Background: Aflatoxin B1 (AFB1) is potent hepatotoxic and hepatocarcinogenic agent. In aflatoxicosis, oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage. The aim of this work was to evaluate the hepatoprotective effect of cactus cladode extract (CCE) on aflatoxin B1-induced liver damage in mice by measuring malondialdehyde (MDA) level, the protein carbonyls generation and the heat shock proteins Hsp 70 and Hsp 27 expressions in liver. We also looked for an eventual protective effect against AFB1-induced genotoxicity as determined by chromosome aberrations test, SOS Chromotest and DNA fragmentation assay. We further evaluated the modulation of p53, bax and bcl2 protein expressions in liver. Methods: Adult, healthy balbC (20-25 g) male mice were pre-treated by intraperitonial administration of CCE (50 mg/Kg.b.w) for 2 weeks. Control animals were treated 3 days a week for 4 weeks by intraperitonial administration of 250 μg/Kg.b.w AFB1. Animals treated by AFB1 and CCE were divided into two groups: the first group was administrated CCE 2 hours before each treatment with AFB1 3 days a week for 4 weeks. The second group was administrated without pre-treatment with CCE but this extract was administrated 24 hours after each treatment with AFB1 3 days a week for 4 weeks. Results: Our results clearly showed that AFB1 induced significant alterations in oxidative stress markers. In addition, it has a genotoxic potential and it increased the expression of pro apoptotic proteins p53 and bax and decreased the expression of bcl2. The treatment of CCE before or after treatment with AFB1, showed (i) a total reduction of AFB1 induced oxidative damage markers, (ii) an anti-genotoxic effect resulting in an efficient prevention of chromosomal aberrations and DNA fragmentation compared to the group treated with AFB1 alone (iii) restriction of the effect of AFB1 by differential modulation of the expression of p53 which decreased as well as its associated genes such as bax and bcl2. Conclusion: We concluded that CCE might have a hepatoprotective effect against aflatoxicosis in mice, probably acting by promoting the antioxidant defence systems.

The consumption of a high‐fat diet is linked to the development of obesity and considered a risk factor for cardiovascular diseases. The aim of this study was to evaluate the effect of the methanolic extract of Moringa oleifera leaves (MEML) on the high‐fat diet‐ (HFD‐) induced obesity and cardiac damage in rats. MEML, at a dose of 200 mg/kg/bw and 400 mg/kg/bw, was orally administrated to obese rats for 12 weeks. M. oleifera leaves were proved to be rich in nutrients and minerals. Diversity of phenolic compounds in MEML was evidenced via LC‐ESI‐MS analysis. The chronic administration of HFD in rats led to an increase in the body weight gain, total cholesterol, and triglycerides and reduction in the HDL‐C levels. The obtained results indicated a significant increase (p < 0.05) in the cardiac marker enzyme level in obese rats. A significant decrease (p < 0.05) in the levels of cardiac catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) activities was accompanied with an increase of malondialdehyde (MDA) level in the high‐fat diet group when compared to those of the control. The treatment with the MEML alleviated abnormalities in the serum biochemical parameters, balanced the antioxidant status, and reestablished the normal histological structure of the heart especially in the case of the higher concentration. Moringa oleifera leaves may be a promising candidate in the management of obesity and its related complications such as heart problems.