炎症体
氧化应激
神经炎症
阿切
乙酰胆碱酯酶
医学
药理学
椰子油
化学
内科学
内分泌学
生物化学
炎症
酶
作者
Baban S. Thawkar,Ginpreet Kaur
标识
DOI:10.1016/j.jtcme.2023.11.001
摘要
Activating NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) is crucial in the pathogenesis of Alzheimer's disease (AD). A multimodal treatment intervention is the most feasible way to alter the course of AD progression. Hence, the current study was conducted to study the combination of betanin (BET) and virgin coconut oil (VCO) on NLRP3 regulation in aluminum chloride-induced AD in Wistar rats. BET (100,200 mg/kg) and VCO (1, 5 g/kg) alone and in combination (BET 100 mg/kg + VCO 1 g/kg and BET 200 mg/kg + VCO 5 g/kg) were given orally for 42 days. On day 21 and 42nd, the behavioral test was performed to check the animal's cognition. Acetylcholinesterase (AChE) activity, oxidative stress markers, estimation of NLRP3 and IL-1β, and histological examinations were conducted in the hippocampus (H) and cortex (C). Treatment with BET and VCO alone or combined improved behavioral characteristics (MWM and PA p < 0.0001; EPM p = 0.5184), inhibited AChE activity (C, p = 0.0101; H, p < 0.0001), and lowered oxidative stress in the brain. Also, combination treatment restored the levels of NLRP3 (C, p = 0.0062; H, p < 0.0001) and IL1β (C, p = 0.0005; H, p = 0.0098). The combination treatment significantly reduced the degree of neuronal degeneration, amyloid deposition, and necrosis in the brain tissue. The current study revealed that the combination strategy effectively controlled neuroinflammation via modulation of the NLRP3 inflammasome pathway, paving the way for the new treatment.
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