ArticleScientific reports2025
Remimazolam attenuated lipopolysaccharide-induced behavioral deficits and neuronal injury via activation of the Nrf2 pathway.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed.
- The role and mechanism of TNFRSF21 in promoting necroptosis of vascular endothelial cells and inducing vascular leakage in sepsis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Discontinuation of the development of remimazolam for ICU sedation in Japan: background and rationale.Journal of intensive care · 2026Review
- Identification and Analysis of Remimazolam's Potential Therapeutic Mechanisms in Murine Sepsis-Associated Encephalopathy via Transcriptomic Analysis.Journal of inflammation research · 2026Article
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7 authors.
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Abstract
Sepsis is a severe disorder that is always accompanied by brain injury and dysfunction. This study aimed to evaluate the effects of remimazolam, a new ultra-short-acting sedative, on LPS-induced neuronal injury, and the role of Nrf2 signaling pathway involved. LPS was administered to Sprague-Dawley rats in the presence or absence of remimazolam. Then the behavior analysis was performed by using the Morris Water Maze and Open Field Test. The levels of the Superoxide Dismutase (SOD) and Malondialdehyde (MDA), the neuronal apoptosis, and the expression of Nrf2, HO-1, and Bcl-2 were detected in the hippocampus. In vitro, primary hippocampal neurons were exposed to LPS with or without remimazolam administration. Then the cell viability, apoptosis, mitochondrial membrane potential (MMP), and intracellular ROS were measured to assess oxidative stress and neuron injury. The expression of Nrf2, and HO-1 was also determined by Western blotting. LPS triggered neuroapoptosis, evoked oxidative stress, and inhibited the expression of Nrf2, and HO-1 in rat hippocampus, which were attenuated by remimazolam treatment. Additionally, remimazolam alleviated LPS-induced cognitive dysfunction and anxiety‑like behaviors in rats. In vitro, remimazolam could ameliorate neuronal damage, decrease the production of ROS, and increase the MMP of neurons exposed to LPS, which was accompanied by an increase in the expression of Nrf2 and HO-1. However, ML385 (an Nrf2 inhibitor) reversed the beneficial effects of remimazolam on primary hippocampal neurons. These findings suggest that remimazolam exerted protective effects on LPS-induced hippocampal neuronal injury in vivo and in vitro, which was associated with activation of Nrf2 signaling. Further experiments are needed to fully explore the exact molecular mechanism of Nrf2 upstream and downstream of remimazolam and its effects on distinct brain regions, which will help to better understand the neural effects of remimazolam.
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