scholarly journals Glia limitans superficialis oxidation and breakdown promotes cortical cell death after repeat head injury

JCI Insight ◽  
2021 ◽  
Author(s):  
Hannah D. Mason ◽  
Alexis M. Johnson ◽  
Nicole A. Mihelson ◽  
Panagiotis Mastorakos ◽  
Dorian B. McGavern
Keyword(s):  
Cell Death ◽  
Head Injury ◽  
Cortical Cell ◽  
Glia Limitans

scholarly journals NMDA Receptor-Mediated Neuroprotective Effect of theScutellaria baicalensisGeorgi Extract on the Excitotoxic Neuronal Cell Death in Primary Rat Cortical Cell Cultures

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Jinsong Yang ◽  
Xiaohong Wu ◽  
Haogang Yu ◽  
Xinbiao Liao ◽  
Lisong Teng
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Cell Cultures ◽  
Neuroprotective Effect ◽  
Neuronal Cell Death ◽  
Cortical Cell ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Phytochemical Analysis ◽  
Cortical Cell Cultures

The objective of the current research work was to evaluate the neuroprotective effect of the ethanol extract ofScutellaria baicalensis(S.B.) on the excitotoxic neuronal cell death in primary rat cortical cell cultures. The inhibitory effects of the extract were qualitatively and quantitatively estimated by phase-contrast microscopy and lactate dehydrogenase (LDH) assays. The extract exhibited a potent and dose-dependent inhibition of the glutamate-induced excitotoxicity in the culture media. Further, using radioligand binding assays, it was observed that the inhibitory effect of the extract was more potent and selective for the N-methyl-D-aspartate (NMDA) receptor-mediated toxicity. The S.B. ethanol extract competed with [3H] MDL 105,519 for the specific binding to the NMDA receptor glycine site with 50% inhibition occurring at 35.1 μg/mL. Further, NMDA receptor inactivation by the S.B. ethanol extract was concluded from the decreasing binding capability of [3H]MK-801 in the presence of the extract. Thus, S.B. extract exhibited neuroprotection against excitotoxic cell death, and this neuroprotection was mediated through the inhibition of NMDA receptor function by interacting with the glycine binding site of the NMDA receptor. Phytochemical analysis of the bioactive extract revealed the presence of six phytochemical constituents including baicalein, baicalin, wogonin, wogonoside, scutellarin, and Oroxylin A.

scholarly journals SUN-211 Active Steroid Hormone Synthesis Renders Adrenocortical Cells Highly Susceptible to Type II Ferroptosis Induction

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Isabel Weigand ◽  
Jochen Schreiner ◽  
Florian Roehrig ◽  
Na Sun ◽  
Landwehr Laura-Sophie ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Treatment Options ◽  
Cortical Cell ◽  
Current Treatment ◽  
Adrenocortical Cells ◽  
Hormone Synthesis ◽  
Steroidogenic Cell ◽  
Coa Ligase ◽  
Dependent Form

Abstract Context: Cell death in the adrenal cortex is ill understood but of high clinical relevance. Resistance of adrenocortical carcinoma (ACC) to current treatment with mitotane and chemotherapy calls for an improved understanding of adrenal cortical cell death processes. Ferroptosis is an iron-dependent form of regulated cell death which is characterized by polyunsaturated lipids adrenic (AdA) and arachidonic acid (AA) peroxidation. Aim: To address the potential role of ferroptosis in the adrenal gland as a potential treatment target of ACC. Methods: Human ACC cells H295R, CU-ACC1 and 2 were used. Protein expression of key enzymes was determined by western blotting. Lipid peroxidation was quantified with BODIPY 581/591 and cell viability with CellTiterGlo after treatment with known inducers and inhibitors of ferroptosis and steroidogenesis, respectively. Results: Adrenocortical tissues are enriched in AdA and AA and express high levels of genes relevant to ferroptosis, such as glutathione peroxidase 4 (GPX4) and long-chain-fatty-acid CoA ligase 4 (ACSL4). Inhibition of GPX4 with RSL3 led to cell death in H295R, CU-ACC1 and 2 cells at EC50 values of 2.4x10-7, 8.1x10-7 and 1.5x10-8 M, respectively. The steroidogenesis inhibitor ketoconazole completely reversed RSL3 cytotoxicity in all three steroidogenic cell lines by reducing lipid peroxidation. Mitotane induced lipid peroxidation but inhibition of ferroptosis with liproxstatin did not protect mitotane-induced cell death. Conclusion: Adrenocortical cells are highly sensitive to ferroptosis due to active steroidogenesis. Triggering this form of cell death could present future novel treatment options against ACC.

Cortical cell death, cell proliferation, macromolecular movements and rTip1 expression pattern in roots of rice ( Oryza sativa L.) under NaCl stress

Planta ◽  
1999 ◽  
Vol 207 (3) ◽  
pp. 354-361 ◽  
Author(s):  
P. K. Samarajeewa ◽  
R. A. Barrero ◽  
C. Umeda-Hara ◽  
M. Kawai ◽  
H. Uchimiya
Keyword(s):  
Cell Proliferation ◽  
Cell Death ◽  
Oryza Sativa ◽  
Expression Pattern ◽  
Oryza Sativa L ◽  
Cortical Cell ◽  
Nacl Stress

Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

2020 ◽  
Vol 39 (9) ◽  
pp. 1200-1212 ◽  
Author(s):  
RS Baty ◽  
KE Hassan ◽  
KF Alsharif ◽  
RE El-Hennamy ◽  
EK Elmahallawy ◽  
...  
Keyword(s):  
Cell Death ◽  
Lead Acetate ◽  
Neuronal Damage ◽  
Cortical Cell ◽  
Flavonoid Compound ◽  
Control Group ◽  
No Production ◽  
Cortical Tissue ◽  
Group 4 ◽  
Group 2

Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg−1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg−1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.

scholarly journals Cortical Death Caused by Striatal Administration of AMPA and Interleukin-1 is Mediated by Activation of Cortical NMDA Receptors

2000 ◽  
Vol 20 (10) ◽  
pp. 1409-1413 ◽  
Author(s):  
Stuart M. Allan ◽  
Nancy J. Rothwell
Keyword(s):  
Cell Death ◽  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Ampa Receptor ◽  
Neuronal Death ◽  
Interleukin 1 ◽  
Cortical Cell ◽  
Nmda Receptor Antagonist ◽  
Interleukin 1Β

Striatal coadministration of interleukin-1β (IL-1β) with α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) in rats results in widespread cortical cell death not caused by either treatment alone. This cortical damage was unaffected by cortical infusion of the AMPA-receptor antagonist NBQX. Cortical infusion of an NMDA-receptor antagonist D-AP5 significantly inhibited (57%; P < 0.05) cortical death, but had no effect on the local striatal death. Thus, cortical neuronal death induced by striatal S-AMPA and human recombinant interleukin-1β (hrIL-1β) is mediated by activation of NMDA receptors in the cortex. The authors propose that IL-1β actions on AMPA-receptor mediated cell death may involve the activation of polysynaptic pathways from the striatum to the cortex.

Cellular dissection of the degradation pattern of cortical cell death during aerenchyma formation of rice roots

Planta ◽  
1998 ◽  
Vol 204 (3) ◽  
pp. 277-287 ◽  
Author(s):  
M. Kawai ◽  
P. K. Samarajeewa ◽  
R. A. Barrero ◽  
M. Nishiguchi ◽  
H. Uchimiya
Keyword(s):  
Cell Death ◽  
Cortical Cell ◽  
Aerenchyma Formation ◽  
Rice Roots ◽  
Degradation Pattern

scholarly journals Experimental Closed Head Injury: Analysis of Neurological Outcome, Blood–Brain Barrier Dysfunction, Intracranial Neutrophil Infiltration, and Neuronal Cell Death in Mice Deficient in Genes for Pro-Inflammatory Cytokines

2000 ◽  
Vol 20 (2) ◽  
pp. 369-380 ◽  
Author(s):  
Philip F. Stahel ◽  
Esther Shohami ◽  
Firas M. Younis ◽  
Karin Kariya ◽  
Viviane I. Otto ◽  
...  
Keyword(s):  
Cell Death ◽  
Head Injury ◽  
Blood Brain Barrier ◽  
Neuronal Cell Death ◽  
Closed Head Injury ◽  
Neuronal Cell ◽  
Brain Barrier ◽  
Blood Brain ◽  
Closed Head ◽  
Deficient Mice

Cytokines are important mediators of intracranial inflammation following traumatic brain injury (TBI). In the present study, the neurological impairment and mortality, blood-brain barrier (BBB) function, intracranial polymorphonuclear leukocyte (PMN) accumulation, and posttraumatic neuronal cell death were monitored in mice lacking the genes for tumor necrosis factor (TNF)/lymphotoxin-α (LT-α) (TNF/LT-α−/−) and interleukin-6 (IL-6) and in wild-type (WT) littermates subjected to experimental closed head injury (total n = 107). The posttraumatic mortality was significantly increased in TNF/LT-α−/− mice (40%; P < 0.02) compared with WT animals (10%). The IL-6−/− mice also showed a higher mortality (17%) than their WT littermates (5.6%), but the difference was not statistically significant ( P > 0.05). The neurological severity score was similar among all groups from 1 to 72 hours after trauma, whereas at 7 days, the TNF/LT-α−/− mice showed a tendency toward better neurological recovery than their WT littermates. Interestingly, neither the degree of BBB dysfunction nor the number of infiltrating PMNs in the injured hemisphere was different between WT and cytokine-deficient mice. Furthermore, the analysis of brain sections by in situ DNA nick end labeling (TUNEL histochemistry) at 24 hours and 7 days after head injury revealed a similar extent of posttraumatic intracranial cell death in all animals. These results show that the pathophysiological sequelae of TBI are not significantly altered in mice lacking the genes for the proinflammatory cytokines TNF, LT-α, and IL-6. Nevertheless, the increased posttraumatic mortality in TNF/LT-α-deficient mice suggests a protective effect of these cytokines by mechanisms that have not been elucidated yet.

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