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Cell Biochem Funct ; 41(8): 1403-1411, 2023 Dec.
Article in English | MEDLINE | ID: mdl-37987234

ABSTRACT

Inflammation is a reaction of the immune system to infection and injury; in fact, it positioned at the center of metabolic disorders, particularly obesity, type 2 diabetes, and cardiovascular diseases. Thus play a major role not only in their development, but also exerts as a crucial linking factor among those diseases. In this regard, one of the strategies for tackling this problem is application of antioxidants to treat such diseases. The present study was performed to evaluate the synergistic effects of punicic acid (PUA) and alpha-lipoic acid (ALA) as antioxidants and radical scavenging reagents on the expression of some inflammatory and metabolism-related genes under oxidative stress in the muscle cells. The experimental treatments consisted of a range of 20, 40, 80, 160, and 320 µM of PUA, and 5, 25, 50, 100, and 200 µM of ALA with a 200 µM concentration of H2 O2 as an oxidative stress inducer. Accordingly, fatty acid treatments were applied for 24 h, and H2 O2 was treated for 1 h. Our results indicated that the simultaneous treatment of PUA and ALA at optimal concentrations (80 and 50 µM, respectively) decreased the expression of inflammation genes and increased the expression of regulatory genes (Pparγ, Pgc-1α) related to metabolism (p < .05). Unexpectedly, H2 O2 treatment increased the Fndc5 expression (p < .05). Maximal upregulation of Pparγ, Pgc-1α were obtained when fatty acids combination (PUA and ALA) were used in the culture of H2 O2 treated cells (p < .05). Therefore, our findings suggest that the simultaneous use of PUA and ALA fatty acids could reduce oxidative stress, and the expression of inflammatory genes, thereby improving the cell metabolism.


Subject(s)
Diabetes Mellitus, Type 2 , Thioctic Acid , Humans , Thioctic Acid/pharmacology , Thioctic Acid/metabolism , PPAR gamma/genetics , PPAR gamma/metabolism , Antioxidants/pharmacology , Oxidative Stress , Linolenic Acids/pharmacology , Inflammation/drug therapy , Myoblasts/metabolism
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