Background: Anesthesia can lead to functional cognitive impairment, which can seriously affect postoperative recovery. To investigate the effect and mechanism of quercetin (Que) in anesthetized rats, the study provided a new therapeutic idea for the prevention of cognitive dysfunction caused by anesthesia.

Methods: Cognitively impaired rats were constructed using Isoflurane (ISO) anesthesia and treated with Que. The capacity of the rats to learn and remember was tested using the Morris water maze test. Rat hippocampal tissues were collected and analyzed for inflammatory factor concentration and miR-138-5p expression using ELISA and qRT-PCR, respectively, and the targeting link between miR-138-5p and LCN2 was verified by dual luciferase reporter.

Results: Que treatment was found to improve ISO-induced cognitive dysfunction and inhibit the level of hippocampal inflammatory factors in rats. miR-138-5p was down-regulated in rats with cognitive dysfunction, while Que treatment increased miR-138-5p expression. The study found that knockdown miR-138-5p can reverse the positive effects of Que therapy, aggravate cognitive dysfunction, and promote the secretion of TNF-α, IL-1β, and IL-6 in the hippocampus. In addition, LCN2, a target gene of miR-138-5p, was significantly up-regulated in the hippocampus after ISO induction.

Conclusion: Que may inhibit ISO-induced hippocampal neuroinflammation and ameliorate functional cognitive deficits in rats by modulating miR-138-5p/ LCN2.

Download full-text PDF

Source
http://dx.doi.org/10.1186/s12871-024-02876-0DOI Listing

Publication Analysis

Top Keywords

cognitive dysfunction
20
mir-138-5p/ lcn2
8
functional cognitive
8
mir-138-5p expression
8
cognitive
7
rats
6
mir-138-5p
6
dysfunction
5
quercetin improve
4
improve anesthesia
4

Similar Publications

Microglial polarization and ferroptosis are important pathological features in Alzheimer's disease (AD). Ghrelin, a brain-gut hormone, has potential neuroprotective effects in AD. This study aimed to explore the potential mechanisms by which ghrelin regulates the progression of AD, as well as the crosstalk between microglial polarization and ferroptosis.

View Article and Find Full Text PDF

The primary objective of this study was to examine neurological disorders and cognitive impairments in patients with secondary hypothyroidism and epilepsy undergoing treatment with antiepileptic medications. The study included 184 patients divided into three groups: Group 1 (subclinical hypothyroidism, n = 60), Group 2 (manifest hypothyroidism, n = 64), and Group 3 (control, n = 60). Patients in Group 2 received levothyroxine therapy (initial dose of 25 μg/day, titrated to 50-100 μg/day), while Groups 1 and 2 were treated with anti-seizure medications (valproic acid, 40 mg/kg/day).

View Article and Find Full Text PDF

Chronic stress exposure has been widely recognized as a significant contributor to numerous central nervous system (CNS) disorders, leading to debilitating behavioral changes such as anxiety, depression, and cognitive impairments. The prolonged activation of the hypothalamic-pituitary-adrenal (HPA) axis during chronic stress disrupts the neuroendocrine balance and has detrimental effects on neuronal function and survival. () Gaertn.

View Article and Find Full Text PDF

Flavonoids are naturally occurring polyphenolic compounds known for their extensive range of biological activities. This review focuses on the inhibitory effects of flavonoids on acetylcholinesterase (AChE) and their potential as therapeutic agents for cognitive dysfunction. AChE, a serine hydrolase that plays a crucial role in cholinergic neurotransmission, is a key target in the treatment of cognitive impairments due to its function in acetylcholine hydrolysis.

View Article and Find Full Text PDF

The Receptor for Advanced Glycation End Products (RAGE), part of the immunoglobulin superfamily, plays a significant role in various essential functions under both normal and pathological conditions, especially in the progression of Alzheimer's disease (AD). RAGE engages with several damage-associated molecular patterns (DAMPs), including advanced glycation end products (AGEs), beta-amyloid peptide (Aβ), high mobility group box 1 (HMGB1), and S100 calcium-binding proteins. This interaction impairs the brain's ability to clear Aβ, resulting in increased Aβ accumulation, neuronal injury, and mitochondrial dysfunction.

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!