yi ◽  
Genlin He ◽  
Ju Yang ◽  
Zhen Luo ◽  
Xuesen Yang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Heat Stroke ◽  
Microscopic Analysis ◽  
Heat Acclimation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Electron Microscopic ◽  
Fluoro Jade B

Background/Aims: The mechanisms underlying the protective role of heat acclimation (HA) in heat stroke (HS)-induced brain injury are still unclear. The autophagy-lysosome pathway is known to pay an important role in protecting stressed or diseased cells from death. Nevertheless, whether autophagy and lysosomes are involved in HA-mediated neuroprotection following HS exposure remains unclear. Methods: The protective effects of HA were assessed by rectal temperature, hematoxylin-eosin staining, transmission electron microscopic analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining, and Fluoro Jade B staining, after mice were subjected to HS. The effects of HA on autophagy and lysosomes were assessed in the presence of the autophagy inhibitor 3-methyladenine (3MA). Autophagy and lysosome-associated proteins were analysed by Western blotting. Results: We found that HA protected against HS-induced death and brain injury. HS can robustly induce autophagy and impair lysosome function. HA pre-conditioning significantly modulated the autophagy level, and improved lysosome function in HS mice. Furthermore, 3MA completely abolished the neuroprotective effect of HA on HS. Conclusion: HS may induce brain injury through lysosomal dysfunction and impaired autophagic flux. HA protected against HS-induced brain injury via a mechanism involving the autophagy-lysosome pathway.

Inhibition of acrolein-induced apoptosis by the antioxidant selenium

2020 ◽  
Vol 36 (2) ◽  
pp. 84-92
Author(s):  
Ayşe Başardı Gökçe ◽  
Banu Eren ◽  
Dilek Sağir ◽  
Burcu Demirel Yilmaz
Keyword(s):  
Chromatin Condensation ◽  
Light And Electron Microscopy ◽  
Environmental Pollutant ◽  
Apoptotic Index ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Control Group ◽  
Albino Rats ◽  
Protective Agent ◽  
Electron Microscopic ◽  
Induced Apoptosis

In this study, the effects of a potent antioxidant, selenium, on apoptosis induced by acrolein, a cytotoxic and genotoxic environmental pollutant, were investigated by immunohistochemical and electron microscopic methods. One hundred adult male Wistar albino rats were used in the study. The rats were divided into four main groups: control, acrolein, selenium, and acrolein + selenium. The animals in the experimental groups were given 1 mg/kg/day selenium and 4 mg/kg/day acrolein daily for 7 days by gavage. After drug administration, each group was divided into subgroups according to the time they were to be euthanized: 12th hour, 1st, 2nd, 3rd, and 5th day. The rats in each group at the determined time were euthanized and their livers were removed. Routine histological procedures were performed for light and electron microscopy examinations. After applying the Terminal Deoxynucleotidyl Transferase dUTP nick end labeling assay on the liver sections, apoptotic index values were calculated. Comparing the liver sections of the rats in the acrolein group and the control group, acrolein was found to cause a significant increase in the apoptotic index. The apoptotic index values of the acrolein + selenium group decreased compared to the acrolein group. In the electron microscopic examinations, apoptotic findings were observed in the liver tissues of the rats given acrolein, such as chromatin condensation in the nucleus of hepatocytes, dilatations in the perinuclear space, and cytoplasmic vacuolization. These apoptotic findings were not observed in the acrolein + selenium group after the 12th hour. These findings show that selenium may potentially be useful as a protective agent for people exposed to acrolein.

scholarly journals Evidence for the infiltration of gas bubbles into the arterial circulation and neuronal injury following “yo-yo” dives in pigs

2016 ◽  
Vol 121 (5) ◽  
pp. 1059-1064
Author(s):  
Dror Ofir ◽  
Yoav Yanir ◽  
Michael Mullokandov ◽  
Ben Aviner ◽  
Yehuda Arieli
Keyword(s):  
Spinal Cord ◽  
Left Ventricle ◽  
Cell Injury ◽  
Neuronal Cell ◽  
Gas Bubbles ◽  
Control Group ◽  
Arterial Circulation ◽  
Increased Risk ◽  
Group B ◽  
The Right

“Yo-yo” diving may place divers at a greater risk of neurologic decompression illness (DCI). Using a rat model, we previously demonstrated that “yo-yo” diving has a protective effect against DCI. In the current study, we evaluated the risk of neurologic DCI following “yo-yo” dives in a pig model. Pigs were divided into four groups. The Control group ( group A) made a square dive, without excursions to the surface (“peeps”). Group B performed two “peeps,” group C performed four “peeps,” and group D did not dive at all. All dives were conducted on air to 5 atm absolute, for 30-min bottom time. Echocardiography was performed to detect cardiac gas bubbles before the dive, immediately after, and at 90-min postdive. Motor performance was observed during the 5-h postdive period. Symptoms increased dramatically following a dive with four “peeps.” Gas bubbles were detected in the right ventricle of all animals except for the sham group and in the left ventricle only after the four-peep dive. Neuronal cell injury was found in the spinal cord in each of the three experimental groups, tending to decrease with an increase in the number of “peeps.” A four-peep “yo-yo” dive significantly increased the risk of neurologic DCI in pigs. Following a four-peep dive, we detected a higher incidence of bubbles in the left ventricle, supporting the common concern regarding an increased risk of neurologic DCI, albeit there was no direct correlation with the frequency of “red neurons” in the spinal cord.

Oxidative Stress: Major Threat in Traumatic Brain Injury

2018 ◽  
Vol 17 (9) ◽  
pp. 689-695 ◽  
Author(s):  
Nidhi Khatri ◽  
Manisha Thakur ◽  
Vikas Pareek ◽  
Sandeep Kumar ◽  
Sunil Sharma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mitochondrial Dysfunction ◽  
Calcium Influx ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Physical Assault ◽  
Mortality And Morbidity ◽  
Primary Injury

Background & Objective: Traumatic Brain Injury (TBI) is one of the major causes of mortality and morbidity worldwide. It represents mild, moderate and severe effects of physical assault to brain which may cause sequential, primary or secondary ramifications. Primary injury can be due to the first physical hit, blow or jolt to one of the brain compartments. The primary injury is then followed by secondary injury which leads to biochemical, cellular, and physiological changes like blood brain barrier disruption, inflammation, excitotoxicity, necrosis, apoptosis, mitochondrial dysfunction and generation of oxidative stress. Apart from this, there is also an immediate increase in glutamate at the synapses following severe TBI. Excessive glutamate at synapses in turn activates corresponding NMDA and AMPA receptors that facilitate excessive calcium influx into the neuronal cells. This leads to the generation of oxidative stress which further leads to mitochondrial dysfunction, lipid peroxidation and oxidation of proteins and DNA. As a consequence, neuronal cell death takes place and ultimately people start facing some serious disabilies. Conclusion: In the present review we provide extensive overview of the role of reactive oxygen species (ROS)-induced oxidative stress and its fatal effects on brain after TBI.

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