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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

(A) Effect of SPP on mice skeletal muscle MDA level. (B) Effect of SPPE on mice skeletal muscle mitochondrial SOD level each bar represent Mean ± SEM (n=10). Significant at ***p-value < 0.001 compared to control; #p-value < 0.05 compared to model.
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Figure 2: (A) Effect of SPP on mice skeletal muscle MDA level. (B) Effect of SPPE on mice skeletal muscle mitochondrial SOD level each bar represent Mean ± SEM (n=10). Significant at ***p-value < 0.001 compared to control; #p-value < 0.05 compared to model.

Mentions: Forced swimming for 90 min resulted in a significant increase in lipid peroxidation; as measured by the formation of TBARS (Figure 2 and Table 1). There is a highly significant increase of tissue MDA level (P < 0.001) in model group (205.68 nmol/mg protein) which undergo forced swimming compare to normal control group (138.84 nmol/mg protein). The current results also demonstrated that SPP inhibited lipid peroxidation at both high and low concentration 171.38 nmol/mg protein and 179.89 nmol/mg protein, respectively (Figure 2 and Table 1) SPP at 200 mg/kg significantly reduce TBARAS level (P < 0.05) but SPP at 400 mg/kg was not statistically significant. Positive control group (CoQ10 200 mg/kg) has also significantly inhibited lipid peroxidation (168.07 nmol/mg protein) compared to model group (P < 0.05).


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
(A) Effect of SPP on mice skeletal muscle MDA level. (B) Effect of SPPE on mice skeletal muscle mitochondrial SOD level each bar represent Mean ± SEM (n=10). Significant at ***p-value < 0.001 compared to control; #p-value < 0.05 compared to model.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: (A) Effect of SPP on mice skeletal muscle MDA level. (B) Effect of SPPE on mice skeletal muscle mitochondrial SOD level each bar represent Mean ± SEM (n=10). Significant at ***p-value < 0.001 compared to control; #p-value < 0.05 compared to model.
Mentions: Forced swimming for 90 min resulted in a significant increase in lipid peroxidation; as measured by the formation of TBARS (Figure 2 and Table 1). There is a highly significant increase of tissue MDA level (P < 0.001) in model group (205.68 nmol/mg protein) which undergo forced swimming compare to normal control group (138.84 nmol/mg protein). The current results also demonstrated that SPP inhibited lipid peroxidation at both high and low concentration 171.38 nmol/mg protein and 179.89 nmol/mg protein, respectively (Figure 2 and Table 1) SPP at 200 mg/kg significantly reduce TBARAS level (P < 0.05) but SPP at 400 mg/kg was not statistically significant. Positive control group (CoQ10 200 mg/kg) has also significantly inhibited lipid peroxidation (168.07 nmol/mg protein) compared to model group (P < 0.05).

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&rsquo;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-&alpha;) elevation. Whereas SPP protected fatigue induced mitochondrial dysfunction through preventing ROS and TNF-&alpha; 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