Neuroprotective role of luteolin against lead acetate-induced cortical damage in rats

Abstract

Luteolin (LUT) is a glycosylated flavonoid compound that has multiple beneficial pharmacological and biological impacts. The current investigation was undertaken to evaluate the putative neuroprotective potency of LUT against neuronal damage induced by lead acetate (PbAc). Twenty-eight rats were placed into four equal groups. Group 1: served as the control group, group 2: rats were supplemented orally with LUT (50 mg kg−1), group 3: rats were intraperitoneally injected with PbAc (20 mg kg−1), and group 4: rats were pretreated with LUT before PbAc injection with the same doses. All animals were treated for 7 days. The exposure to PbAc increased the concentration of lead in the cortical tissue, neuronal lipid peroxidation, and nitric oxide (NO) production and decreased the antioxidant enzymes. Additionally, PbAc enhanced a neuroinflammatory response in the cortical tissue through increasing the pro-inflammatory cytokines secretion and inducible NO synthase expression. Moreover, cortical cell death was recorded following PbAc intoxication as evidenced by the enhancement of the proapoptotic and inhibiting the antiapoptotic markers. Interestingly, LUT supplementation reversed the cortical adverse reactions induced by PbAc. Taken together, these findings may suggest that LUT may be useful for attenuating neuronal damage induced by PbAc through inhibiting the oxidative damage, neuroinflammation, and the cortical cell death.

Synergistic protective effect of Beta vulgaris with meso-2,3-dimercaptosuccinic acid against lead-induced neurotoxicity in male rats

“…High levels of ROS lead to oxidation of the cellular biomolecules, especially, the biomembrane lipids causing lipid peroxidation 44 . These results are agreed with the previous studies 18,26,32,36,45 . Inflammation is considered as a beneficial process under normal condition via controlling the innate response to biological or physical triggers such as trauma, infection and other pathogens that may disrupt homeostasis and cause diseases 46 .…”

“…The brain is the most critical organ for lead toxicity 9 . Both of the PNS and the CNS are affected by lead toxicity 19 but, the mechanisms of lead neurotoxicity are complex and still not clearly understood 17,32 . However, in adults, the PNS is more affected, while in children, the CNS is more affected 33 .…”

Moringa oleifera Lam. extract rescues lead‐induced oxidative stress, inflammation, and apoptosis in the rat cerebral cortex

“…Lead has a high affinity for thiol groups or metal cofactors in enzymatic and non‐enzymatic antioxidants and molecules, the binding of which results in a decline in antioxidant enzyme activities, including SOD, CAT, GPx, and GR activities (Baty et al., 2020). Our experimental findings are in accordance with those of AL‐Megrin, Soliman, et al (2020), who reported a prominent elevation in hepatic MDA levels and a marked depletion in enzymatic and non‐enzymatic antioxidants and molecules.…”

“…Furthermore, Baty et al. (2020) revealed that activation of the caspase cascade and concurrent extracellular signal‐regulated kinase dephosphorylation is the most operative pathway directly associated with apoptotic signals triggered by PbAc in vivo. Caspase‐3 hyperactivity can induce DNA breakage, chromatin condensation, and apoptosis of neurons.…”

Neuroprotective effects of flavone luteolin in neuroinflammation and neurotrauma

“…45 Luteolin can suppress neuroinflammation through several mechanisms, including decreasing the release of cytokines/chemokines, NO, reactive oxygen species (ROS), protein kinase C (PKC), Ca ++ influx, and inhibiting Akt, and nuclear transcription factor-κB (NF-κB) in SH-SY5Y human neuroblastoma cells in vitro. 27,46,47 Additionally, luteolin can suppress the activation of NF-kB, signal transducer and activator of transcription 3 (STAT3), c-Jun N-terminal kinases (JNK), p38, and extracellular signal-regulated kinases 1/2 (ERK1/2) that are involved in the glial cell activation and inflammatory mediator release. 48 Neurotrauma is a known risk factor for neurodegenerative diseases through TBIassociated secondary injury, and luteolin administration can protect from these neurodegenerative diseases.…”