ß-sitosterol Protects against Aluminium Chloride-mediated Neurotoxicity.

OBJECTIVE: The objective of this study is to investigate the neuroprotective effects of ß- sitosterol using the AlCl3 model of Alzheimer's Disease. METHODS: AlCl3 model was used to study cognition decline and behavioral impairments in C57BL/6 mice. Animals were randomly assigned into 4 groups with the following treatments: Group 1 received normal saline for 21 days, Group 2 received AlCl3 (10 mg/kg) for 14 days; Group 3 received AlCl3(10 mg/kg) for 14 days + ß-sitosterol (25mg/kg) for 21 days; while Group 4 was administered ß-sitosterol (25mg/kg) for 21 days. On day 22, we performed the behavioral studies using a Y maze, passive avoidance test, and novel object recognition test for all groups. Then the mice were sacrificed. The corticohippocampal region of the brain was isolated for acetylcholinesterase (AChE), acetylcholine (ACh), and GSH estimation. We conducted histopathological studies using Congo red staining to measure ß -amyloid deposition in the cortex and hippocampal region for all animal groups. RESULTS: AlCl3 successfully induced cognitive decline in mice following a 14-day induction period, as shown by significantly decreased (p < 0.001) in step-through latency, % alterations, and preference index values. These animals also exhibited a substantial decrease in ACh (p <0.001) and GSH (p < 0.001) and a rise in AChE (p < 0.001) compared to the control group. Mice administered with AlCl3 and ß-sitosterol showed significantly higher step-through latency time, % alteration time, and % preference index (p < 0.001) and higher levels of ACh, GSH, and lower levels of AChE in comparison to the AlCl3 model. AlCl3-administered animals also showed higher ß-amyloid deposition, which got significantly reduced in the ß-sitosterol treated group. CONCLUSION: AlCl3 was effectively employed to induce a cognitive deficit in mice, resulting in neurochemical changes and cognitive decline. ß -sitosterol treatment mitigated AlCl3-mediated cognitive impairment.

Pharmacological Actions and Underlying Mechanisms of Catechin: A Review.

BACKGROUND: Catechin is a phytochemical and is a major component of our daily use beverages, which has shown great potential in improving general health and fighting against several medical conditions. Clinical studies have confirmed its effectiveness in conditions ranging from acute upper respiratory tract infection, neuroprotection, to cardio-protection effects. Though most studies relate their potential to anti-oxidative action and radical scavenging action, still the mechanism of action is not clearly understood. OBJECTIVE: The present review article is focused on addressing various pharmacological actions and underlying mechanisms of catechin. Additionally, we will try to figure out the major adverse effect and success in trials with catechin and lead to a conclusion for its effectiveness. METHODS: This review article is based on the recent/ most cited papers of PubMed and Scopus databases. DESCRIPTION: Catechin can regulate Nrf2 and NFkB pathways in ways that impact oxidative stress and inflammation by influencing gene expression. Other pathways like MAPKs and COMT and receptor tyrosine kinase are also affected by catechin and EGCG that alter their action and barge the cellular activity. This review article explored the structural aspect of catechin and its different isomers and analogs. It also evaluated its various therapeutic and pharmacological arrays. CONCLUSION: Catechin and its stereo-isomers have shown their effectiveness as anti-inflammatory, anti-diabetic, anti-cancer, anti-neuroprotective, bactericidal, memory enhancer, anti-arthritis, and hepato-protective mainly through its activity to alter the pathway by NF-κB, Nrf-2, TLR4/NF-κB, COMT, and MAPKs.