Evidence map›Paper›PMID 39548856›Full record

ArticleThe Kaohsiung journal of medical sciences2024

Nuciferine inhibits osteoclast formation through suppressing glycolysis metabolic programming and ROS production.

Wen-Hui Guo, Guan-Qi Zhen, Feng Wu, Yun-Peng Lv, Jing-Long Yan, Jia-Ning Zu, Cheng-Chao Song

Abstract read
In one paragraph

Article in The Kaohsiung journal of medical sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. 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

7 authors.

Wen-Hui GuoDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Guan-Qi ZhenDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Feng WuDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yun-Peng LvDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Jing-Long YanDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Jia-Ning ZuDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Cheng-Chao SongDepartment of Orthopedics, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.ORCID https://orcid.org/0000-0002-0129-4325

Funding

2023 Heilongjiang Provincial Universities Basic Scientific Research Business Expenses Scientific Research Project 2023-KYYWF-0190Heilongjiang Postdoctoral Financial Assistance LBH-Z22228National Natural Science Foundation of China 82072472Natural Science Foundation of Heilongjiang Province LH2023H040New Era Longjiang Outstanding Master's and Doctoral Dissertations Project Funding LJYXL2022-070
6 · The paper itself

Abstract

Nuciferine (NCF) is a bioactive compound from lotus leaves and has been proven to prevent osteoclastogenesis and ovariectomy-induced osteoporosis by our previous research. However, the underlying mechanism is still unclear. In this research, Raw264.7 cells were induced into osteoclast with or without NCF. CCK-8 and Edu assays were performed to detect the effects of 30 μM NCF on cell viability and proliferation. TRAP staining and bone resorption assays were performed to observe the role of NCF in osteoclastogenesis and bone resorption. RT-PCR and Western blot were performed to detect the effects of NCF on osteoclast-related genes, glycolysis-related genes, and reactive oxygen species (ROS)-related genes. Seahorse assays, lactate concentration and glucose consumption were performed to observe cell metabolism change. DCFH-DA fluorescent probe was used to detect ROS level. In this work, 30 μM NCF could not influence cell viability and cell proliferation. Osteoclast differentiation could be inhibited by 30 μM NCF. Bone resorption assay could also observe that bone resorption ability was successfully inhibited by 30 μM NCF. In seahorse assay, we discovered that NCF could decrease extracellular acid rate and increase oxygen consumption. RT-PCR and Western blot results showed that NCF could decrease the expression of hexokinase2, pyruvate kinase muscle 2, and lactate dehydrogenase A and that NCF could also weaken the concentration of lactate. However, pyruvate kinase muscle 2 activator (GC69716) and lactate addition could promote osteoclastogenesis and bone resorption and promote the expression of c-Fos and nuclear factor of activated T cells c1. Besides, NCF could also inhibit the production of ROS. In conclusion, NCF might inhibit osteoclast formation through inhibiting glycolysis metabolism and ROS production.

Indexed as

Cell ProliferationGlycolysisOsteoclastsOsteogenesisReactive Oxygen SpeciesAnimalsBone ResorptionCell DifferentiationCell SurvivalHexokinaseMetabolic ReprogrammingMiceRAW 264.7 CellsHexokinaseReactive Oxygen SpeciesglycolysisNuciferineosteoclastROS

Identifiers

PMID39548856
PMCPMC11618493

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.