Neuroprotective Effect of Cardamom Oil Against Aluminum Induced Neurotoxicity in Rats

Abstract

Acetylcholinesterase (AChE) is an enzyme involved in the progression of Alzheimer's disease (AD). Cardamom oil (CO) has been reported to have acetylcholinesterase inhibitory, antioxidant and anti-anxiety effects. Hence, we studied the effect of cardamom oil in aluminum chloride induced neurotoxicity in rats. AD like symptoms were induced in Wistar rats with aluminum chloride (100 mg/kg, p.o .). Cardamom oil was administered concomitantly by oral route at doses of 100 and 200 mg/kg for 42 days. Behavioral parameters like Morris water maze, elevated plus maze, passive avoidance test and locomotor activity were evaluated on day 21 and 42. AChE activity, oxidative stress parameters, histopathological studies and immunohistochemistry studies were carried out in hippocampus and cortex. Cardamom oil treatment showed significant improvement in behavioral parameters, inhibition of AChE activity ( p < 0.001) and reduction in oxidative stress in the brain. Histopathological studies of hippocampus and cortex by hematoxylin & eosin (H. & E.) and congo red stain showed inhibition of neuronal damage and amyloid β plaque formation with cardamom oil treatment. Immunohistochemistry showed, CO treatment inhibited amyloid β expression and upregulated brain-derived neurotrophic factor (BDNF). The present study showed that, cardamom oil has neuroprotective effect in aluminum chloride induced neurotoxicity linked with inhibition of AChE activity and reduction in oxidative damage. This effect of cardamom oil may be useful in management of Alzheimer's disease.

Biotin, coenzyme Q10, and their combination ameliorate aluminium chloride‐induced Alzheimer's disease via attenuating neuroinflammation and improving brain insulin signaling

“…Accumulation of Aβ is the primary clinical and pathological hallmark of AD and a potential pharmacological target of AD. [4] In consistent with this fact, our results displayed a highly significant increase in the protein levels of Aβ in AlCl 3 -intoxicated rats, a result which is consistent with those of Auti and Kulkarni, [47] Justin Thenmozhi et al, [48] Mustafa, [52] and Khalifa et al [64] Oxidative stress has important implication in the aggregation of Aβ; [3] therefore, via their antioxidant properties, the protein levels of Aβ were significantly alleviated by oral supplementation of CoQ10, biotin, and their combination concomitantly with AlCl 3 . Our results confirm the protective role of CoQ10 against deleterious effects induced by Aβ in AD.…”

“…[63] In the present study, oxidative stress was indicated by the elevated levels of MDA along with depletion in the levels of the antioxidants; GSH and SOD. These results are in agreement with Auti and Kulkarni, [47] Justin Thenmozhi et al, [48] Ahmad Rather et al, [51] and Khalifa et al [64] Elevated MDA is an index of oxidation of polyunsaturated fatty acid in cell membrane leading to membrane rupture, cell damage, and neurodegeneration. Aluminium may cause such effect by stimulating Fenton reaction [65] and, so, enhancing the iron-evoked oxidative damage in brain.…”

“…Aluminium is a well-known neurotoxicant that can induce neurodegeneration and AD-like symptoms. [47,48] Aluminium exerts such effects via different mechanisms including oxidative stress, [47][48][49] enhanced deposition of Aβ, [47,50] neuroinflammation, [41] and apoptosis. [39,48,51] It is documented that the Aβ-induced neuroinflammation disturbs insulin signaling in brain leading to the loss of its critical role in memory and neuronal survival.…”

“…The result is consistent with previous works on AlCl 3 -induced AD. [47,48,51,[52][53][54] Earlier studies reported that the accumulation of Aβ (as revealed in Figure 6A) has a great contribution to cognitive impairment in both human and animal AD. [55][56][57] In addition, evidence supports the beneficial impact of insulin signaling on memory and learning; [10][11][12] biotin.…”

Histomorphological evaluations on the frontal cortex extrapyramidal cell layer following administration of N-Acetyl cysteine in aluminum induced neurodegeneration rat model

“…In furtherance to our rationale to use 200 mg/kg, Hanaa et al (2015) and Chiroma et al (2018) reported it to be the best dose to model AD in animal study, as it shows the crucial pathogenesis of AD. Mode of administration was according to Auti and Kulkarni (2019) whereby, 200 mg/kg of Aluminum chloride (AlCl 3 ) was given an hour before 1000 mg/kg of N-Acetyl Cysteine (NAC) for 21 days (three weeks). AlCl 3 was dissolved in distilled water at dose of 200 mg/kg bw and given orally.…”