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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.


Mitochondrial structure of mice skeletal muscle under electron microscopy. (A,B) control, (C,D) model, (E,F) SPP-200 mg/kg, (G,H) SPP-400 mg/kg, (I,J) CoQ 10 200 mg/kg at 4.0 K (upper) and 20.0 K (lower) magnification. Scale bar represent 2 um and 200 nm respectively.
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Figure 1: Mitochondrial structure of mice skeletal muscle under electron microscopy. (A,B) control, (C,D) model, (E,F) SPP-200 mg/kg, (G,H) SPP-400 mg/kg, (I,J) CoQ 10 200 mg/kg at 4.0 K (upper) and 20.0 K (lower) magnification. Scale bar represent 2 um and 200 nm respectively.

Mentions: Ultra structural analysis of mice skeletal muscle biopsies revealed an enormous change in mice skeletal muscle mitochondrial structure in model group compared to normal control group. Generally Model group showed various abnormalities including increased number and size of mitochondria, pleomorphism, compartmentalization, and zigzag cristae as shown in (Figure 1). This proves use of forced swimming model to induce mitochondrial dysfunction due to chronic fatigue worked very well. Whereas, in SPP 200 mg/kg and 400 mg/kg the size of mitochondria is almost similar to control group while in positive control (CoQ10) group mitochondrial size is slightly larger than normal control group but smaller compared to model group. The other most remarkable abnormality seen was on internal structure of mitochondria which produced an appearance of compartmentalization, apparently produced by branching and fusion of the cristae. In model group almost all mitochondrion’s lost their normal parallel arrangement of cristae at the sites of the branching and fusion, some of mitochondrion’s in SPP 400 mg/kg and positive control (CoQ10) group also lost some of their parallel arrangement of cristae, only occasional mitochondria showed compartmentalization. But in SPP 200 mg/kg the arrangement of cristae was as intact as normal control group. Moreover the outer and inner membrane of mitochondria was lysed in forced swimming model group while it was intact in rest of other group. The results have shown SPP have protected mitochondrial dysfunction by maintaining the normal structure and through preserving outer and inner membrane integrity.


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
Mitochondrial structure of mice skeletal muscle under electron microscopy. (A,B) control, (C,D) model, (E,F) SPP-200 mg/kg, (G,H) SPP-400 mg/kg, (I,J) CoQ 10 200 mg/kg at 4.0 K (upper) and 20.0 K (lower) magnification. Scale bar represent 2 um and 200 nm respectively.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 1: Mitochondrial structure of mice skeletal muscle under electron microscopy. (A,B) control, (C,D) model, (E,F) SPP-200 mg/kg, (G,H) SPP-400 mg/kg, (I,J) CoQ 10 200 mg/kg at 4.0 K (upper) and 20.0 K (lower) magnification. Scale bar represent 2 um and 200 nm respectively.
Mentions: Ultra structural analysis of mice skeletal muscle biopsies revealed an enormous change in mice skeletal muscle mitochondrial structure in model group compared to normal control group. Generally Model group showed various abnormalities including increased number and size of mitochondria, pleomorphism, compartmentalization, and zigzag cristae as shown in (Figure 1). This proves use of forced swimming model to induce mitochondrial dysfunction due to chronic fatigue worked very well. Whereas, in SPP 200 mg/kg and 400 mg/kg the size of mitochondria is almost similar to control group while in positive control (CoQ10) group mitochondrial size is slightly larger than normal control group but smaller compared to model group. The other most remarkable abnormality seen was on internal structure of mitochondria which produced an appearance of compartmentalization, apparently produced by branching and fusion of the cristae. In model group almost all mitochondrion’s lost their normal parallel arrangement of cristae at the sites of the branching and fusion, some of mitochondrion’s in SPP 400 mg/kg and positive control (CoQ10) group also lost some of their parallel arrangement of cristae, only occasional mitochondria showed compartmentalization. But in SPP 200 mg/kg the arrangement of cristae was as intact as normal control group. Moreover the outer and inner membrane of mitochondria was lysed in forced swimming model group while it was intact in rest of other group. The results have shown SPP have protected mitochondrial dysfunction by maintaining the normal structure and through preserving outer and inner membrane integrity.

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.