The 6-AF Evaluation of Neuroprotective Activity against Cd- Induced Oxidative Stress and Degenerative Brain Disease including PD in Mice

Abstract

Background: The neurotoxicity caused by Cadmium (Cd) has been researched internationally. Since it has a wide range of unfavorable effects on people, it is believed to be one of the primary tissue-inducing target agents. Using adult male albino mice, the therapeutic potential of 6-AF to reduce memory impairment, neurodegeneration, and neuroinflammation caused by Cadmium Chloride (CdCl2) was evaluated in the current study for the first time. Methodology: The male adult mice were distributed into 4 sub-groups; Control, Cd treated (1 mg/kg thrice weeks), Cd (1 mg/kg 3 weeks) + 6-AF (30 mg/kg 3 a week for last 2 weeks) and 6-AF treated (30 mg/kg thrice a week for the last two weeks). After the initial seven-day Cdcl2 dosing cycle, the 6-Aminoflavone was administered interpretively intravenously for the following around 14 days (three per week). After receiving Cdcl2 injections for 30 days, behavior tests were conducted. Western blot analysis was performed after the hippocampus was extracted, and the results were then used to develop the X-rays. Results: Our results demonstrate that 6-AF significantly enhanced behavior as assessed by the Y-maze and Morris Water Maze (MWM) and that this enhancement was followed by an inhibition of phospho C-Jun N Terminal Kinase (p-JNK) and its downstream signaling, including tumor necrosis factor-alpha (TNF-alpha), Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-KB), and Poly (ADP-ribose In addition, 6-AF also reduced the expression of NRF-2 proteins in adult mice exposed to oxidative stress caused by cadmium chloride. Conclusion: 6-AF is an effective neuroprotective drug in disorders causing neurodegeneration.