Evidence map›Paper›PMID 36514079›Full record

ArticleBMC musculoskeletal disorders2022

Treadmill training mitigates bone deterioration via inhibiting NLRP3/Caspase1/IL-1β signaling in aged rats.

Qi Wu, Peirui Zhong, Pengyun Ning, Lu Tan, Xiarong Huang, Ting Peng, Linwei Yin, Fu Luo, Mengjian Qu, Jun Zhou

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC musculoskeletal disorders, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Qi WuDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Peirui ZhongDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Pengyun NingDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Lu TanDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Xiarong HuangDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Ting PengDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Linwei YinDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Fu LuoDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Mengjian QuDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China.
Jun ZhouDepartment of Rehabilitation, Hengyang Medical School, The First Affiliated Hospital, University of South China, No. 69, Chuanshan Road, Hengyang, Hunan Province, 421001, Hengyang, People's Republic of China. zhoujun8005@163.com.
University of South China · CN

Funding

National Natural Science Foundation of China 81973917the key project of University of South China USCKF201902K02the Natural Science Foundation of Hunan Province 2020JJ4085
6 · The paper itself

Abstract

introductionAlthough aerobic physical exercise may improve osteoporosis during ageing, the underlying mechanism of the favorable effects remains unclear. The aim of this study was to examine the localized and generalized proinflammatory indicators and the adaptive skeletal responses to treadmill training in aged rats to explore the potential mechanisms by which treadmill training impacts bone deterioration in a natural aged rat model. MATERIALS AND

methodsA total of 24 Sprague Dawley (SD) rats were included in this study. Sixteen of all these animals were twenty-four months natural aged male SD rats, which were distributed into two groups (n = 8/group): AC group with sham treadmill training, and AT group with 8 weeks treadmill training. The remaining 8 were six months male SD rats matched subline and supplier, which were used as the adult control group with sham treadmill training (YC group, n = 8). The serum, bone marrow, fresh femur, tibia, and lumbar spine were harvested for molecular biological analysis, bone mineral density (BMD) testing, and micro-CT analysis after 8 weeks of treadmill training.

resultsAfter 8 weeks of intervention, the results showed that treadmill training increased BMD and inhibited deterioration of bone microarchitecture of hind limb bones. Further analysis showed that treadmill training increased serum P1CP concentration and decreased serum CTX-1level. Interestingly, treadmill training down-regulated the protein expressions of proinflammatory indicators, including NLRP3, proCaspase1, cleaved Caspase1, IL-1β, and GSDMD-N, and the mRNA levels of NLRP3, Caspase1, and IL-1β of the bone marrow. In addition, treadmill training also inhibited serum TNF-α and IL-1β concentration. However, 8 weeks of treadmill training did not increase BMD and bone microarchitecture in the lumbar spine.

conclusionTreadmill training mitigates the ageing-induced bone loss and reverses the deterioration of bone microarchitecture in hind limbs probably through inhibiting NLRP3/Caspase1/IL-1β signaling to attenuate low-grade inflammation and improve the inflammatory bone microenvironment.

Indexed as

Bone DensityNLR Family, Pyrin Domain-Containing 3 ProteinPhysical Conditioning, AnimalAnimalsLumbar VertebraeMaleRatsRats, Sprague-DawleyNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratAerobic physical exerciseAgeingBone microenvironmentNLRP3-mediated inflammationOsteoporosis

Identifiers

PMID36514079
PMCPMC9746211
OpenAlexW4312095716

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.