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Sulforaphane reverses glucocorticoid-induced apoptosis in osteoblastic cells through regulation of the Nrf2 pathway

Overview of attention for article published in Drug Design, Development and Therapy, July 2014
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (84th percentile)
  • Good Attention Score compared to outputs of the same age and source (78th percentile)

Mentioned by

blogs
1 blog
twitter
2 tweeters
video
1 video uploader

Citations

dimensions_citation
35 Dimensions

Readers on

mendeley
28 Mendeley
Title
Sulforaphane reverses glucocorticoid-induced apoptosis in osteoblastic cells through regulation of the Nrf2 pathway
Published in
Drug Design, Development and Therapy, July 2014
DOI 10.2147/dddt.s65410
Pubmed ID
Authors

Hao Lin, Bo Wei, Guangsheng Li, Jinchang Zheng, Jiecong Sun, Jiaqi Chu, Rong Zeng, Yanru Niu

Abstract

Apoptosis of osteoblasts triggered by high-dose glucocorticoids (GCs) has been identified as a major cause of osteoporosis. However, the underlying molecular mechanisms accounting for this action remain elusive, which has impeded the prevention and cure of this side effect. Sulforaphane (SFP) is a naturally occurring isothiocyanate that has huge health benefits for humans. In this study, by using osteoblastic MC3T3-E1 cells as a model, we demonstrate the protective effects of SFP against dexamethasone (Dex)-induced apoptosis and elucidate the underlying molecular mechanisms. The results show that SFP could effectively inhibit the Dex-induced growth inhibition and release of lactate dehydrogenase in MC3T3-E1 cells. Treatment with Dex induced caspase-dependent apoptosis in MC3T3-E1 cells, as evidenced by an increase in the Sub-G1 phase, chromatin condensation, and deoxyribonucleic acid fragmentation, which were significantly suppressed by coincubation with SFP. Mitochondria-mediated apoptosis pathway contributed importantly to Dex-induced apoptosis, as revealed by the activation of caspase-3/-9 and subsequent cleavage of poly adenosine diphosphate ribose polymerase, which was also effectively blocked by SFP. Moreover, treatments of Dex strongly induced overproduction of reactive oxygen species and inhibited the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and the downstream effectors HO1 and NQO1. However, cotreatment with SFP effectively reversed this action of Dex. Furthermore, silencing of Nrf2 by small interfering ribonucleic acid significantly blocked the cytoprotective effects of SFP against Dex-induced apoptosis, which suggest the important role of Nrf2 signaling pathway and cell apoptosis induced by Dex. Taken together, this study provides a novel strategy for molecular intervention against Dex-induced osteoporosis using phytochemicals.

Twitter Demographics

The data shown below were collected from the profiles of 2 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Canada 1 4%
Unknown 27 96%

Demographic breakdown

Readers by professional status Count As %
Student > Master 10 36%
Student > Bachelor 4 14%
Student > Ph. D. Student 3 11%
Student > Doctoral Student 2 7%
Researcher 2 7%
Other 4 14%
Unknown 3 11%
Readers by discipline Count As %
Agricultural and Biological Sciences 8 29%
Biochemistry, Genetics and Molecular Biology 6 21%
Pharmacology, Toxicology and Pharmaceutical Science 2 7%
Nursing and Health Professions 2 7%
Veterinary Science and Veterinary Medicine 1 4%
Other 4 14%
Unknown 5 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 9. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 28 March 2019.
All research outputs
#2,475,970
of 16,117,257 outputs
Outputs from Drug Design, Development and Therapy
#122
of 1,614 outputs
Outputs of similar age
#30,117
of 195,172 outputs
Outputs of similar age from Drug Design, Development and Therapy
#4
of 19 outputs
Altmetric has tracked 16,117,257 research outputs across all sources so far. Compared to these this one has done well and is in the 84th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,614 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.0. This one has done particularly well, scoring higher than 92% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 195,172 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 84% of its contemporaries.
We're also able to compare this research output to 19 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 78% of its contemporaries.