Cannabidiol Alleviates LPS-Induced Depressive-Like Behaviors Via Improving Mitochondria Function.

Junning Zhao, Qian Liu, Xin Wang, Yusen Xiao, Baiyi Yao, Jiale Liu, Cailin Wang, Gongping Liu, Xiaoyue Hong

Abstract read

In one paragraph

Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it

0cells of the map it votes in

1citing papers in PubMed

–field-weighted citation impact

1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

Low Dose Ketamine Preconditions Astrocyte Mitochondria to Achieve Antidepressant Efficacy via Adenosine, Humanin, and Melatonin Upregulation and Efflux.Alpha psychiatry · 2026
Article

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Junning ZhaoDepartment of Neurology, Xuanwu Hospital Capital Medical University, National Center for Neurological Disorders, Beijing, 100053, China.

Qian LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Xin WangDepartment of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

Yusen XiaoThe First Clinical Medical School, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Baiyi YaoThe Second Clinical Medical School, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Jiale LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Cailin WangDepartment of Neurology, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou Peoples Hospital, No.100 of Minjiang Street, Quzhou, 32400, China.

Gongping LiuDepartment of Pathophysiology, School of Basic Medicine, Key Laboratory of Education Ministry of China/Hubei Province for Neurological Disorders, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Xiaoyue HongDepartment of Laboratory Medicine, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China. zn003955@whu.edu.cn.

Funding

Health and Wellness Science and Technology Project of Hubei Province WJ2025Q090National Natural Science Foundation of China 82201589

6 · The paper itself

Abstract

Mitochondrial autophagy has been regarded as a new signaling pathway for the action of antidepressant drugs. The neuroprotective properties of the non-psychoactive cannabinoid cannabidiol (CBD) have been demonstrated in different animal models of neurological disorders. However, the therapeutic effect of cannabidiol on neuroinflammation-induced depression and its underlying molecular mechanisms involved has not been comprehensively studied. In this study, depressive-like behaviors were induced in male C57BL/6 mice by LPS injection, with intragastric administration of CBD (70 or 140 mg/kg/day) for 6 days. Our results demonstrated that CBD treatment significantly attenuated lipopolysaccharide (LPS)-induced depressive-like behaviors, accompanied by a marked amelioration of synaptic healthiness in the hippocampal region. CBD effectively inhibited reactive oxygen species production, normalized the levels of oxidative stress markers, and restored superoxide dismutase activity, involving a mechanism that promotes mitochondrial biogenesis and mitophagy. In addition, LPS-induced neuroinflammation was reduced by CBD, as evidenced by a marked decrease in neuroinflammatory activation markers. CBD also inhibited LPS-activated inflammasome activation by targeting NLRP3/IL-1β/Caspase-1 signaling pathway. These findings suggest that CBD may be a potential therapeutic drug for managing major depressive disorder.

Indexed as

Behavior, AnimalCannabidiolDepressionMitochondriaAnimalsAntidepressive AgentsHippocampusInflammasomesInterleukin-1betaLipopolysaccharidesMaleMiceMice, Inbred C57BLNLR Family, Pyrin Domain-Containing 3 ProteinOxidative StressReactive Oxygen SpeciesAntidepressive AgentsCannabidiolInflammasomesInterleukin-1betaLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesCannabidiolDepressionMitochondriaMitophagyNeuroinflammationNLRP3

Identifiers

PMID41484536

DOI10.1007/s12035-025-05614-w

What OpenQuestion holds

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.