Expression of bax and bcl2 Genes in MDMA-induced Hepatotoxicity on Rat Liver Using Quantitative Real-Time PCR Method through Triggering Programmed Cell Death.
Mitra Behroozaghdam, Mehrdad Hashemi, Gholamreza Javadi, Reza Mahdian, Mansoureh Soleimani
Iranian Red Crescent medical journal November 26, 2015 DOI: 10.5812/ircmj.24609 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Controlled experimental animal study Peer reviewed |
|---|---|
| Sample size | 20 |
| Population | Adult male Wistar rats weighing 250-300 grams |
| Interventions | MDMA Pentoxifylline |
| Dose | MDMA 7.5 mg/kg, three doses with two hours between doses |
| Measures | Real-Time quantitative PCR (bax and bcl2 gene expression) |
| Topics | MDMA |
| Keywords | Anti-apoptotic gene Pentoxifylline Pro-apoptotic gene Qreal-time pcr |
| Key findings | MDMA altered liver expression of apoptosis-related genes, increasing bcl2 93.80-fold and bax 2.13-fold, which the authors interpret as MDMA prompting hepatic apoptosis. Pentoxifylline given after MDMA produced the highest bcl2 (340.45-fold) and lowest bax (1.55-fold), while pentoxifylline before MDMA gave bcl2 47.13-fold and bax 10.44-fold; the authors conclude pentoxifylline protected against MDMA-induced hepatotoxicity in both schedules. |
Abstract
Background: 3-4methylenedioxymethamphetamine (MDMA) is a synthetic and psychoactive drug, which is known popularly as Ecstasy and has toxic effects on human organs.
Objectives: Considering the potential toxic interaction, this study was performed to quantify the expression of bax and bcl2 genes in MDMA-induced hepatotoxicity on rat liver. Subsequently, we evaluated pentoxifylline as a possible protective drug on hepatotoxicity.
Materials and Methods: Adult male Wistar rats weighting 250 - 300 grams were used in the study. The rats were equally distributed into four experimental groups (5 rat/group). MDMA was dissolved in PBS and injected intraperitoneally (IP) including untreated control, MDMA (MDMA dissolved in PBS), treated-1 (MDMA followed by PTX) and treated-2 (PTX followed by MDMA). All animals given MDMA received 3 doses of 7.5mg/kg with two hours gap between doses. Liver tissue was removed after anaesthetizing. Subsequently, RNA isolation, cDNA synthesis and Real-Time PCR were performed. Finally, data analyzed statistically to determine significantly differences between the groups (P value < 0.05).
Results: Using Real-Time quantitative PCR results, the gene expression ratio of bcl2 were calculated 93.80±20.64, 340.45 ± 36.60 and 47.13 ± 5.84 fold in MDMA, treated-1 and treated-2 groups, respectively. Furthermore, this ratio for bax gene obtained 2.13±0.33 fold in MDMA, 1.55 ± 0.26 fold in treated-1 and 10.44 ± 1.56 fold in treated-2 groups.
Conclusions: The present study focused on molecular mechanism of MDMA in programmed cell death using gene expression quantification of a pro-apoptotic and anti-apoptoic gene in MDMA-induced hepatotoxocity. The results showed that MDMA prompted apoptosis in liver and pentoxifylline protected against hepatotoxicity before and after taking MDMA.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
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