Chrysanthemum Morifolium-Derived Nanovesicles Reduce Lactate-Associated Histone Lactylation and Modulate Microglia-Mediated Neuroinflammation in Sepsis-Associated Encephalopathy.
5 affiliations
- 1Center for Laboratory Medicine, Allergy center, Department of Transfusion medicine, Zhejiang Provincial People's Hospital (Affiliated People's Hospital), Hangzhou Medical College, Hangzhou, Zhejiang, China.
- 2Key Laboratory of Biomarkers and In Vitro Diagnosis Translation of Zhejiang Province, Hangzhou, Zhejiang, China.
- 3College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou, Zhejiang, China.
- 4Department of Pharmacy, Taizhou Municipal Hospital (Taizhou University Affiliated Municipal Hospital), School of Medicine, Taizhou University, Taizhou, Zhejiang, China.
- 5State Key Laboratory of Fluid Power and Mechatronic Systems, School of Mechanical Engineering, Zhejiang University, Hangzhou, Zhejiang, China.
Abstract
Sepsis-associated encephalopathy (SAE)-a complication of the central nervous system in patients with sepsis-markedly diminishes cognitive functions and is linked to hippocampal neuritis-induced injury. Plant exosome-like nanovesicles can transport proteins, lipids, and molecular compounds between neural cells and the periphery, thereby modulating target cells. This study examined the therapeutic potential of Chrysanthemum morifolium-derived exosome-like nanovesicles (CRELNVs) in an animal model of lipopolysaccharide-induced SAE, revealing their ability to effectively cross the blood-brain barrier, be internalized by microglia, and alleviate nerve injury and memory impairment by reducing lactate levels in microglia at the hippocampus. CRELNVs decreased lactylation levels in microglia, thus promoting the conversion of microglial cells from the detrimental M1 metabolic phenotype to the protective M2 one. Mechanistically, our finding suggest CRELNVs reduced proinflammatory cytokine release is associated with the inhibition of NF-κB activation. Thus, CRELNVs were concluded to exert their protective effects by modulating the H3K18la/NF-κB axis and regulate microglia-mediated neuroinflammation by responding to the hippocampal neuritis-induced injury in SAE.
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BibTeX
@article{li2026chrysanthemum,
title = {{Chrysanthemum Morifolium-Derived Nanovesicles Reduce Lactate-Associated Histone Lactylation and Modulate Microglia-Mediated Neuroinflammation in Sepsis-Associated Encephalopathy.}},
author = {Kaiqiang Li and Xuling Luo and Xiaoting Zhang and Chengwen He and Wei Xu and Aibo Xu and Shushan Hua and Liping Wang and Liang Ma and Ke Hao and Youmin Ying and Zhen Wang},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
year = {2026},
month = oct,
doi = {10.1002/advs.78330},
url = {https://europepmc.org/article/MED/42875879},
note = {CC BY},
}
RIS
TY - JOUR
TI - Chrysanthemum Morifolium-Derived Nanovesicles Reduce Lactate-Associated Histone Lactylation and Modulate Microglia-Mediated Neuroinflammation in Sepsis-Associated Encephalopathy.
AU - Kaiqiang Li
AU - Xuling Luo
AU - Xiaoting Zhang
AU - Chengwen He
AU - Wei Xu
AU - Aibo Xu
AU - Shushan Hua
AU - Liping Wang
AU - Liang Ma
AU - Ke Hao
AU - Youmin Ying
AU - Zhen Wang
PY - 2026
DA - 2026/10/14
JO - Advanced science (Weinheim, Baden-Wurttemberg, Germany)
DO - 10.1002/advs.78330
UR - https://europepmc.org/article/MED/42875879
AB - Sepsis-associated encephalopathy (SAE)-a complication of the central nervous system in patients with sepsis-markedly diminishes cognitive functions and is linked to hippocampal neuritis-induced injury. Plant exosome-like nanovesicles can transport proteins, lipids, and molecular compounds between neural cells and the periphery, thereby modulating target cells. This study examined the therapeutic potential of Chrysanthemum morifolium-derived exosome-like nanovesicles (CRELNVs) in an animal model of lipopolysaccharide-induced SAE, revealing their ability to effectively cross the blood-brain barrier, be internalized by microglia, and alleviate nerve injury and memory impairment by reducing lactate levels in microglia at the hippocampus. CRELNVs decreased lactylation levels in microglia, thus promoting the conversion of microglial cells from the detrimental M1 metabolic phenotype to the protective M2 one. Mechanistically, our finding suggest CRELNVs reduced proinflammatory cytokine release is associated with the inhibition of NF-κB activation. Thus, CRELNVs were concluded to exert their protective effects by modulating the H3K18la/NF-κB axis and regulate microglia-mediated neuroinflammation by responding to the hippocampal neuritis-induced injury in SAE.
SN - 2198-3844
ER -