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.

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
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