AI Article Synopsis
- Methamphetamine (MA) abuse leads to serious cardiovascular issues, making myocardial injury and oxidative stress key concerns, with the Nrf2 pathway playing a crucial role in these processes.
- In an experiment, MA was administered to mice, resulting in significant increases in markers of cardiac injury and oxidative stress, highlighting the harmful effects of MA on the heart.
- Activation of the Nrf2 pathway reduced the damage caused by MA, while knocking out Nrf2 worsened the injury, indicating that Nrf2 has a protective role against MA-induced heart damage.
Article Abstract
Objectives: Methamphetamine (MA) abuse is a serious social problem worldwide. Cardiovascular complications were the second leading cause of death among MA abusers. We aimed to clarify the effects of MA on myocardial injury, oxidative stress, and apoptosis in myocardial cells and to explore the potential mechanism of nuclear factor-erythroid factor 2-related factor 2 (Nrf2) in MA-induced oxidative stress and apoptosis.
Methods: An acute cardiac toxicity model of MA was established by intraperitoneal injection of MA (2 mg/kg) for 5 days. Nrf2 activation (by sulforaphane (SFN) 1 h before MA injection) and gene knockout were performed to explore the regulatory effects of Nrf2 on cardiac toxicity.
Results: The protein expressions of Nrf2 ( < .001) and heme oxygenase-1 (HO-1) were increased ( < .01), suggesting that MA activated the Nrf2/HO-1 pathway. In the MA group, cardiac injury score ( < .001) and cardiac troponin I (cTnI) protein expression increased ( < .01). Malondialdehyde (MDA) content increased ( < .001), superoxide dismutase (SOD) activity decreased ( < .05). Protein expressions of Caspase-3 ( < .001) and Bax ( < .001) increased, and Bcl-2 decreased ( < .001) as well. These changes were reversed by activation of Nrf2 but became more pronounced after Nrf2 knockout, suggested that the activation and knockout of Nrf2 attenuated and aggravated MA-induced myocardial injury, oxidative stress and apoptosis in myocardial cells, respectively.
Conclusions: MA administration induced myocardial injury, oxidative stress, and apoptosis in mice. Nrf2 attenuated MA-induced myocardial injury by regulating oxidative stress and apoptosis, thus playing a protective role.
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| http://dx.doi.org/10.1177/09603271231219488 | DOI Listing |
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