AI Article Synopsis

  • The study examines how long-term use of antiretroviral therapy (HAART) affects brain health in HIV-infected individuals, focusing on toxic interactions between the prefrontal cortex and hippocampus.
  • Treatment with Epigallocatechin gallate (EGCG) shows potential in reversing neurodegenerative damage caused by HAART, as evidenced by improved brain architecture and function in a rat model.
  • EGCG significantly boosts antioxidant levels while reducing harmful markers, suggesting it may offer a protective effect against the toxicities associated with antiretroviral medications.

Article Abstract

The contribution of prefrontal-hippocampal interactions to brain function of people infected with HIV may be aggravated by toxicities due to long-term use of antiretroviral agents. This study was designed to investigate the curative potential of Epigallotatechin gallate (EGCG) in the treatment of neurodegenerative disorders as a possible consequence of antiretroviral toxicity. Twenty-four adult male Wistar rats, weighing 80~100g, were divided into four groups and treated as follows: control A (distilled water), B (HAART), C (EGCG 2.5mg/kg), D (EGCG 2.5mg/kg) + HAART) Brain histology, immunohistochemistry, and oxidative stress markers such as superoxide dismutase (SOD), glutathione (GSH),catalase (CAT)  and malondialdehyde (MDA) were examined. The use of highly active antiretroviral therapy (HAART) showed extensive architectural deformation with pyknotic neuronal cells and obliterated neurons in the hippocampus and prefrontal cortex. Expression of inflammasome cells was also evident in this group. MDA levels increased significantly with a significant reduction in the levels of GSH, as well as antioxidant enzyme (SOD and CAT) activities compared to other treatment groups. Treatment with EGCG resulted in partial neuronal restoration of histopathological alterations, and modulation of NLRP3 inflammasome in the hippocampus and prefrontal cortex. EGCG also showed significant improvements in terms of increased antioxidant levels of SOD, GSH, CAT and a reduced MDA level and well-preserved brain architecture. Epigallocatechin gallate improves brain morphology and function with a reversal of HAART-induced alterations.

Download full-text PDF

Source
http://dx.doi.org/10.54548/njps.v37i2.7DOI Listing

Publication Analysis

Top Keywords

hippocampus prefrontal
12
prefrontal cortex
12
wistar rats
8
epigallocatechin gallate
8
egcg 25mg/kg
8
egcg
5
cortex anti-retroviral
4
anti-retroviral therapy
4
therapy adult
4
adult wistar
4

Similar Publications

Background: As a non drug and non invasive therapy, both transcranial alternating current stimulation (tACS) and transcranial direct current stimulation (tDCS) may modulate cortical rhythms and serve as potentially effective approaches to cognitive decline in Alzheimer's disease (AD). However, studies using animal models of AD are quite limited.

Methods: This study investigates the aftereffects of tACS and tDCS on brain EEG activity and associated exploratory behavior in normal aged and APP/PS1 transgenic mice (15 months old).

View Article and Find Full Text PDF

Protective effect of sub-hypothermic mechanical perfusion combined with membrane lung oxygenation on a yorkshire model of brain injury after traumatic blood loss.

Chin J Traumatol

December 2024

Beijing Key Lab of Regenerative Medicine in Orthopedics, Key Laboratory of Musculoskeletal Trauma and War Injuries PLA, Department of Orthopedics, The Fourth Medical Center, Chinese PLA General Hospital, Beijing, 100048, China. Electronic address:

Purpose: To investigate the protective effect of sub-hypothermic mechanical perfusion combined with membrane lung oxygenation on ischemic hypoxic injury of yorkshire brain tissue caused by traumatic blood loss.

Methods: This article performed a random controlled trial. Brain tissue of 7 yorkshire was selected and divided into the sub-low temperature anterograde machine perfusion group (n = 4) and the blank control group (n = 3) using the random number table method.

View Article and Find Full Text PDF

Amelioration of Gap Junction Dysfunction in a Depression Model by Loganin: Involvement of GSK-3β/β-Catenin Signaling.

J Ethnopharmacol

December 2024

School of Life Sciences & School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing 100029, People's Republic of China. Electronic address:

Ethnopharmacological Relevance: Comus officinalis Sieb. et Zucc has significant neuroprotective activity and has been widely studied for its potential to improve cognitive function. Our team's previous research has found that loganin isolated from Comus officinalis has an antidepressant effect.

View Article and Find Full Text PDF

Electrophysiological Insights into Alzheimer's Disease: A Review of Human and Animal Studies.

Neurosci Biobehav Rev

December 2024

Interdisciplinary Neuroscience Program, University of Nevada, Las Vegas; Department of Psychology, University of Nevada, Las Vegas.

This review highlights the crucial role of neuroelectrophysiology in illuminating the mechanisms underlying Alzheimer's disease (AD) pathogenesis and progression, emphasizing its potential to inform the development of effective treatments. Electrophysiological techniques provide unparalleled precision in exploring the intricate networks affected by AD, offering insights into the synaptic dysfunction, network alterations, and oscillatory abnormalities that characterize the disease. We discuss a range of electrophysiological methods, from non-invasive clinical techniques like electroencephalography and magnetoencephalography to invasive recordings in animal models.

View Article and Find Full Text PDF

Background/objectives: Antipsychotic medicines are used to treat several psychological disorders and some symptoms caused by dementia and schizophrenia. Haloperidol (Hal) is a typical antipsychotic usually used to treat psychosis; however, its use causes motor or extrapyramidal symptoms (EPS) such as catalepsy. Hal blocks the function of presynaptic D2 receptors on cholinergic interneurons, leading to the release of acetylcholine (ACh), which is hydrolyzed by the enzyme acetylcholinesterase (AChE).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!