Evidence map›Paper›PMID 38203507›Full record

ArticleInternational journal of molecular sciences2023

Delayed Reaction of Radiation on the Central Nervous System and Bone System in C57BL/6J Mice.

Yi Ru, Xianxie Zhang, Baoying Shen, Chunqi Yang, Huijing Yu, Zuoxu Liu, Xiangjun Wu, Fangyang Li, Jialu Cui, Chengcai Lai and 2 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.1field-weighted citation impact, top 20% of its field
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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Phenylethanoid Glycosides fromInternational journal of molecular sciences · 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

12 authors.

Yi RuDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Xianxie ZhangDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Baoying ShenDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Chunqi YangDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.ORCID 0000-0003-3028-0739
Huijing YuDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Zuoxu LiuDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Xiangjun WuDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Fangyang LiDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Jialu CuiDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Chengcai LaiDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Yuguang WangDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.
Yue GaoDepartment of Pharmaceutical Sciences, Beijing Institute of Radiation Medicine, Beijing 100850, China.

Funding

National Natural Science Foundation of China 82004054National Natural Science Foundation of China 82192911
6 · The paper itself

Abstract

The aim of this study was to provide a suitable mouse model of radiation-induced delayed reaction and identify potential targets for drug development related to the prevention and treatment of radiation injury. C57BL/6J mice were subjected to singular (109 cGy/min, 5 Gy*1) and fractional (109 cGy/min, 5 Gy*2) total body irradiation. The behavior and activity of mice were assessed 60 days after ionizing radiation (IR) exposure. After that, the pathological changes and mechanism of the mouse brain and femoral tissues were observed by HE, Nissl, Trap staining micro-CT scanning and RNA sequencing (RNA-Seq), and Western blot. The results show that singular or fractional IR exposure led to a decrease in spatial memory ability and activity in mice, and the cognitive and motor functions gradually recovered after singular 5 Gy IR in a time-dependent manner, while the fractional 10 Gy IR group could not recover. The decrease in bone density due to the increase in osteoclast number may be relative to the down-regulation of RUNX2, sclerostin, and beta-catenin. Meanwhile, the brain injury caused by IR exposure is mainly linked to the down-regulation of BNDF and Tau. IR exposure leads to memory impairment, reduced activity, and self-recovery, which are associated with time and dose. The mechanism of cognitive and activity damage was mainly related to oxidative stress and apoptosis induced by DNA damage. The damage caused by fractional 10 Gy TBI is relatively stable and can be used as a stable multi-organ injury model for radiation mechanism research and anti-radiation medicine screening.

Indexed as

Brain InjuriesCentral Nervous SystemAnimalsBone DensityMiceMice, Inbred C57BLOsteoclastsbone lossbrain injurydelayed radiation damageionizing radiationradiation injury

Identifiers

PMID38203507
PMCPMC10779003
OpenAlexW4390236642

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.