Evidence map›Paper›PMID 40008134›Full record

ArticleFrontiers in pharmacology2025

Neoandrographolide inhibits mature osteoclast differentiation to alleviate bone loss and treat osteoporosis.

Kai Tang, Wei Deng, Zhiying Huang, Simin Chen, Zilin Zhu, Shukun Lin, Lubin Zhong, Quanxin Zheng, Wenhua Zhao, Zhida Zhang and 1 more

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2025. 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
–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

2 citing papers in PubMed.

  1. Review
  2. 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

11 authors.

Kai Tang *Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Wei Deng *Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Zhiying Huang *Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Simin ChenGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Zilin ZhuGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Shukun LinGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Lubin ZhongGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Quanxin ZhengGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Wenhua ZhaoDepartment of Spine Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Zhida ZhangDepartment of Spine Surgery, The Second Affiliated Hospital of Guangzhou Medical University, Guangzhou, Guangdong, China.
Ling MoGuangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Osteoporosis (OP), as the prevalent systemic metabolic bone disease worldwide, progresses insidiously and slowly. The clinical discomfort and complications associated with OP impose a significant burden on patients. Therefore, finding more effective treatments for OP remains an urgent challenge. Method: We first conducted Results: NEO exhibits no significant cytotoxic effects on BMMs at concentrations less than or equal to 30 μM while exerting inhibitory effects on OC differentiation during its early and middle stages. RT-PCR and Western blot results reveal that NEO suppresses the expression of genes and proteins including CTSK,c-Fos,MMP9,NFATc1. Western blot findings also indicate that NEO inhibits the phosphorylation of ERK, P38, JNK, and P65 but does not reverse the degradation of IκB-α. Additionally, NEO affects the phosphorylation of proteins in the PI3K/AKT, GSK3β, and PPARγ signaling pathways, demonstrating that NEO can inhibit OC formation through multiple pathways and targets. Conclusion: NEO has the potential to serve as a therapeutic agent for OP by targeting multiple sites and inhibiting the formation of mature OC through various signaling pathways.

Indexed as

GSK3βMAPKneoandrographolideNF-κBosteoclastogenesisPI3K/AKTPPARγ

Identifiers

PMID40008134
PMCPMC11851123

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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.