Cassia tora Mitigates Aluminium Chloride Induced Alterations in Pro-inflammatory Cytokines, Neurotransmitters, and Beta-amyloid and Tau Protein Markers in Wistar Rats

Background and Aim: Exposure to Aluminium (Al) has been reported to cause neurotoxicity in laboratory animals. Amyloid-β (Aβ) plaque formation, tau protein hyperphosphorylation, and neuroinflammation have been indicated as the possible mechanism of Al-induced neurodegeneration. The present study aimed to understand the mechanism of aluminium chloride (AlCl3)-induced neurotoxicity in Wistar rats and to assess the neuroprotective effect of methanolic extract of Cassia tora leaves (MECT). Material and Methods: Seventy-two male Wistar rats were randomly divided into nine groups. AlCl3 (100 mg/kg bw) and MECT (300 mg/kg bw) were given orally by gavage and memantine (MEM) was administered intraperitoneally (20 mg/kg bw) to rats, daily for 60 days. The spatial learning memory and recognition memory were evaluated using the Morris Water Maze (MWM) test. The levels of oxidative stress, neurotransmitter markers, pro-inflammatory markers, Aβ proteins plaques formation and tau protein hyperphosphorylation were evaluated. Histopathology of brain tissue was performed to assess the extent of tissue damage on AlCl3 exposure. Results: MECT significantly improved cognitive behaviours in AlCl3-exposed rats during the MWM test. Treatment with MECT resulted in a significant recovery of antioxidant enzyme function, the activity of neurotransmitter markers and pro-inflammatory cytokine levels. MECT prevented the aggregation of Aβ proteins and tau protein phosphorylation. Also, it inhibited the loss of neuronal integrity in the cortex and hippocampus regions of the brain in AlCl3-exposed rats. Conclusion: The findings demonstrate that a methanolic extract of Cassia tora leaves ameliorated AlCl3-induced neurodegeneration in Wistar rats.