article · Frontiers in Pharmacology
Aluminium accumulation in the brain contributes to neurodegenerative conditions such as Alzheimer's disease, creating an urgent need for protective interventions. This research investigates the combined use of sesamol, a compound derived from sesame, and the probiotic bacterium Lactobacillus rhamnosus to protect against aluminium chloride-induced brain and liver damage in rats. Testing revealed that this dual treatment significantly lowered levels of brain amyloid-beta, phosphorylated tau, and inflammatory markers, whilst increasing protective Wnt3a and beta-catenin levels. In liver tissue, the combined treatment reduced inflammatory, fibrotic, and apoptotic indicators while enhancing beneficial receptor expression. Behavioural and tissue examinations confirmed that administering Lactobacillus rhamnosus alongside sesamol effectively mitigated aluminium-induced neurotoxicity and hepatotoxicity. The findings demonstrate that adding probiotics to sesamol presents an effective strategy against tissue damage caused by aluminium toxicity.
Aluminium exposure is linked to serious neurodegenerative diseases and systemic organ damage. Finding accessible, low-toxicity interventions is critical for safeguarding brain and liver health. Demonstrating that a combined regimen of sesamol and a common probiotic bacterium counters toxic damage in animal models provides valuable evidence for multi-target nutritional or therapeutic approaches aimed at mitigating metal-induced health risks.
This early-stage preclinical research suggests potential applications in developing dietary supplements, functional foods, or adjunctive therapeutics targeting metal-induced neurotoxicity and liver injury. Potential commercial users include nutraceutical companies and pharmaceutical developers researching neurodegenerative disease interventions. Because the findings are currently limited to an animal model in rats, significant further preclinical testing and human clinical trials are required before practical deployment can occur.
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Introduction: Aluminium (Al) is accumulated in the brain causing neurotoxicity and neurodegenerative disease like Alzheimer's disease (AD), multiple sclerosis, autism and epilepsy. Hence, attenuation of Al-induced neurotoxicity has become a “hot topic“ in looking for an intervention that slow down the progression of neurodegenerative diseases. Objective: Our study aims to introduce a new strategy for hampering aluminum chloride (AlCl3)-induced neurotoxicity using a combination of sesamol with the probiotic bacteria; Lactobacillus rhamnosus (L. rhamnosus) and also to test their possible ameliorative effects on AlCl 3 -induced hepatotoxicity. Methods: Sprague-Dawley male rats were randomly divided into five groups (n = 10/group) which are control, AlCl 3 , AlCl 3 + Sesamol, AlCl 3 + L. rhamnosus and AlCl 3 + Sesamol + L. rhamnosus . We surveilled the behavioral, biochemical, and histopathological alterations centrally in the brain and peripherally in liver. Results: This work revealed that the combined therapy of sesamol and L. rhamnosus produced marked reduction in brain amyloid-β, p-tau, GSK-3β, inflammatory and apoptotic biomarkers, along with marked elevation in brain free β-catenin and Wnt3a, compared to AlCl 3 -intoxicated rats. Also, the combined therapy exerted pronounced reduction in hepatic expressions of JAK-2/STAT-3, inflammatory (TNF-α, IL-6, NF-κB), fibrotic (MMP-2, TIMP-1, α-SMA) and apoptotic markers, (caspase-3), together with marked elevation in hepatic PPAR-γ expression, compared to AlCl 3 -intoxicated rats. Behavioral and histopathological assessments substantiated the efficiency of this combined regimen in halting the effect of neurotoxicity. Discussion: Probiotics can be used as an add-on therapy with sesamol ameliorate AlCl 3 -mediated neurotoxicity and hepatotoxicity.
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DOI: 10.3389/fphar.2023.1208252
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