Moringa oleifera Lam. extract rescues lead-induced oxidative stress, inflammation, and apoptosis in the rat cerebral cortex
J Food Biochem. 2021 Jan;45(1):e13579. doi: 10.1111/jfbc.13579. Epub 2020 Dec 9.
ABSTRACT
In this study, we investigate the potential protective effect of Moringa oleifera Lam. extract (MOE) against lead-induced neurotoxicity. Wistar rats were allocated equally into (a) a control group, (b) a lead acetate (PbAc) group intraperitoneally injected with 20 mg/kg PbAc, (c) a MOE group orally gavaged with MOE (250 mg/kg), and (d) a MOE + PbAc group orally gavaged with MOE 3 hr before receiving intraperitoneal injections of PbAc. All rats were treated for 14 days. Our results revealed that PbAc-induced brain injury, accompanied by increased levels of oxidative stress markers. Moreover, Pb enhanced the inflammatory response and triggered neuronal apoptosis, as well as significantly depleted glutathione content and inhibited antioxidant enzyme activity. Interestingly, concurrent treatment with MOE ameliorated oxidative stress, inflammation, and apoptosis in the brain cortex. The current study provides evidence that MOE has the potential to protect neuronal tissues in PbAc-exposed rats via attenuation of nuclear factor-kappa B (NF-κB) signaling. PRACTICAL APPLICATIONS: This study reports the potential neuroprotective effect of Moringa oleifera Lam. (MOE) against lead-induced cortical brain toxicity. Our data reveal that PbAc-induced oxidative stress, neuroinflammation, and apoptosis in cortical tissues. However, simultaneous treatment of rats with MOE abrogated cortical brain inflammatory biomarkers, mitigated cortical tissue damage, and restrained oxidative stress, programmed cell death, and nuclear factor-kappa B (NF-κB) translocation. In addition, MOE stimulated detoxifying enzymes in PbAc-treated rats. These findings provide evidence that simultaneous treatment with MOE has the potential to attenuate PbAc-induced brain damage in rats by restraining oxidative stress, neuroinflammation, and apoptosis via attenuation of NF-κB signaling.
PMID:33300136 | DOI:10.1111/jfbc.13579