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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.


(A) Effect of SPP on mice serum TNF-α level. (B) Effect of SPP on mice serum IL-6 level. Each bar represent M±SEM (n=10). Significant at ***p-value < 0.001 compared control; ###p-value < 0.001, ##p-value < 0.01 compared to model. * indicates significance compared to control.
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Figure 3: (A) Effect of SPP on mice serum TNF-α level. (B) Effect of SPP on mice serum IL-6 level. Each bar represent M±SEM (n=10). Significant at ***p-value < 0.001 compared control; ###p-value < 0.001, ##p-value < 0.01 compared to model. * indicates significance compared to control.

Mentions: To elucidate whether forced swimming could increase serum TNF-α level, and to see the effect SPP on cytokines level serum TNF-α level was measured as shown in (Figure 3 and Table 2). Forced swimming of mice for 90 min resulted in a significant increase in serum TNF-α level of model group (91.82 ng/l) compared to normal control group (81.07 ng/l) P-value < 0.001. On the other hand, treatment of mice with SPP 200 and 400 mg/kg significantly reduced serum TNF-α level 80.42 and 84.12 ng/l, respectively. SPP at lower dose inhibited serum TNF-α level (P < 0.001) better than SPP at high dose (P < 0.01) compared to normal control group. Moreover, positive control mice taking CoQ10 200 mg/kg have also showed a significant inhibition of TNF-α (P-value < 0.001).


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 serum TNF-α level. (B) Effect of SPP on mice serum IL-6 level. Each bar represent M±SEM (n=10). Significant at ***p-value < 0.001 compared control; ###p-value < 0.001, ##p-value < 0.01 compared to model. * indicates significance compared to control.
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Related In: Results  -  Collection

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

Figure 3: (A) Effect of SPP on mice serum TNF-α level. (B) Effect of SPP on mice serum IL-6 level. Each bar represent M±SEM (n=10). Significant at ***p-value < 0.001 compared control; ###p-value < 0.001, ##p-value < 0.01 compared to model. * indicates significance compared to control.
Mentions: To elucidate whether forced swimming could increase serum TNF-α level, and to see the effect SPP on cytokines level serum TNF-α level was measured as shown in (Figure 3 and Table 2). Forced swimming of mice for 90 min resulted in a significant increase in serum TNF-α level of model group (91.82 ng/l) compared to normal control group (81.07 ng/l) P-value < 0.001. On the other hand, treatment of mice with SPP 200 and 400 mg/kg significantly reduced serum TNF-α level 80.42 and 84.12 ng/l, respectively. SPP at lower dose inhibited serum TNF-α level (P < 0.001) better than SPP at high dose (P < 0.01) compared to normal control group. Moreover, positive control mice taking CoQ10 200 mg/kg have also showed a significant inhibition of TNF-α (P-value < 0.001).

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.