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Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue

Overview of attention for article published in Frontiers in Pharmacology, September 2016
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Title
Placenta Peptide Can Protect Mitochondrial Dysfunction through Inhibiting ROS and TNF-α Generation, by Maintaining Mitochondrial Dynamic Network and by Increasing IL-6 Level during Chronic Fatigue
Published in
Frontiers in Pharmacology, September 2016
DOI 10.3389/fphar.2016.00328
Pubmed ID
Authors

Rekik A. Muluye, Yuhong Bian, Li Wang, Paulos N. Alemu, Huantian Cui, Xiaofei Peng, Shanshan Li

Abstract

Background: Level of fatigue is related to the metabolic energy available to tissues and cells, mainly through mitochondrial respiration, as well fatigue is the most common symptom of poorly functioning mitochondria. Hence, dysfunction of these organelles may be the cause of the fatigue seen in Chronic fatigue (CF). Placenta has been used for treatment of fatigue and various disease, moreover peptides has known protect mitochondrial viability, and alleviate fatigue. These properties of placenta and peptides may link with its effect on mitochondria; therefore, it is highly important to investigate the effectiveness of placenta peptide on fatigue and mitochondrial dysfunction. Methods: After administration of sheep placenta peptide (SPP) for 1 month, mice's were forced to swim till exhaustion for 90 min to induce chronic fatigue. Electron microscopic examination of skeletal muscle mitochondrial structure, tissue Malondialdehyde (MDA), mitochondrial SOD and serum inflammatory cytokines level were investigated in order to determine the potential effect of SPP on mitochondria during CF. Rat skeletal muscle (L6 cell) were also treated with different concentration of SPP to determine the effect of SPP on cell viability using Thiazoyl blue tetrazolium assay. Results: Our finding revealed that forced swimming induced fatigue model can cause mitochondrial damage through Reactive oxygen species (ROS) mediated lipid peroxidation and Tumor Necrosis factor alpha (TNF-α) elevation. Whereas SPP protected fatigue induced mitochondrial dysfunction through preventing ROS and TNF-α generation, by maintaining mitochondrial dynamic network and by increasing serum IL-6 level. Conclusion: SPP can protect damage in mitochondrial components which will allow proper functioning of mitochondria that will in turn inhibit progression of chronic fatigue. Therefore, SPP may represent a novel therapeutic advantage for preventing mitochondrial dysfunction in patients with chronic fatigue.

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The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

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 4 20%
Student > Ph. D. Student 2 10%
Unspecified 1 5%
Other 1 5%
Student > Doctoral Student 1 5%
Other 2 10%
Unknown 9 45%
Readers by discipline Count As %
Medicine and Dentistry 6 30%
Agricultural and Biological Sciences 2 10%
Biochemistry, Genetics and Molecular Biology 1 5%
Unspecified 1 5%
Nursing and Health Professions 1 5%
Other 0 0%
Unknown 9 45%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 25 September 2017.
All research outputs
#14,210,614
of 22,889,074 outputs
Outputs from Frontiers in Pharmacology
#4,644
of 16,187 outputs
Outputs of similar age
#183,592
of 322,819 outputs
Outputs of similar age from Frontiers in Pharmacology
#67
of 158 outputs
Altmetric has tracked 22,889,074 research outputs across all sources so far. This one is in the 37th percentile – i.e., 37% of other outputs scored the same or lower than it.
So far Altmetric has tracked 16,187 research outputs from this source. They receive a mean Attention Score of 4.9. This one has gotten more attention than average, scoring higher than 70% 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 322,819 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 42nd percentile – i.e., 42% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 158 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 57% of its contemporaries.