Evidence map›Paper›PMID 26392752›Full record

ArticleDrug design, development and therapy2015

Regulation of bone formation by baicalein via the mTORC1 pathway.

Sheng-fa Li, Jia-jun Tang, Jian Chen, Pei Zhang, Ting Wang, Tian-yu Chen, Bo Yan, Bin Huang, Liang Wang, Min-jun Huang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

27 citing papers in PubMed, 37 citations in OpenAlex.

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  12. Anti-Osteoporosis Effect ofMolecules (Basel, Switzerland) · 2022
    Article
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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

12 authors at 2 institutions in 1 country.

Sheng-fa LiAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Jia-jun TangAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Jian ChenAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China ; Three Gorges Central Hospital of Chongqing, Chongqing, People's Republic of China.
Pei ZhangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Ting WangDepartment of Cell Biology, School of Basic Medical Science, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Tian-yu ChenAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Bo YanAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Bin HuangAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Liang WangAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Min-jun HuangAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Zhong-min ZhangAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Da-di JinAcademy of Orthopedics of Guangdong Province, Guangzhou, People's Republic of China ; Department of Orthopedics, The Third Affiliated Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Third Affiliated Hospital of Southern Medical University · CNSouthern Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteoporosis is a systemic skeletal disease that is characterized by low bone density and microarchitectural deterioration of bone tissue. The increasing prevalence of osteoporosis has attracted much attention. In this study, MC3T3-E1 pre-osteoblasts were treated with the natural compound, baicalein (0.1 μmol/L, 1 μmol/L, 10 μmol/L), to stimulate differentiation over a 14-day period. In addition, a canonical ovariectomized (OVX) mouse model was used to investigate the effect of 3-month baicalein treatment (10 mg/kg per day) in preventing postmenopausal osteoporosis. In vitro, we found that baicalein induced activation of alkaline phosphatase, stimulated the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway, and induced expression of osteoblast differentiation markers, ie, osteocalcin, osterix, collagen Iα1, and runt-related transcription factor 2 (RUNX2), in osteoblasts. In vivo, several bone parameters, including trabecular thickness, trabecular bone mineral density, and trabecular number, in the distal femoral metaphysis were significantly increased in OVX mice treated intragastrically with baicalein for 3 months compared with OVX mice that were not treated with baicalein. We also found that expression of osteocalcin and RUNX2 was decreased in primary ossified tissue from the OVX group, and baicalein increased the levels of osteocalcin and RUNX2 in OVX mice. These data suggest that baicalein can stimulate MC3T3-E1 cells to differentiate into osteoblasts via activation of the mTORC1 signaling pathway, which includes protein kinases and transcription factors such as P-4E/BP1 and P-S6K1.

Indexed as

AnimalsCell LineCore Binding Factor Alpha 1 SubunitDose-Response Relationship, DrugFemaleFlavanonesHumansMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMultiprotein ComplexesOsteoblastsOsteocalcinOsteogenesisOsteoporosis, PostmenopausalOvariectomybaicaleinCore Binding Factor Alpha 1 SubunitFlavanonesMechanistic Target of Rapamycin Complex 1Multiprotein ComplexesOsteocalcinTOR Serine-Threonine KinasesmenopausemTORosteoblastosteoporosis

Identifiers

PMID26392752
PMCPMC4572734
OpenAlexW1441005930

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.