Neuroprotective effects of crude extracts, compounds, and isolated molecules obtained from plants in the central nervous system injuries: a systematic review.

The number of people with central nervous system (CNS) injuries increases worldwide and only a few therapies are used to mitigate neurological damage. Crude extracts, compounds, and isolated molecules obtained from plants have neuroprotective effects; however, their actions on the central nervous system are still not fully understood. This systematic review investigated the neuroprotective effects of crude extracts, compound, and isolated molecules obtained from plants in different CNS lesions. This PICO (Population/Problem, Intervention, Control, Outcome) systematic review included in vivo and in vitro studies that used small rodents as experimental models of CNS injuries (P) treated with crude extracts, compounds, and/or isolated molecules obtained from plants (I), compared to non-intervention conditions (C), and that showed a neuroprotective effect (O). Fourteen out of 5,521 studies were selected for qualitative analysis. Several neuroprotective effects (improvement of antioxidant activity, modulation of the inflammatory response, tissue preservation, motor and cognitive recovery) in the brain and spinal cord were reported after treatment with different doses of crude extracts (10 studies), compounds (2 studies), and isolated molecules (2 studies). Crude extracts, compounds, or isolated molecules obtained from plants showed promising neuroprotective effects against several CNS injuries in both the brain and spinal cord, regardless of gender and age, through the modulation of inflammatory activity and oxidative biochemistry, tissue preservation, and recovery of motor and cognitive activity.

Putative Activation of the CB1 Cannabinoid Receptors Prevents Anxiety-Like Behavior, Oxidative Stress, and GABA Decrease in the Brain of Zebrafish Submitted to Acute Restraint Stress.

Anxiety disorder is a well-recognized condition observed in subjects submitted to acute stress. Although the brain mechanisms underlying this disorder remain unclear, the available evidence indicates that oxidative stress and GABAergic dysfunction mediate the generation of stress-induced anxiety. Cannabinoids are known to be efficient modulators of behavior, given that the activation of the cannabinoid receptors type-1 (CB1 receptors) induces anxiolytic-like effects in animal models. In the present study, we aimed to describe the effects of the stimulation of the CB1 receptors on anxiety-like behavior, oxidative stress, and the GABA content of the brains of zebrafish submitted to acute restraint stress (ARS). The animals submitted to the ARS protocol presented evident anxiety-like behavior with increased lipid peroxidation in the brain tissue. The evaluation of the levels of GABA in the zebrafish telencephalon presented decreased levels of GABA in the ARS group in comparison with the control. Treatment with ACEA, a specific CB1 receptor agonist, prevented ARS-induced anxiety-like behavior and oxidative stress in the zebrafish brain. ACEA treatment also prevented a decrease in GABA in the telencephalon of the animals submitted to the ARS protocol. Overall, these preclinical data strongly suggest that the CB1 receptors represent a potential target for the development of the treatment of anxiety disorders elicited by acute stress.