The neuroprotective effects of (−)deprenyl in the gerbil hippocampus following transient global ischemia

2000 ◽  
Vol 107 (7) ◽  
pp. 779-786 ◽  
Author(s):  
J. Kuhmonen ◽  
J. Jolkkonen ◽  
A. Haapalinna ◽  
J. Sivenius
Keyword(s):  
Global Ischemia ◽  
Neuroprotective Effects ◽  
Transient Global Ischemia

LC-MS/MS profiling and neuroprotective effects of Mentat® against transient global ischemia and reperfusion–induced brain injury in rats

Nutrition ◽  
2015 ◽  
Vol 31 (7-8) ◽  
pp. 1008-1017 ◽  
Author(s):  
Gollapalle Lakshminarayanashastry Viswanatha ◽  
Lakkavalli Mohan Sharath Kumar ◽  
Mohamed Rafiq ◽  
Kethaganahalli Jayaramaiah Kavya ◽  
Agadi Hiremath Thippeswamy ◽  
...  
Keyword(s):  
Brain Injury ◽  
Global Ischemia ◽  
Ischemia And Reperfusion ◽  
Neuroprotective Effects ◽  
Transient Global Ischemia

Neuroprotective Effects of Dexmedetomidine in the Gerbil Hippocampus after Transient Global Ischemia 

1997 ◽  
Vol 87 (2) ◽  
pp. 371-377 ◽  
Author(s):  
Johanna Kuhmonen ◽  
Jaroslav Pokorny ◽  
Riitta Miettinen ◽  
Antti Haapalinna ◽  
Jukka Jolkkonen ◽  
...  
Keyword(s):  
Neuronal Death ◽  
Global Ischemia ◽  
Neuroprotective Effects ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Adrenoceptor Agonists ◽  
Transient Global Ischemia ◽  
Alpha2 Adrenoceptor ◽  
Alpha2 Receptor ◽  
Dentate Hilus

Background Cerebral ischemia induces a massive release of norepinephrine associated with neuronal death in the brain. It has been demonstrated that alpha2-adrenoceptor agonists decrease the release and turnover of noradrenaline, and this might prove advantageous in counteracting the neurodegeneration in ischemic brain. Therefore, in the present study, the authors tested whether dexmedetomidine, a selective alpha2-receptor agonist, has neuroprotective effects in a gerbil transient global ischemia model. Methods Ischemia was induced by bilateral carotid occlusion for 5 min in diethylether-anesthetized normothermic gerbils. Dexmedetomidine was administered subcutaneously in four different treatment paradigms (6-8 animals/group): 3 or 30 microg/kg 30 min before and thereafter at 3, 12, 24, and 48 h after the occlusion, or 3 or 30 microg/kg at 3, 12, 24, and 48 h after the occlusion. Control animals were subjected to forebrain ischemia but received only saline injections. One week after occlusion, animals were transcardially perfused for histochemistry. Neuronal death in the CA1 and CA3 regions of the hippocampus and in the hilus of the dentate gyrus was evaluated in silver-stained 60-microm coronal sections. Results Compared with saline-treated ischemic animals, dexmedetomidine at a dose of 3 microg/kg given before and continued after the induction of ischemia reduced the number of damaged neurons in the CA3 area (2 +/- 3 vs. 17 +/- 20 degenerated neurons/mm2; P < 0.05). Also in the dentate hilus, the number of damaged neurons was reduced by dexmedetomidine (3 microg/kg) given before and continued after ischemia (5 +/- 7 vs. 56 +/- 42 degenerated neurons/mm2; P < 0.01). Conclusions The present data demonstrate that dexmedetomidine effectively prevents delayed neuronal death in CA3 area and in the dentate hilus in gerbil hippocampus when the management is started before the onset of ischemia and continued for 48 h after reperfusion. Inhibition of ischemia-induced norepinephrine release may be associated with neuroprotection by dexmedetomidine.

Neuroprotective Effects of Curcumin Against Transient Global Ischemia are Dose and Area Dependent

2016 ◽  
Vol 3 (2) ◽  
Author(s):  
Fatemeh Attari ◽  
Zahra Nadia Sharifi ◽  
Shabnam Movassaghi ◽  
Hadi Aligholi ◽  
Tahereh Alizamir ◽  
...  
Keyword(s):  
Global Ischemia ◽  
Neuroprotective Effects ◽  
Transient Global Ischemia

Neuroprotective effects of valproic acid following transient global ischemia in rats

Life Sciences ◽  
2012 ◽  
Vol 90 (11-12) ◽  
pp. 463-468 ◽  
Author(s):  
Aiguo Xuan ◽  
Dahong Long ◽  
Jianhua Li ◽  
Weidong Ji ◽  
Lepeng Hong ◽  
...  
Keyword(s):  
Valproic Acid ◽  
Global Ischemia ◽  
Neuroprotective Effects ◽  
Transient Global Ischemia

scholarly journals HIF-1α Activation Attenuates IL-6 and TNF-α Pathways in Hippocampus of Rats Following Transient Global Ischemia

2016 ◽  
Vol 39 (2) ◽  
pp. 511-520 ◽  
Author(s):  
Jihong Xing ◽  
Jian Lu
Keyword(s):  
Cerebral Ischemia ◽  
Caspase 3 ◽  
Global Ischemia ◽  
Rat Hippocampus ◽  
Global Cerebral Ischemia ◽  
Control Group ◽  
Signal Pathways ◽  
Neuroprotective Effects ◽  
Tnf Α ◽  
Transient Global Ischemia

Background/Aims: This study was to examine the role played by hypoxia inducible factor-1 (HIF-1α) in regulating pro-inflammatory cytokines (PICs) pathway in the rat hippocampus after cardiac arrest (CA) induced-transient global ischemia followed by cardiopulmonary resuscitation (CPR). Those PICs include interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Methods: A rat model of CA induced by asphyxia was used in the current study. Following CPR, the hippocampus CA1 region was obtained for ELISA to determine the levels of HIF-1α and PICs; and Western Blot analysis to determine the protein levels of PIC receptors. Results: Our data show that IL-1β, IL-6 and TNF-α were significant elevated in the hippocampus after CPR as compared with control group. This was companied with increasing of HIF-1α and the time courses for HIF-1α and PICs were similar. In addition, PIC receptors, namely IL-1R, IL-6R and TNFR1 were upregulated in CA rats. Also, stimulation of HIF-1α by systemic administration of ML228, HIF-1α activator, significantly attenuated the amplified IL-6/IL-6R and TNF-α /TNFR1 pathway in the hippocampus of CA rats, but did not modify IL-1β and its receptor. Moreover, ML228 attenuated upregulated expression of Caspase-3 indicating cell apoptosis evoked by CA. Conclusion: Transient global ischemia induced by CA increases the levels of IL-1β, IL-6 and TNF-α and thereby leads to enhancement in their respective receptor in the rat hippocampus. Stabilization of HIF-1α plays a role in attenuating amplified expression IL-6R, TNFR1 and Caspase-3 in the processing of transient global ischemia. Results of our study suggest that PICs contribute to cerebral injuries evoked by transient global ischemia and in this pathophysiological process activation of HIF-1α improves tissues against ischemic injuries. Our data revealed specific signaling pathways in alleviating CA-evoked global cerebral ischemia by elucidating that HIF-1α plays an important role in regulating PIC signal pathways and Caspase-3. The subsequent induction of HIF-1α and its target signals is likely a part of the intrinsic neuroprotective effects aimed at attenuating damage as a result of global cerebral ischemia. Thus, targeting one or more of these signaling molecules has clinical implications for treatment and improvement of CA-evoked global cerebral ischemia often observed in clinics.

Inhibition of microRNA-155 Alleviates Neurological Dysfunction Following Transient Global Ischemia and Contribution of Neuroinflammation and Oxidative Stress in the Hippocampus

2020 ◽  
Vol 25 (40) ◽  
pp. 4310-4317 ◽  
Author(s):  
Lichao Sun ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Oxidative Stress ◽  
Brain Edema ◽  
Severity Score ◽  
Global Ischemia ◽  
Signal Pathways ◽  
Neurological Severity Score ◽  
Tnf Α ◽  
Transient Global Ischemia ◽  
And Oxidative Stress

Background/Aims: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine the role of microRNA- 155 (miR-155) in regulating IL-1β, IL-6 and TNF-α in the hippocampus of rats with induction of CA. We further examined the levels of products of oxidative stress 8-isoprostaglandin F2α (8-iso PGF2α, indication of oxidative stress); and 8-hydroxy-2’-deoxyguanosine (8-OHdG, indication of protein oxidation) after cerebral inhibition of miR-155. Methods: CA was induced by asphyxia and followed by cardiopulmonary resuscitation in rats. ELISA and western blot analysis were used to determine the levels of PICs and products of oxidative stress; and the protein expression of NADPH oxidase (NOXs) in the hippocampus. In addition, neurological severity score and brain edema were examined to assess neurological functions. Results: We observed amplification of IL-1β, IL-6 and TNF-α along with 8-iso PGF2α and 8-OHdG in the hippocampus of CA rats. Cerebral administration of miR-155 inhibitor diminished upregulation of PICs in the hippocampus. This also attenuated products of oxidative stress and upregulation of NOX4. Notably, inhibition of miR-155 improved neurological severity score and brain edema and this was linked to signal pathways of PIC and oxidative stress. Conclusion: We showed the significant role of blocking miR-155 signal in improving the neurological function in CA rats likely via inhibition of signal pathways of neuroinflammation and oxidative stress, suggesting that miR-155 may be a target in preventing and/or alleviating development of the impaired neurological functions during CA-evoked global cerebral ischemia.

Amiloride Alleviates Neurological Deficits Following Transient Global Ischemia and Engagement of Central IL-6 and TNF-α Signal

2019 ◽  
Vol 19 (8) ◽  
pp. 597-604
Author(s):  
Li Pang ◽  
Shouqin Ji ◽  
Jihong Xing
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Caspase 3 ◽  
Global Ischemia ◽  
Neurological Deficits ◽  
Global Cerebral Ischemia ◽  
Caspase 9 ◽  
Tnf Α ◽  
The Central Nervous System ◽  
Transient Global Ischemia

Background: Central pro-inflammatory cytokine (PIC) signal is involved in neurological deficits after transient global ischemia induced by cardiac arrest (CA). The present study was to examine if blocking acid sensing ion channels (ASICs) using amiloride in the Central Nervous System can alleviate neurological deficits after the induction of CA and further examine the participation of PIC signal in the hippocampus for the effects of amiloride. Methods: CA was induced by asphyxia and then cardiopulmonary resuscitation was performed in rats. Western blot analysis and ELISA were used to determine the protein expression of ASIC subunit ASIC1 in the hippocampus, and the levels of PICs. As noted, it is unlikely that this procedure is clinically used although amiloride and other pharmacological agents were given into the brain in this study. Results: CA increased ASIC1 in the hippocampus of rats in comparison with control animals. This was associated with the increase in IL-1β, IL-6 and TNF-α together with Caspase-3 and Caspase-9. The administration of amiloride into the lateral ventricle attenuated the upregulation of Caspase-3/Caspase-9 and this further alleviated neurological severity score and brain edema. Inhibition of central IL-6 and TNF-α also decreased ASIC1 in the hippocampus of CA rats. Conclusion: Transient global ischemia induced by CA amplifies ASIC1a in the hippocampus likely via PIC signal. Amiloride administered into the Central Nervous System plays a neuroprotective role in the process of global ischemia. Thus, targeting ASICs (i.e., ASIC1a) is suggested for the treatment and improvement of CA-evoked global cerebral ischemia.

scholarly journals Estradiol protects against hippocampal damage and impairments in fear conditioning resulting from transient global ischemia in mice

2012 ◽  
Vol 1443 ◽  
pp. 64-74 ◽  
Author(s):  
Jennah L. Durham ◽  
Katherine A. Jordan ◽  
Marijke J. DeVos ◽  
Erika K. Williams ◽  
Noah J. Sandstrom
Keyword(s):  
Fear Conditioning ◽  
Global Ischemia ◽  
Hippocampal Damage ◽  
Transient Global Ischemia
Sign in / Sign up

Export Citation Format

Share Document