Baicalin improved the spatial learning ability of global ischemia/reperfusion rats by reducing hippocampal apoptosis

2012 ◽  
Vol 1470 ◽  
pp. 111-118 ◽  
Author(s):  
Oumei Cheng ◽  
Zhenhua Li ◽  
Yu Han ◽  
Qingsong Jiang ◽  
Yong Yan ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Ischemia Reperfusion ◽  
Global Ischemia ◽  
Learning Ability ◽  
Hippocampal Apoptosis

scholarly journals Treadmill exercise enhances spatial learning ability through suppressing hippocampal apoptosis in Huntington’s disease rats

2015 ◽  
Vol 11 (3) ◽  
pp. 133-139 ◽  
Author(s):  
Eun-Sang Ji ◽  
You-Mi Kim ◽  
Mal-Soon Shin ◽  
Chang-Ju Kim ◽  
Kwang-Sik Lee ◽  
...  
Keyword(s):  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Spatial Learning ◽  
Treadmill Exercise ◽  
Learning Ability ◽  
Hippocampal Apoptosis

scholarly journals Pelargonidin ameliorates MCAO-induced cerebral ischemia/reperfusion injury in rats by the action on the Nrf2/HO-1 pathway

2021 ◽  
Vol 12 (1) ◽  
pp. 020-031
Author(s):  
Kong Fu ◽  
Miancong Chen ◽  
Hua Zheng ◽  
Chuanzi Li ◽  
Fan Yang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neurological Function ◽  
Learning Ability ◽  
Morris Water Maze Test ◽  
Cerebral Ischemia Reperfusion ◽  
Tnf Α ◽  
Cerebral Ischemia Reperfusion Injury

Abstract Background Morbidity and mortality remain high for ischemic stroke victims, and at present these patients lack effective neuroprotective agents, which improve the cure rate. In recent years, studies have shown that pelargonidin has many biological actions. However, few studies are available regarding the pelargonidin treatment of cerebral ischemia. Methods The rat middle cerebral artery occlusion (MCAO) model was established to investigate the neuroprotective effect of pelargonidin on cerebral ischemia/reperfusion injury. Reperfusion was performed 2 h after ischemia; magnetic resonance imaging (MRI) and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining were used to measure the volume of cerebral ischemia. Both modified neurological severity scores (mNSSs) and Morris water maze test were used to assess the neurological functions. ELISA was applied to determine the levels of TNF-α, TGF-β, IL-6, IL-10, MDA, and SOD. The expression of Nuclear factor-E2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) protein in brain tissue was measured by immunofluorescence and Western blot assays. Results The results showed that pelargonidin could effectively reduce the volume of cerebral ischemia and improve the neurological function in MCAO rats, thereby improving memory and learning ability. With the corresponding decreases in the expression of TNF-α, TGF-β, IL-6, and MDA, the level of IL-10 and SOD increased and also promoted the nuclear metastasis of Nrf2 and the expression of HO-1 in ischemic brain tissues. Conclusions Our data demonstrated that pelargonidin ameliorated neurological function deficits in MCAO rats, and its potential mechanism of action was associated with overexpression of the Nrf2/HO-1-signaling pathway. This study will provide a new approach to treat cerebral ischemia/reperfusion injury.

Effect of soya phosphatidylcholine and possible underlying mechanism on ischemia/reperfusion injury in isolated perfused rat heart: an experimental and computational study

2022 ◽  
pp. 1-7
Author(s):  
Anita A. Mehta ◽  
Purav Patel ◽  
Vandana R. Thakur ◽  
Jayesh V. Beladiya
Keyword(s):  
Ischemia Reperfusion Injury ◽  
Computational Study ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Left Ventricular ◽  
Global Ischemia ◽  
Mechanistic Study ◽  
Cardiac Damage ◽  
Nitric Oxide Synthase Inhibitor ◽  
Triton X

This study was designed to assess the effect of soya phosphatidylcholine (SPC) against ischemia/reperfusion (I/R) injury and the possible underlying mechanism using experimental and computational studies. I/R injury was induced by global ischemia for 30 min followed by reperfusion for 120 min. The perfusion of the SPC was performed for 10 min before inducing global ischemia. In the mechanistic study, the involvement of specific cellular pathways was identified using various inhibitors such as ATP-dependent potassium channel (KATP) inhibitor (glibenclamide), protein kinase C (PKC) inhibitor (chelerythrine), non-selective nitric oxide synthase inhibitor (L-NAME), and endothelium remover (Triton X-100). The computational study of various ligands was performed on toll-like receptor 4 (TLR4) protein using AutoDock version 4.0. SPC (100 μM) significantly decreased the levels of cardiac damage markers and %infarction compared with the vehicle control (VC). Furthermore, cardiodynamics (indices of left ventricular contraction (dp/dtmax), indices of left ventricular relaxation (dp/dtmin), coronary flow, and antioxidant enzyme levels were significantly improved as compared with VC. This protective effect was attenuated by glibenclamide, chelerythrine, and Triton X-100, but it was not attenuated by L-NAME. The computational study showed a significant bonding affinity of SPC to the TLR4-MD2 complex. Thus, SPC reduced myocardial I/R injury in isolated perfused rat hearts, which might be governed by the KATP channel, PKC, endothelium response, and TLR4-MyD88 signaling pathway.

scholarly journals Neonatal Rat Hearts Cannot Be Protected by Ischemic Postconditioning

2015 ◽  
pp. 789-794 ◽  
Author(s):  
J. DOUL ◽  
Z. CHARVÁTOVÁ ◽  
I. OŠŤÁDALOVÁ ◽  
M. KOHUTIAR ◽  
H. MAXOVÁ ◽  
...  
Keyword(s):  
Isometric Force ◽  
Ischemia Reperfusion ◽  
Force Transducer ◽  
Global Ischemia ◽  
Ischemic Postconditioning ◽  
Neonatal Rat ◽  
Postnatal Life ◽  
Protective Effects ◽  
Rat Hearts ◽  
Ldh Release

Although there are abundant data on ischemic postconditioning (IPoC) in the adult myocardium, this phenomenon has not yet been investigated in neonatal hearts. To examine possible protective effects of IPoC, rat hearts isolated on days 1, 4, 7 and 10 of postnatal life were perfused according to Langendorff. Developed force (DF) of contraction was measured by an isometric force transducer. Hearts were exposed to 40 or 60 min of global ischemia followed by reperfusion up to the maximum recovery of DF. IPoC was induced by three cycles of 10, 30 or 60 s periods of global ischemia/reperfusion. To further determine the extent of ischemic injury, lactate dehydrogenase (LDH) release was measured in the coronary effluent. Tolerance to ischemia did not change from day 1 to day 4 but decreased to days 7 and 10. None of the postconditioning protocols tested led to significant protection on the day 10. Prolonging the period of sustained ischemia to 60 min on day 10 did not lead to better protection. The 3x30 s protocol was then evaluated on days 1, 4 and 7 without any significant effects. There were no significant differences in LDH release between postconditioned and control groups. It can be concluded that neonatal hearts cannot be protected by ischemic postconditioning during first 10 days of postnatal life.

scholarly journals Reduced Adolescent-Age Spatial Learning Ability Associated with Elevated Juvenile-Age Superoxide Levels in Complex I Mouse Mutants

PLoS ONE ◽  
2015 ◽  
Vol 10 (4) ◽  
pp. e0123863 ◽  
Author(s):  
Johannes Mayer ◽  
Gesine Reichart ◽  
Tursonjan Tokay ◽  
Falko Lange ◽  
Simone Baltrusch ◽  
...  
Keyword(s):  
Spatial Learning ◽  
Complex I ◽  
Learning Ability ◽  
Mouse Mutants ◽  
Juvenile Age
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