African mesquite elicits neuroprotective activity against quaternary metal mixture -induced olfactory bulb-hippocampal oxido-inflammatory stress via nrf2-hmox-1pathway.

African mesquite AM is widely used as an anti-inflammatory agent in sub-Sahara Africa especially Nigeria. Given its strong anti-inflammatory potency, this study has evaluated the neuroprotective properties of AM in the hippocampus HIP and olfactory bulb OB of rats exposed to Cd, As, Hg, and Pb. Twenty-five albino Sprague Dawley rats were randomly divided into five groups in this experiment. Group 1, the control received only water. Group 2 received heavy metal mixture HMM (PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), HgCl2 (0.40 mg/kg), and NaAsO3 (10 mg/kg), for 60 days. Groups 3, 4, and 5 were treated with HMM along with AM at doses of 500, 1000, and 1500 mg/kg, respectively. AM decreased the Cd, As, Hg, and Pb levels in OB and HIP, restored the activities of antioxidants, Hmox-1, reduced the activities of AChE, NRF2 and NFkB and improved histopathology.

Prosopis africana exerts neuroprotective activity against quaternary metal mixture-induced memory impairment mediated by oxido-inflammatory response via Nrf2 pathway.

The beneficial effects of Prosopis africana (PA) on human health have been demonstrated; however, its protective effects against heavy metals (HM) are not yet understood. This study evaluated the potential neuroprotective effects of PA in the cerebral cortex and cerebellum. To accomplish this, we divided 35 albino Sprague Dawley rats into five groups. Group I did not receive either heavy metal mixture (HMM) or PA. Group II received a HMM of PbCl2 (20 mg/kg), CdCl2 (1.61 mg/kg), HgCl2 (0.40 mg/kg), and NaAsO3 (10 mg/kg) orally for a period of two months. Groups III, IV, and V received HMM along with PA at doses of 500, 1000, and 1500 mg/kg, respectively. PA caused decreased levels of HM accumulation in the cerebral cortex and cerebellum and improved performance in the Barnes maze and rotarod tests. PA significantly reduced levels of IL-6 and TNF-α. PA increased concentrations of SOD, CAT, GSH, and Hmox-1 and decreased the activities of AChE and Nrf2. In addition, levels of MDA and NO decreased in groups III, IV, and V, along with an increase in the number of live neurons. In conclusion, PA demonstrates a complex neuroprotective effect with the potential to alleviate various aspects of HM-induced neurotoxicity.

Essential Trace Elements Prevent the Impairment in the Retention Memory, Cerebral Cortex, and Cerebellum Damage in Male Rats Exposed to Quaternary Metal Mixture by Up-regulation, of Heme Oxygynase-1 and Down-regulation of Nuclear Factor Erythroid 2-related Factor 2-NOs Signaling Pathways.

In the present study, we examined adverse effects of metals and metalloids in the Cerebral cortex (CC) and Cerebellum (CE). Group 1 comprised from the controls while other four groups of male Wistar rats were treated with following pattern: Group II (Heavy Metal Mixture HMM only: PbCl2, 20 mg·kg-1; CdCl2, 1.61 mg·kg-1; HgCl2, 0.40 mg·kg-1, and NaAsO3,10 mg·kg-1), Groups III (HMM + ZnCl2); Group IV (HMM + Na2SeO3) and Group V (HMM + ZnCl2 + Na2SeO3) for 60 days per os. HMM promoted oxidative stress in the CC and CE of treated rats compared to controls; moreover, exposure to HMM led to increased activity of the AChE and pro-inflammatory cytokines; also, HMM promoted accumulation of caspase 3 and other transcriptional factors such as Nrf2 and decreased levels of Hmox-1. Essential metals reduced increased bioaccumulation of Pb, Cd, As and Hg in CC and CE caused by HMM exposure. Also, all mentioned adverse effects were diminished by essential metals treatment (Se and Zn). HMM exposed rats had considerably less escape dormancy than controls. Histopathological analysis revealed moderate cell loss at the intermediate (Purkinje cell) and granular layer. Zinc and selenium supplementations could reverse adverse effects of heavy metals at various cellular levels in neurons.