Plant extracts can be therapeutic alternatives for depression and anxiety. However, some plant-derived preparations can also be toxic. Moringa oleifera leaves are used in human nutrition due to their high nutritional value and antioxidant activity. This study investigated a saline extract from M. oleifera leaves (MoLE) for secondary metabolites, proteins, cytotoxicity, hemolytic activity, in vivo acute oral toxicity, and neurobehavioral effects. MoLE contains flavonoids (rutin and vitexin), lectin, and a trypsin inhibitor. It is neither cytotoxic nor hemolytic for human cells and did not present acute oral toxicity (2000 mg/kg) to mice. The elevated plus maze test showed that MoLE (500, 1000, and 2000 mg/kg, p.o.) significantly increased the number of entries as well as the time spent by mice in open arms, while it decreased the number of entries and the time spent in closed arms when compared to the control. MoLE (500, 1000, and 2000 mg/kg, p.o.) reduced immobility time of mice in the tail suspension and forced swimming tests, compared to the control. The anxiolytic-like effect of MoLE is possibly mediated by a GABA mimetic action once it is prevented by pre-treatment with flumazenil. The present study demonstrated that MoLE has antidepressant and anxiolytic effects in mice and is a promising herbal medicine.

Moringa oleifera Lam. (horseradish tree) leaves demonstrate high nutritional value, are rich in proteins, and are widely used in folk medicine and food. This study investigated the presence of secondary metabolites and antinutritional proteins in leaf extract (LE) and the protein-rich fraction (PRF) derived from M. oleifera leaves, as well as the cytotoxicity to human cells, hemolytic activity, and in vivo acute toxicity and genotoxicity in mice. The flavonoids rutin and vitexin as well as trypsin inhibitors and lectins were detected in LE and PRF. Neither sample demonstrated toxicity against human peripheral blood mononuclear cells and both showed low hemolytic action. In vivo, LE and PRF did not show antinutritional effects and caused no death. The hematological parameters of the animals in the treated group were similar to those of the control. A significant increase in the serum levels of alanine aminotransferase and a discrete leukocyte infiltration with cytoplasmic vacuolization of the hepatocytes in the liver were detected in LE-treated animals. The preparations were not genotoxic or mutagenic. This study shows that LE and PRF are not antinutritional agents and presented low acute toxicity and no genotoxicity or mutagenicity. The present study contributes to the determination of the safety of using M. oleifera leaf proteins.

Euphorbia hirta L. is traditionally used to treat tumors and has demonstrated anticancer effects. This study evaluated the phytochemical composition, toxicity, and antitumor activity of saline extract (SE) from E. hirta leaves in mice. Phytochemical analysis included thin layer chromatography, high-performance liquid chromatography, and quantification of phenols, flavonoids, and proteins. Acute toxicity (2000 mg/kg) assessed mortality, hematological, biochemical, histological parameters, water/feed intake, and body weight. Genotoxicity was evaluated via comet and micronucleus assays. Antitumor activity was tested in vitro and in vivo on sarcoma 180. SE contained 107.3 mg GAE/g phenolics and 22.9 mg QE/g flavonoids; the presence of gallic and ellagic acids was detected. Protein concentration was 12.16 mg/mL with lectin activity present. No mortality, organ damage, or genotoxic effects occurred in toxicity tests. SE demonstrated in vitro cytotoxicity against sarcoma cells (IC₅₀: 10 µg/mL). In vivo, SE (50–200 mg/kg) reduced tumor weight by 70.2–72.3%. SE modulated IL-2, IL-4, IL-6, IL-17, IFN-γ, and TNF-α in tumor environment. Tumors showed inflammatory infiltrate, necrosis, and fibrosis after treatment. These findings position the extract as a promising candidate for further development as a safe, plant-based antitumor agent.

The authors would like to make the following correction to their published paper