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Nutritional Neuroscience 2019-May

Protective effect of Curcuma amada acetone extract against high-fat and high-sugar diet-induced obesity and memory impairment.

Rakstu tulkošanu var veikt tikai reģistrēti lietotāji
Ielogoties Reģistrēties
Saite tiek saglabāta starpliktuvē
Lakshmi Rao
Eswar Kilari
Phani Kola

Atslēgvārdi

Abstrakts

Objectives:Curcuma amada Roxb. (Mango ginger) was evaluated for anti-obesity, anti-amnesic and neuroprotection using high-fat and high-sugar diet (HFHS)-induced obesity and cognitive impairment in rats. Methods: Animals were exposed to HFHS diet to evaluate lipid parameters and subjected to Y maze test and Pole climbing test to evaluate the memory. In addition, oxidative stress parameters, acetyl cholinesterase activity (AChE), neurochemicals and histopathology were assessed in the brain. Results: HFHS diet led to increased body weight and lipid parameters (total cholesterol, low-density lipoprotein [LDL], and very low-density lipoprotein [VLDL], triglycerides [TG]) but not high-density lipoprotein (HDL). Elevated serum glutamate oxalate transaminase (SGOT) and serum glutamate pyruvate transaminase (SGPT), oxidative biomarker, decreased enzymatic and non-enzymatic antioxidants, Acetylcholinesterase (AChE) activity and reduced percentage of spontaneous alternation behaviour (% SAB in Y-maze test) as well as reduced serotonin and dopamine levels and neurodegeneration were observed in HFHS diet-fed rats. Curcuma amada (CAAE1, 100 mg/kg and CAAE2, 300 mg/kg) treatment to HFHS diet-fed rats (21 days after HFHS diet feeding alone) showed dose-dependent activity and ameliorated the HFHS diet-induced alterations in lipid parameters related to obesity, hepatological parameters, memory, oxidative stress, neurochemicals and neurodegeneration. Furthermore, 300 mg/kg of C. amada (CAAE2) augmented the memory by inhibiting acetylcholinesterase (AChE) activity; it also ameliorated the effect of antioxidants such as glutathione, superoxide dismutase (SOD), and total thiol and mitigated the effect of malondialdehyde (MDA). CAAE2 also controlled the level of dopamine and serotonin and reduced the neurodegeneration in the hippocampus CA1 region. Discussion: The results of the present study indicated that treatment with C. amada 300 mg/kg (CAAE2) attenuated the HFHS diet-induced obesity, memory loss, oxidative stress, and neurodegeneration. These study results indicated that the administration of C. amada offers a potential treatment option for obesity and memory loss, and it requires further preclinical and clinical evaluations.

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