Toxicity effects of Nerium oleander, basic and clinical evidence: A comprehensive review.

INTRODUCTION: Nerium oleander is a plant that is frequently grown in gardens and public areas. N. oleander is distributed originally in subtropical Asia but is now growing in many parts of the world, such as the United States, Australia, China, and Middle East countries. Pharmacological effects of plant including antinociceptive, anti-inflammatory, and anticancer activity were reported, but the potential toxic effects of all parts of the shrub either fresh or dried on animal and human body were documented. METHOD: The data of this review article were obtained from Medline/Pubmed, Scopusand Google Scholar databases in English until September 2019. To include all publications in this field, keywords such as N. oleander and toxicity were used. RESULTS: The poisoning effects of plant or their active alkaloids induced infiltration of cells with hemorrhage and sever negative changes in the lung, induce lesions, and infiltration of inflammatory cells into the portal spaces with scattered necrosis of hepatocytes in the liver, cardiac toxicity of the plant in the heart were included, induced varying degrees of hemorrhage, myocardial degeneration, and necrosis. It also induced arrhythmia, sinus bradycardia, and prolonged P-R interval in electrocardiographic records. CONCLUSIONS: The toxic effects of N. oleander are mostly related to its inhibitory effects on the Na+-K+ ATPase pump in the cellular membrane. However, the exact molecular mechanism involved in the toxicity of N. oleander is not clear.

Corticotropin-releasing factor as well as opioid and dopamine are involved in tail-pinch-induced food intake of rats.

Several kinds of stress such as psychological stress, restraint, and foot shock inhibit feeding behavior through corticotropin-releasing factor (CRF). In contrast, a mild tail pinch increases food intake in rats. Although dopamine and opioid are thought to be involved in tail-pinch-induced food intake, it is unknown whether CRF participates in this phenomenon. Therefore, we attempted to clarify this issue using rats. A 30-s tail pinch increased food intake in 30 min after the tail pinch, and this increase was blocked by intraperitoneal injection of CRF receptor type 1 selective antagonist. CRF increased food intake in 30 min after intracerebroventricular injection at a dose of 2 or 10 ng, and this increase was also blocked by CRF receptor type 1 antagonist. Tail-pinch- or CRF-induced food intake was blocked by naloxone, pimozide, and spiperone. These results suggest that CRF, through CRF receptor type 1 as well as opioid and dopaminergic systems, are involved in the mechanism of tail-pinch-induced food intake. The results also suggest that brain CRF has dual effects on food intake, hyperphagia and anorexia, in a stress-dependent manner.