ArticleBosnian journal of basic medical sciences2022
Resveratrol ameliorates neuronal apoptosis and cognitive impairment by activating the SIRT1/RhoA pathway in rats after anesthesia with sevoflurane.
Article in Bosnian journal of basic medical sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 13 citations in OpenAlex.
- Loganin alleviates sevoflurane-induced cognitive dysfunction and neuroinflammation in aged mice via modulation of SIRT1/NF-κB signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Role and mechanism of LINC00662 via targeting let-7 g-5p in sevoflurane-induced cognitive impairment in rats.BMC anesthesiology · 2026Article
- STUB1-mediated PGC-1α ubiquitination promotes postoperative cognitive dysfunction in aged mice via modulating autophagy-lysosome machinery.European journal of medical research · 2025Article
- Impact of dietary ingredients on radioprotection and radiosensitization: a comprehensive review.Annals of medicine · 2024Review
- Sevoflurane-induced overexpression of extrasynaptic α5-GABAAging cell · 2024Article
- Natural Radiosensitizers in Radiotherapy: Cancer Treatment by Combining Ionizing Radiation with Resveratrol.International journal of molecular sciences · 2022Review
- Resveratrol Alleviates Cognitive Impairment in Chronic Cerebral Hypoperfusion by Targeting Lingo-1, NgR1, p75, and RhoA/ROCK-2 Pathways.Iranian journal of pharmaceutical research : IJPRArticle
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4 authors at 1 institution in 1 country.
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Abstract
Studies have shown that long-term exposure to sevoflurane (SEV) may cause postoperative cognitive dysfunction. This study aimed to investigate the effects of resveratrol (RES) treatment on the changes in the cognitive function of rats after prolonged anesthesia with SEV. Seventy-six adult male rats were used in this study. The SEV model was established under continuous anesthesia for 6 h. Rats were randomly classified into four groups as follows: control, SEV+vehicle, SEV+pre-RES (RES was administered 24 h before establishing the SEV model), and SEV+post-RES (RES was administered 1 h after establishing the SEV model) groups. Neurobehavioral outcomes and the potential mechanism underlying RES-mediated neuroprotection through the SIRT1/RhoA signaling pathway were evaluated. The water maze test showed that long-term exposure to SEV may lead to loss of learning and memory ability in rats (p<0.05). Compared with the SEV+vehicle group, the RES treatment groups showed significantly improved neurobehavioral scores (p<0.05). Additionally, the SEV+pre-RES group had a better outcome than the SEV+vehicle group on days 1 or 2 (p<0.05), unlike the SEV+post-RES group (p>0.05). Western blotting showed that SIRT1, RhoA, and cleaved Caspase-3 (CC3) expression significantly increased in the SEV+vehicle group (p<0.05), while Bcl2 expression decreased (p < 0.05). RES treatment further upregulated SIRT1 and Bcl2 expression and downregulated the expression of RhoA and CC3 (p<0.05). In conclusion, RES treatment improved cognitive dysfunction by reducing neuronal apoptosis in adult rats exposed to SEV. RES partly exerted a neuroprotective effect through the activation of the SIRT1/RhoA signaling pathway.
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