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Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression

Overview of attention for article published in Brazilian Journal of Medical and Biological Research, January 2018
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Title
Andrographolide protects mouse astrocytes against hypoxia injury by promoting autophagy and S100B expression
Published in
Brazilian Journal of Medical and Biological Research, January 2018
DOI 10.1590/1414-431x20177061
Pubmed ID
Authors

Juan Du, Chunyan Zhang, Xueqing Na, Aizhi Li, Qingfeng Zhang, Kezhong Li, Yongbo Ding

Abstract

Andrographolide (ANDRO) has been studied for its immunomodulation, anti-inflammatory, and neuroprotection effects. Because brain hypoxia is the most common factor of secondary brain injury after traumatic brain injury, we studied the role and possible mechanism of ANDRO in this process using hypoxia-injured astrocytes. Mouse cortical astrocytes C8-D1A (astrocyte type I clone from C57/BL6 strains) were subjected to 3 and 21% of O2 for various times (0-12 h) to establish an astrocyte hypoxia injury model in vitro. After hypoxia and ANDRO administration, the changes in cell viability and apoptosis were assessed using CCK-8 and flow cytometry. Expression changes in apoptosis-related proteins, autophagy-related proteins, main factors of JNK pathway, ATG5, and S100B were determined by western blot. Hypoxia remarkably damaged C8-D1A cells evidenced by reduction of cell viability and induction of apoptosis. Hypoxia also induced autophagy and overproduction of S100B. ANDRO reduced cell apoptosis and promoted cell autophagy and S100B expression. After ANDRO administration, autophagy-related proteins, S-100B, JNK pathway proteins, and ATG5 were all upregulated, while autophagy-related proteins and s100b were downregulated when the jnk pathway was inhibited or ATG5 was knocked down. ANDRO conferred a survival advantage to hypoxia-injured astrocytes by reducing cell apoptosis and promoting autophagy and s100b expression. Furthermore, the promotion of autophagy and s100b expression by ANDRO was via activation of jnk pathway and regulation of ATG5.

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Mendeley readers

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The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 20 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 5 25%
Student > Postgraduate 2 10%
Student > Master 2 10%
Professor 1 5%
Other 1 5%
Other 2 10%
Unknown 7 35%
Readers by discipline Count As %
Medicine and Dentistry 5 25%
Biochemistry, Genetics and Molecular Biology 4 20%
Neuroscience 2 10%
Immunology and Microbiology 1 5%
Unknown 8 40%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. 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 26 April 2018.
All research outputs
#20,663,600
of 25,382,440 outputs
Outputs from Brazilian Journal of Medical and Biological Research
#901
of 1,254 outputs
Outputs of similar age
#343,505
of 449,583 outputs
Outputs of similar age from Brazilian Journal of Medical and Biological Research
#45
of 85 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 10th percentile – i.e., 10% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,254 research outputs from this source. They receive a mean Attention Score of 4.9. This one is in the 18th percentile – i.e., 18% of its peers scored the same or lower than it.
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 449,583 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 13th percentile – i.e., 13% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 85 others from the same source and published within six weeks on either side of this one. This one is in the 36th percentile – i.e., 36% of its contemporaries scored the same or lower than it.