Evidence map›Paper›PMID 31057410›Full record

ArticleFrontiers in pharmacology2019

Geniposide Alleviates Glucocorticoid-Induced Inhibition of Osteogenic Differentiation in MC3T3-E1 Cells by ERK Pathway.

Baocheng Xie, Jiahuan Wu, Yongmei Li, Xuejun Wu, Zhanwei Zeng, Chenhui Zhou, Daohua Xu, Longhuo Wu

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
–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

26 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  15. Iridoid fromEvidence-based complementary and alternative medicine : eCAM · 2023
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  18. Inhibitory Effect ofMedicina (Kaunas, Lithuania) · 2022
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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

8 authors.

Baocheng XieGuangdong Key Laboratory for Research and Development of Natural Drugs, The Public Service Platform of South China Sea for R&D Marine Biomedicine Resources, Marine Biomedical Research Institute, Guangdong Medical University, Zhanjiang, China.
Jiahuan WuGuangdong Key Laboratory for Research and Development of Natural Drugs, The Public Service Platform of South China Sea for R&D Marine Biomedicine Resources, Marine Biomedical Research Institute, Guangdong Medical University, Zhanjiang, China.
Yongmei LiDepartment of Pharmacology, Institute of Traditional Chinese Medicine and New Pharmacy Development, Guangdong Medical University, Dongguan, China.
Xuejun WuDepartment of Pharmacology, Institute of Traditional Chinese Medicine and New Pharmacy Development, Guangdong Medical University, Dongguan, China.
Zhanwei ZengDepartment of Pharmacology, Institute of Traditional Chinese Medicine and New Pharmacy Development, Guangdong Medical University, Dongguan, China.
Chenhui ZhouSchool of Nursing, Guangdong Medical University, Dongguan, China.
Daohua XuGuangdong Key Laboratory for Research and Development of Natural Drugs, The Public Service Platform of South China Sea for R&D Marine Biomedicine Resources, Marine Biomedical Research Institute, Guangdong Medical University, Zhanjiang, China.
Longhuo WuCollege of Pharmacy, Gannan Medical University, Ganzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid (GC) therapy is the leading cause of secondary osteoporosis and the therapeutic and preventative drugs for GC-induced osteoporosis are limited. In this study, we investigated the protective effects of geniposide on dexamethasone (DEX)-induced osteogenic inhibition in MC3T3-E1 cells. The results showed that there was no obvious toxicity on MC3T3-E1 cells when geniposide was used at the doses ranging from 1 to 75 μM. In DEX-treated MC3T3-E1 cells, geniposide promoted the alkaline phosphatase (ALP) activity and the mineralization. In addition, geniposide also significantly increased the mRNA and protein expression of osteopontin (OPN), Runt-related transcription factor 2 (Runx2), and Osterix (Osx) in DEX-treated MC3T3-E1 cells. Furthermore, geniposide activated ERK pathway in DEX-treated MC3T3-E1 cells. The ERK activation inhibitor U0126 and glucagon-like peptide-1 (GLP-1) receptor antagonist exendin 9-39 abolished the geniposide-induced activation of ERK and inhibited the protective effect of geniposide. Taken together, our study revealed that geniposide alleviated GC-induced osteogenic suppression in MC3T3-E1 cells. The effect of geniposide was at least partially associated with activating ERK signaling pathway via GLP-1 receptor. Geniposide might be a potential therapeutic agent for GC-induced osteoporosis.

Indexed as

ERK pathwaygeniposideGLP-1 receptorglucocorticoidosteogenic differentiationosteoporosis

Identifiers

PMID31057410
PMCPMC6482204

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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.