Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy

Introduction:Dysregulation of parvalbumin (PV) interneurons has been implicated in sepsis-associated encephalopathy (SAE), yet the underlying mechanisms remain poorly understood, and effective treatments are lacking. Given the high energy demands of PV interneurons and the emerging role of mitochond...

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Main Authors: Lei Dai, Shuxin Gu, Yibao Zhang, Siqi Ma, Peishan Wang, Jingyun Zhang, Cai Wang, Gaowei Su, Qun Fu, Wei Zhou, Yunxia Fan
Format: Article
Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Pharmacology
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Online Access:https://www.frontiersin.org/articles/10.3389/fphar.2025.1525028/full
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author Lei Dai
Lei Dai
Shuxin Gu
Shuxin Gu
Yibao Zhang
Siqi Ma
Peishan Wang
Peishan Wang
Jingyun Zhang
Jingyun Zhang
Cai Wang
Cai Wang
Gaowei Su
Gaowei Su
Qun Fu
Wei Zhou
Yunxia Fan
Yunxia Fan
author_facet Lei Dai
Lei Dai
Shuxin Gu
Shuxin Gu
Yibao Zhang
Siqi Ma
Peishan Wang
Peishan Wang
Jingyun Zhang
Jingyun Zhang
Cai Wang
Cai Wang
Gaowei Su
Gaowei Su
Qun Fu
Wei Zhou
Yunxia Fan
Yunxia Fan
author_sort Lei Dai
collection DOAJ
description Introduction:Dysregulation of parvalbumin (PV) interneurons has been implicated in sepsis-associated encephalopathy (SAE), yet the underlying mechanisms remain poorly understood, and effective treatments are lacking. Given the high energy demands of PV interneurons and the emerging role of mitochondrial dynamics in SAE pathophysiology, this study aimed to investigate whether the mitochondrial fission inhibitor Mdivi-1 could alleviate PV interneuron dysfunction and cognitive impairments in a mouse model of SAE.Methods:C57BL/6 male mice were injected with lipopolysaccharide (LPS) to establish an animal model of SAE. Mdivi-1 was administered intraperitoneally 1 h before LPS challenge. Hippocampal tissues were harvested 24 h after LPS challenge for biochemical and histochemical analyses, and mitochondrial morphology was evaluated using transmission electron microscopy. In vivo electrophysiology and behavioral tests were performed between 2 and 4 days after LPS challenge to measure neural oscillations in the hippocampus and assess cognitive function.ResultsOur results showed that LPS induced neuroinflammation, mitochondrial fission abnormalities, ATP depletion, and downregulation of PV interneurons in the hippocampus, collectively contributing to reduced gamma oscillations and cognitive impairments in mice. However, these effects were mitigated by Mdivi-1 treatment.Conclusion:Our study suggests that Mdivi-1 may offer a promising therapeutic approach for attenuating PV interneurons dysfunction and cognitive impairments in SAE.
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spelling doaj-art-0dd44f2cbec04bdb8352bbe1c91ea1ff2025-08-20T02:22:20ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-06-011610.3389/fphar.2025.15250281525028Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathyLei Dai0Lei Dai1Shuxin Gu2Shuxin Gu3Yibao Zhang4Siqi Ma5Peishan Wang6Peishan Wang7Jingyun Zhang8Jingyun Zhang9Cai Wang10Cai Wang11Gaowei Su12Gaowei Su13Qun Fu14Wei Zhou15Yunxia Fan16Yunxia Fan17Department of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, ChinaDepartment of Anesthesiology, Jinling Hospital, Medical School of Nanjing University, Nanjing, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaDepartment of Anesthesiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, ChinaDepartment of Anesthesiology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, ChinaDepartment of Anesthesiology, Jintan Affiliated Hospital of Jiangsu University, Changzhou, ChinaJiangsu Key Laboratory of Medical Science and Laboratory Medicine, School of Medicine, Jiangsu University, Zhenjiang, Jiangsu, ChinaIntroduction:Dysregulation of parvalbumin (PV) interneurons has been implicated in sepsis-associated encephalopathy (SAE), yet the underlying mechanisms remain poorly understood, and effective treatments are lacking. Given the high energy demands of PV interneurons and the emerging role of mitochondrial dynamics in SAE pathophysiology, this study aimed to investigate whether the mitochondrial fission inhibitor Mdivi-1 could alleviate PV interneuron dysfunction and cognitive impairments in a mouse model of SAE.Methods:C57BL/6 male mice were injected with lipopolysaccharide (LPS) to establish an animal model of SAE. Mdivi-1 was administered intraperitoneally 1 h before LPS challenge. Hippocampal tissues were harvested 24 h after LPS challenge for biochemical and histochemical analyses, and mitochondrial morphology was evaluated using transmission electron microscopy. In vivo electrophysiology and behavioral tests were performed between 2 and 4 days after LPS challenge to measure neural oscillations in the hippocampus and assess cognitive function.ResultsOur results showed that LPS induced neuroinflammation, mitochondrial fission abnormalities, ATP depletion, and downregulation of PV interneurons in the hippocampus, collectively contributing to reduced gamma oscillations and cognitive impairments in mice. However, these effects were mitigated by Mdivi-1 treatment.Conclusion:Our study suggests that Mdivi-1 may offer a promising therapeutic approach for attenuating PV interneurons dysfunction and cognitive impairments in SAE.https://www.frontiersin.org/articles/10.3389/fphar.2025.1525028/fullsepsis-associated encephalopathyMdivi-1parvalbumin interneuronsneuroinflammationcognitive impairment
spellingShingle Lei Dai
Lei Dai
Shuxin Gu
Shuxin Gu
Yibao Zhang
Siqi Ma
Peishan Wang
Peishan Wang
Jingyun Zhang
Jingyun Zhang
Cai Wang
Cai Wang
Gaowei Su
Gaowei Su
Qun Fu
Wei Zhou
Yunxia Fan
Yunxia Fan
Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
Frontiers in Pharmacology
sepsis-associated encephalopathy
Mdivi-1
parvalbumin interneurons
neuroinflammation
cognitive impairment
title Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
title_full Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
title_fullStr Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
title_full_unstemmed Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
title_short Mitochondrial fission inhibitor Mdivi-1 alleviates lipopolysaccharide-induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis-associated encephalopathy
title_sort mitochondrial fission inhibitor mdivi 1 alleviates lipopolysaccharide induced parvalbumin interneurons dysregulation and cognitive impairments in a mouse model of sepsis associated encephalopathy
topic sepsis-associated encephalopathy
Mdivi-1
parvalbumin interneurons
neuroinflammation
cognitive impairment
url https://www.frontiersin.org/articles/10.3389/fphar.2025.1525028/full
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