Prenatal methamphetamine hydrochloride exposure downregulates miRNA-151-3p and CACNA1C in testis rats' offspring.

Autor:	Bakhshaei R; Men's Health and Reproductive Health Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran. rominabakhshaeiaz48@gmail.com., Zare N; Department of Anatomical Sciences and Cognitive Neuroscience, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. nura.1389@yahoo.com., Baghi Zadeh Z; Department of Medical Science, Islamic Azad University Sari Branch, Iran. zahrabghzd@gmail.com., Ghorbani Yekta B; Department of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Bahareh59gh@yahoo.com.
Jazyk:	angličtina
Zdroj:	Cellular and molecular biology (Noisy-le-Grand, France) [Cell Mol Biol (Noisy-le-grand)] 2024 Jul 28; Vol. 70 (7), pp. 212-217. Date of Electronic Publication: 2024 Jul 28.
DOI:	10.14715/cmb/2024.70.7.31
Abstrakt:	Due to the widespread use of methamphetamine (METH) among reproductive-aged women, the effects of intrauterine exposure to METH need to be investigated, as previous studies on this topic have been limited. The goal of this study is to examine the influence of two regulatory genes (miRNA-151-3p and CACNA1C) on the intrauterine life of mice exposed to METH. Pregnant mice received doses of 2 and 5 mg/kg of METH and saline from day 10 of pregnancy until the end. Their offspring were then evaluated for miRNA-151-3p and CACNA1C gene expression levels using real-time PCR. The findings indicated that exposure to METH reduced the expression levels of both miRNA-151-3p and CACNA1C genes in offspring compared to the control group (p≤0.001). In conclusion, intrauterine exposure to METH leads to a decrease in expression levels of both miRNA-151-3p and CACNA1C genes, potentially disrupting regulatory pathways involving these genes and having an impact on male reproductive health.
Databáze:	MEDLINE
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