scholarly journals Therapeutic Effects of Hydroalcoholic Extracts from the Ancient Apple Mela Rosa dei Monti Sibillini in Transient Global Ischemia in Rats

2021 ◽  
Vol 14 (11) ◽  
pp. 1106
Author(s):  
Hasan Yousefi-Manesh ◽  
Ahmad Reza Dehpour ◽  
Seyed Mohammad Nabavi ◽  
Malihe Khayatkashani ◽  
Mohammad Hossein Asgardoon ◽  
...  
Keyword(s):  
Chemical Constituents ◽  
Central Italy ◽  
Global Ischemia ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Apple Variety ◽  
Quercetin Derivatives ◽  
Severity Scores ◽  
Transient Global Ischemia ◽  
The Brain

The Mela Rosa dei Monti Sibillini is an ancient apple variety cultivated by Romans in the foothills of the Sibillini Mountains, central Italy, showing potential as a source of nutraceuticals. The purpose of this study was to evaluate the protective effects of the hydroalcoholic extracts from the peel (APE) and pulp (APP) of this fruit in an animal model of transient global ischemia. Chemical constituents were analyzed by liquid chromatography–mass spectrometry (LC-DAD-MSn) indicating several polyphenols such as B-type procyanidins, quercetin derivatives and hydroxycinnamic acids as the main bioactive components. Acute pre-treatment of extracts (30 mg/kg, i.p.) significantly decreased the brain levels of the pro-inflammatory cytokines IL-1β (p < 0.01) and TNF-α (p < 0.001 and p < 0.01 for APE and APP, respectively), the expression of caspase-3 (p < 0.01, For APE) and MDA (p < 0.05), a lipid peroxidation biomarker in rats. Both extracts restricted the pathological changes of the brain induced by ischemic stroke in hematoxylin and eosin assay. Moreover, they improved the scores of behavioral tests in grid-walking and modified neurological severity scores (mNSS) tests. In conclusion, these results proved this ancient Italian apple is a source of nutraceuticals able to protect/prevent damage from brain ischemia.

Transient global ischemia in rat brain promotes different NMDA receptor regulation depending on the brain structure studied

2009 ◽  
Vol 54 (3-4) ◽  
pp. 180-185 ◽  
Author(s):  
Severiano Dos-Anjos ◽  
Beatriz Martínez-Villayandre ◽  
Sheyla Montori ◽  
Marta M. Regueiro-Purriños ◽  
José M. Gonzalo-Orden ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Rat Brain ◽  
Brain Structure ◽  
Global Ischemia ◽  
Receptor Regulation ◽  
Transient Global Ischemia ◽  
The Brain

scholarly journals Verapamil Inhibits Mitochondria-Induced Reactive Oxygen Species and Dependent Apoptosis Pathways in Cerebral Transient Global Ischemia/Reperfusion

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Ehsan Jangholi ◽  
Zahra Nadia Sharifi ◽  
Mohammad Hoseinian ◽  
Mohammad-Reza Zarrindast ◽  
Hamid Reza Rahimi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prefrontal Cortex ◽  
Mitochondrial Dysfunction ◽  
Antioxidant Defense ◽  
Ischemia Reperfusion ◽  
Mitochondrial Damage ◽  
Morphological Features ◽  
Global Ischemia ◽  
Transient Global Ischemia ◽  
The Brain

The prefrontal cortex is the largest lobe of the brain and is consequently involved in stroke. There is no comprehensive practical pharmacological strategy for ameliorating prefrontal cortex injury induced by cerebral ischemia. Therefore, we studied the neuroprotective properties of verapamil (Ver) on mitochondrial dysfunction and morphological features of apoptosis in transient global ischemia/reperfusion (I/R). Ninety-six Wistar rats were allocated into four groups: control, I/R, I/R+Ver (10 mg/kg twice 1 hour prior to ischemia and 1 hour after reperfusion phase), and I/R+NaCl (vehicle). Animals were sacrificed, and mitochondrial dysfunction parameters (i.e., mitochondrial swelling, mitochondrial membrane potential, ATP concentration, ROS production, and cytochrome c release), antioxidant defense (i.e., superoxide dismutase, malondialdehyde, glutathione peroxidase, catalase, and caspase-3 activation), and morphological features of apoptosis were determined. The results showed that mitochondrial damage, impairment of antioxidant defense system, and apoptosis were significantly more prevalent in the I/R group in comparison with the other groups. Ver decreased mitochondrial damage by reducing oxidative stress, augmented the activity of antioxidant enzymes in the brain, and decreased apoptosis in the I/R neurons. The current study confirmed the role of oxidative stress and mitochondrial dysfunction in I/R progression and indicated the possible antioxidative mechanism of the neuroprotective activities of Ver.

scholarly journals Mitochondrial-Protective Effects of R-Phenibut after Experimental Traumatic Brain Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Einars Kupats ◽  
Gundega Stelfa ◽  
Baiba Zvejniece ◽  
Solveiga Grinberga ◽  
Edijs Vavers ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Tissue ◽  
Aminobutyric Acid ◽  
Drug Candidate ◽  
H2o2 Production ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
The Impact ◽  
The Brain

Altered neuronal Ca2+ homeostasis and mitochondrial dysfunction play a central role in the pathogenesis of traumatic brain injury (TBI). R-Phenibut ((3R)-phenyl-4-aminobutyric acid) is an antagonist of the α2δ subunit of voltage-dependent calcium channels (VDCC) and an agonist of gamma-aminobutyric acid B (GABA-B) receptors. The aim of this study was to evaluate the potential therapeutic effects of R-phenibut following the lateral fluid percussion injury (latFPI) model of TBI in mice and the impact of R- and S-phenibut on mitochondrial functionality in vitro. By determining the bioavailability of R-phenibut in the mouse brain tissue and plasma, we found that R-phenibut (50 mg/kg) reached the brain tissue 15 min after intraperitoneal (i.p.) and peroral (p.o.) injections. The maximal concentration of R-phenibut in the brain tissues was 0.6 μg/g and 0.2 μg/g tissue after i.p. and p.o. administration, respectively. Male Swiss-Webster mice received i.p. injections of R-phenibut at doses of 10 or 50 mg/kg 2 h after TBI and then once daily for 7 days. R-Phenibut treatment at the dose of 50 mg/kg significantly ameliorated functional deficits after TBI on postinjury days 1, 4, and 7. Seven days after TBI, the number of Nissl-stained dark neurons (N-DNs) and interleukin-1beta (IL-1β) expression in the cerebral neocortex in the area of cortical impact were reduced. Moreover, the addition of R- and S-phenibut at a concentration of 0.5 μg/ml inhibited calcium-induced mitochondrial swelling in the brain homogenate and prevented anoxia-reoxygenation-induced increases in mitochondrial H2O2 production and the H2O2/O ratio. Taken together, these results suggest that R-phenibut could serve as a neuroprotective agent and promising drug candidate for treating TBI.

Protective effects of hydroalcoholic extracts from an ancient apple variety ‘Mela Rosa dei Monti Sibillini’ against renal ischemia/reperfusion injury in rats

2019 ◽  
Vol 10 (11) ◽  
pp. 7544-7552 ◽  
Author(s):  
Hasan Yousefi-Manesh ◽  
Sara Hemmati ◽  
Samira Shirooie ◽  
Seyed Mohammad Nabavi ◽  
Azita Talebzadeh Bonakdar ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Central Italy ◽  
Renal Ischemia ◽  
Protective Effects ◽  
Apple Variety ◽  
Renal Ischemia Reperfusion Injury

The purpose of this work was to investigate the effect of hydroalcoholic extracts from the peel and pulp of a traditional apple variety of central Italy on the damage caused by renal ischemia/reperfusion injury in rats.

scholarly journals Thiazoline-related TRPA1 agonist odorants orchestrate survival fate in mice

2020 ◽  
Author(s):  
Tomohiko Matsuo ◽  
Tomoko Isosaka ◽  
Lijun Tang ◽  
Tomoyoshi Soga ◽  
Reiko Kobayakawa ◽  
...  
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Cardiopulmonary Arrest ◽  
Ischemia Reperfusion ◽  
Crisis Response ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Immune Functions ◽  
Term Survival ◽  
The Brain ◽  
Innate Fear

SummaryTherapeutic hypothermia protects the brain after cardiopulmonary arrest. Innate fear has evolved to orchestrate protective effects in life-threatening situations. Thus, strong fear perception may induce a specialized life-protective metabolism based on hypothermia/hypometabolism; however, such phenomena and their inducers are yet to be elucidated. Here, we report that thiazoline-related fear odors (tFOs), which are TRPA1 agonists and induce robust innate fear in mice, induced hibernation-like systemic hypothermia/hypometabolism, accelerated glucose uptake in the brain, and suppressed aerobic metabolism via phosphorylation of pyruvate dehydrogenase, thereby enabling long-term survival in a lethal hypoxic environment. In contrast to hibernation, during which immune functions are generally suppressed, tFO-stimulation induced a crisis-response immune state characterized by potentiated innate immune functions but suppressed inflammation with anti-hypoxic ability. Collectively, these responses exerted potent therapeutic effects in cutaneous and cerebral ischemia/reperfusion injury models. Whole brain mapping and chemogenetic activation revealed that sensory representation of tFOs orchestrate survival fate via brain stem Sp5/NST to midbrain PBN pathway. TFO-induced strong crisis perception maximizes latent life-protective effects by shifting metabolism to a crisis response mode characterized by hypothermia, hypometabolism and crisis immunity.

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