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Effects of N-Acetyl cysteine on gene expression of Protein kinase C-α and Ankyrin repeat domain-containing protein 1 in the cardiac tissue of rats exposed to lead
Publication year - 2021
Publication title -
iranian red crescent medical journal
Language(s) - English
Resource type - Journals
ISSN - 2074-1804
DOI - 10.32592/ircmj.2022.24.1.1584
Subject(s) - cardiotoxicity , oxidative stress , protein kinase c , malondialdehyde , chemistry , antioxidant , pharmacology , inflammation , gene expression , biochemistry , toxicity , medicine , gene , signal transduction , organic chemistry
Objective: This study aimed to evaluate the effects of N-acetylcysteine (NAC) on the oxidative damage, inflammation and expression of PKC-α and ANKRD1 genes in the cardiac tissue of rats exposed to lead (Pb).Methods: Rats were randomly divided into five groups including G1 (control), G2 (single dose of Pb), G3 (continuous dose of Pb), G4 (single dose of Pb + NAC), and G5 (continuous dose of Pb + NAC). Levels of malondialdehyde (MDA), total antioxidant capacity (TAC), IL-10 and TNF-α were measured. Expression of PKC-α and ANKRD1 genes was considered using RT-PCR.Results: Continuous exposure to Pb caused a significant decrease in serum levels of TAC and IL-10, but increased MDA and TNF-α contents (p<0.001). Continuous dose of Pb also dramatically increased the expression of PKC-α and ANKRD1 genes in the cardiac tissue by 4.27-fold and 3.07-fold, respectively (p<0.001). NAC treatments not only improved morphological changes, oxidative stress and inflammatory biomarkers, but also compensated antioxidant capacity and expression of PKC-α and ANKRD1 genes in cardiac tissue. Conclusion: Pb exposure is strongly associated with cardiotoxicity through inducing oxidative stress, inflammation, and antioxidant depletion. NAC ameliorates Pb-induced cardiotoxicity by elevating antioxidants capacity, mitigating oxidative stress and down-regulating of PKC-α and ANKRD1 genes.

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