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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

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

Effect of SPP on mitochondrial functioning during chronic fatigue. SPP in red color shows inhibitory effect, SPP in blue color shows promotor effect.
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Figure 5: Effect of SPP on mitochondrial functioning during chronic fatigue. SPP in red color shows inhibitory effect, SPP in blue color shows promotor effect.

Mentions: Generally our finding revealed that forced swimming chronic fatigue model can cause mitochondrial dysfunction by increasing TNF-α level as well as attacking mitochondrial component through ROS induced lipid peroxidation and also by disturbing mitochondrial dynamic network. Whereas, SPP showed to protect forced swimming induced mitochondrial dysfunction and protect damage to mitochondrial component through preventing ROS and TNF-α generation, by maintaining mitochondrial dynamic network and by increasing serum IL-6 level, that may linked to its effect to inhibit mitochondrial ROS and also increase glucose up take to alleviate stress that occur during chronic fatigue (Figure 5).


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
Effect of SPP on mitochondrial functioning during chronic fatigue. SPP in red color shows inhibitory effect, SPP in blue color shows promotor effect.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5037131&req=5

Figure 5: Effect of SPP on mitochondrial functioning during chronic fatigue. SPP in red color shows inhibitory effect, SPP in blue color shows promotor effect.
Mentions: Generally our finding revealed that forced swimming chronic fatigue model can cause mitochondrial dysfunction by increasing TNF-α level as well as attacking mitochondrial component through ROS induced lipid peroxidation and also by disturbing mitochondrial dynamic network. Whereas, SPP showed to protect forced swimming induced mitochondrial dysfunction and protect damage to mitochondrial component through preventing ROS and TNF-α generation, by maintaining mitochondrial dynamic network and by increasing serum IL-6 level, that may linked to its effect to inhibit mitochondrial ROS and also increase glucose up take to alleviate stress that occur during chronic fatigue (Figure 5).

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus