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. 2022 Sep;22(9):858-865.
doi: 10.1007/s12012-022-09761-7. Epub 2022 Jul 28.

Maternal Ethanol Exposure-Induced Cardiac Fibrosis is Associated with Changes in TGF-β and SIRT1/FOXO3a Signaling in Male Rat Offspring: A Three-Month Follow-up Study

Alireza Shirpoor  1   2 , Roya Naderi  3   4
Affiliations

Maternal Ethanol Exposure-Induced Cardiac Fibrosis is Associated with Changes in TGF-β and SIRT1/FOXO3a Signaling in Male Rat Offspring: A Three-Month Follow-up Study

Alireza Shirpoor et al. Cardiovasc Toxicol. 2022 Sep.

Abstract

Ethanol exposure during pregnancy induces cardiac fibrosis in the fetal heart. However, the mechanisms by which consumption of ethanol induces fibrotic changes are not known. Pregnant rats were received ethanol 4.5 g/kg BW once per day from the 7th day of pregnancy (GD7) throughout lactation. Our findings demonstrated that, area of fibrosis increased in cardiac tissue in the pups on both postnatal day twenty one (PN21) and postnatal day ninety (PN90) after prenatal and early postnatal period ethanol treatment compared with the controls. It was accompanied by a decline in the expression of SIRT1 protein along with the elevation of FOXO3a and TGF-β protein expressions which were determined by western blot. Overall, our data reveal that prenatal alcohol usage increase in fibrotic regions in the pup hearts possibly by regulating TGF-β, FOXO3a and SIRT1 protein levels. These are potential therapeutic molecular targets that can be modulated to protect heart against maternal ethanol exposure.

Keywords: Ethanol; FOXO3a; Heart; Offspring; SIRT1; TGF-β.

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References

    1. Jones, K. L., & Smith, D. W. (1973). Recognition of the fetal alcohol syndrome in early infancy. Lancet (London, England), 302(7836), 999–1001. - DOI
    1. Henderson, G. I., Devi, B. G., Perez, A., & Schenker, S. (1995). In utero ethanol exposure elicits oxidative stress in the rat fetus. Alcoholism, Clinical and Experimental Research, 19(3), 714–720. - PubMed - DOI
    1. Daft, P. A., Johnston, M. C., & Sulik, K. K. (1986). Abnormal heart and great vessel development following acute ethanol exposure in mice. Teratology, 33(1), 93–104. - PubMed - DOI
    1. Shirpoor, A., Gaderi, R., & Naderi, R. (2019). Ethanol exposure in prenatal and early postnatal induced cardiac injury in rats: Involvement of oxidative stress, Hsp70, ERK 1/2, JNK, and apoptosis in a 3-month follow-up study. Cell Stress & Chaperones, 24(5), 917–926. - DOI
    1. Patel, V. B., Why, H. J., Richardson, P. J., & Preedy, V. R. (1997). The effects of alcohol on the heart. Adverse Drug Reactions and Toxicological Reviews, 16(1), 15–43. - PubMed

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