ArticleFood science & nutrition2022
Protective effects of chlorogenic acid on isoflurane-induced cognitive impairment of aged mice.
Article in Food science & nutrition, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- PGK1 Drives Glial Glycolytic Reprogramming to Mediate Isoflurane-Induced Cognitive Impairment in Aged Mice.Journal of cellular and molecular medicine · 2026Article
- Therapeutic potential and microRNA regulating properties of phytochemicals in Alzheimer's disease.Molecular therapy. Nucleic acids · 2025Review
- Quercetin can improve anesthesia induced neuroinflammation and cognitive dysfunction by regulating miR-138-5p/ LCN2.BMC anesthesiology · 2025Article
- Review
- Neuroprotective Effects ofAntioxidants (Basel, Switzerland) · 2022Article
- Protective effects of chlorogenic acid on isoflurane-induced cognitive impairment of aged mice.Food science & nutrition · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Postoperative cognitive dysfunction (POCD) is characterized by impairment in cognitive functions in patients following anesthesia and surgery. Chlorogenic acid (CGA) is a plant-derived compound possessing numerous bioactive properties. The aim of this study was to investigate the therapeutic potential of CGA in isoflurane (ISO)-induced cognitive dysfunction of aged mice, and further identify the mechanisms involved in the protective effects of CGA. A total of 80 male C57BL/6 mice, 20-month-old, were randomly divided into control group, isoflurane group (ISO), and ISO + 30 mg/kg CGA group and ISO + 60 mg/kg CGA. CGA was given orally once daily for 7 days to the mice and they were exposed to ISO (1.5%; 4 h). The open-field and Morris water maze tests were used to investigate the cognitive function of mice. Pretreatment with CGA significantly attenuated ISO-induced cognitive impairment. The levels of IL-1β, TNF-α, IL-6, nuclear p65 NF-kB, cleaved caspase-3, and Bax were significantly increased, while the levels of IkBα and Bcl-2 were decreased in the hippocampus 24 h after the ISO anesthesia. All the mentioned effects induced by ISO were reversed by CGA pretreatment. Furthermore, ISO exposure induced marked downregulation of SOD, CAT, HO-1, and NQO-1 and elevation of MDA and nuclear translocation of Nrf2 in the hippocampus tissue. All these parameters were reversed by CGA treatment. Importantly, the higher dose of CGA (60 mg/kg) showed a greater neuroprotective effect. In conclusion, these findings suggest that CGA attenuates the ISO-induced cognitive impairment via its anti-inflammatory, anti-oxidative, and anti-apoptotic properties in aged mice.
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