Neuro-amelioration of Ficus lyrata (fiddle-leaf fig) extract conjugated with selenium nanoparticles against aluminium toxicity in rat brain: relevance to neurotransmitters, oxidative, inflammatory, and apoptotic events.
Sara S ElganzouryMohamed S AbdelfattahOla A HabottaManal El-KhadragyAhmed E Abdel MoneimMohga S AbdallaPublished in: Environmental science and pollution research international (2023)
Aluminium is a non-essential metal, and its accumulation in the brain is linked with potent neurotoxic action and the development of many neurological diseases. This investigation, therefore, intended to examine the antagonistic efficacy of Ficus lyrata (fiddle-leaf fig) extract (FLE) conjugated with selenium nanoparticles (FLE-SeNPs) against aluminium chloride (AlCl 3 )-induced hippocampal injury in rats. Rats were allocated to five groups: control, FLE, AlCl 3 (100 mg/kg), AlCl 3 + FLE (100 mg/kg), and AlCl 3 + FLE-SeNPs (0.5 mg/kg). All agents were administered orally every day for 42 days. The result revealed that pre-treated rats with FLE-SeNPs showed markedly lower acetylcholinesterase and Na + /K + -ATPase activities in the hippocampus than those in AlCl 3 group. Additionally, FLE-SeNPs counteracted the oxidant stress-mediated by AlCl 3 by increasing superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione contents in rat hippocampus. Besides, the formulated nanoparticles decreased the hippocampal malondialdehyde, carbonyl protein, and nitric oxide levels of AlCl 3 -exposed animals. Furthermore, FLE-SeNPs attenuated neural tissue inflammation, as demonstrated by decreased interleukin-1 beta, interleukin-6, nuclear factor kappa B, and glial fibrillary acidic protein. Remarkable anti-apoptotic action was exerted by FLE-SeNPs by increasing B cell lymphoma 2 and decreasing caspase-3 and Bcl-2-associated-X protein in AlCl 3 -exposed rats. The abovementioned results correlated well with the hippocampal histopathological findings. Given these results, SeNPs synthesized with FLE imparted a remarkable neuroprotective action against AlCl 3 -induced neurotoxicity by reversing oxidative damage, neuronal inflammation, and apoptosis in exposed rats.
Keyphrases
- oxidative stress
- cerebral ischemia
- nuclear factor
- cell death
- anti inflammatory
- diabetic rats
- nitric oxide
- subarachnoid hemorrhage
- hydrogen peroxide
- toll like receptor
- blood brain barrier
- high glucose
- endothelial cells
- multiple sclerosis
- cell cycle arrest
- drug induced
- photodynamic therapy
- endoplasmic reticulum stress
- signaling pathway
- diffuse large b cell lymphoma
- temporal lobe epilepsy
- protein protein
- neuropathic pain
- white matter
- single cell
- heat stress