A dual action of alpha-lipoic acid in the brain: an electrophysiological evaluation

Oxidative stress causes metabolic and structural abnormalities during reperfusion. In an animal model of electrophysiological evaluation of cerebral ischemia-reperfusion, alpha-lipoic acid effect on the oxidative stress was studied by mean absolute amplitude of EEG spectra evaluation. The left carotideal infusion of 3.03 mM alpha-lipoic acid in Wistar rats after cerebral ischemia and reperfusion caused initial reduction and partial final recuperation of the various EEG spectral frequency mean absolute amplitudes (p<0.05). The left intracarotideal infusion of 6.06 mM alpha-lipoic acid significantly reverted the induced depression of mean absolute amplitude of theta and delta spectra. Nevertheless there was an increasing pattern of ischemia demonstrated by mean absolute amplitude depression of almost all EEG spectra with 60.6 mM alpha-lipoic acid infusion. These observations suggest that, depending on the administered concentration, alpha-lipoic acid may act in a dual way, protecting from ischemia at lower concentrations and worsening this process at higher doses.

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Effect of alpha-lipoic acid on oxidative stress status in rat kidney subjected to ischemia/reperfusion injury

Egyptian Journal of Biochemistry and Molecular Biology ◽

10.4314/ejbmb.v25i1.35946 ◽

2007 ◽

Vol 25 (1) ◽

Author(s):

M M El-Sawalhi ◽

M Raafat

Keyword(s):

Oxidative Stress ◽

Reperfusion Injury ◽

Lipoic Acid ◽

Ischemia Reperfusion Injury ◽

Rat Kidney ◽

Ischemia Reperfusion ◽

Alpha Lipoic Acid ◽

Oxidative Stress Status

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Neuroprotection of chromobox 7 knockout in the mouse after cerebral ischemia-reperfusion injury via nuclear factor E2-related factor 2/hemeoxygenase-1 signaling pathway

Human & Experimental Toxicology ◽

10.1177/09603271211036122 ◽

2021 ◽

pp. 096032712110361

Author(s):

Hai-Tao Zhang ◽

Xi-Zeng Wang ◽

Qing-Mei Zhang ◽

Han Zhao

Keyword(s):

Oxidative Stress ◽

Cerebral Ischemia ◽

Infarct Size ◽

Water Content ◽

Cell Apoptosis ◽

Ischemia Reperfusion ◽

Related Factor ◽

Nuclear Factor ◽

Cerebral Ischemia Reperfusion ◽

And Oxidative Stress

Objective To explore the mechanism of chromobox 7 (CBX7)-mediated nuclear factor E2-related factor 2 (Nrf2)/hemeoxygenase-1 (HO-1) signaling pathway in the cerebral ischemia/reperfusion (I/R) injury. Methods The experimental wild-type (WT) and CBX7-/- mice were used to establish cerebral I/R models using the middle cerebral artery occlusion (MCAO) surgery to determine CBX7 levels at different time points after MCAO injury. For all mice, neurological behavior, infarct size, water content, and oxidative stress–related indicators were determined, and transferase (TdT)-mediated dUTP-biotin nick-end labeling (terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL)) staining method was employed to observe cell apoptosis, while Western blot to measure the expression of CBX7 and Nrf/HO-1 pathway-related proteins. Results At 6 h, 12 h, 24 h, 3 days, and 7 days after mice with MCAO, CBX7 expression was gradually up-regulated and the peak level was reached at 24 h. Mice in the WT + MCAO group had increased infarct size, with significant increases in the modified neurological severity scores and water content in the brain, as well as the quantity of TUNEL-positive cells. For the oxidative stress-indicators, an increase was seen in the content of MDA (malondial dehyde), but the activity of SOD (superoxide dismutase) and content of GSH-PX (glutathione peroxidase) and CAT (catalase) were decreased; meanwhile, the protein expression of CBX7, HO-1, and nuclear Nrf2 was up-regulated, while the cytoplasmic Nrf2 was down-regulated. Moreover, CBX7 knockout attenuated I/R injury in mice. Conclusion Knockout of CBX7 may protect mice from cerebral I/R injury by reducing cell apoptosis and oxidative stress, possibly via activating the Nrf2/HO-1 pathway.

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