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Ligularia fischeri: A boon to diabetic cognitive deficits by protecting neuronal apoptosis via insulin signaling pathway

Sang Hyun Park, Seon Kyeong Park, Jin Yong Kang, Jong Min Kim, Jeong Eun Kang, Chang Jun Lee, Bong Seok Kwon, Su Bin Park, Dae Ok Kim, Ho Jin Heo

Abstract


This study investigated the effect of ethyl acetate fraction from Ligularia fischeri (EFLF) on learning and memory deficits and potential mechanisms involved in diabetic mice.

The diabetic mice were induced by injecting STZ (60 mg/kg of body weight) dissolved in sodium citrate buffer (0.1 M, pH 4.5) once a day for 2 consecutive days in the abdominal cavity. Then diabetic mice were orally administered EFLF for 4 weeks and then their diabetes and improving effect on cognitive function was evaluated. In addition, the changes of oxidative damage and protein expression, related in insulin signaling pathway, in brain were examined.

Administration of EFLF (100 and 200 mg/kg of body weight) remarkably improved high glucose states and improved learning and memory deficits, as confirmed through the Y-maze, passive avoidance, and Morris water maze (MWM) tests. Moreover, diabetic mice showed elevation of acetylcholinesterase (AChE) activity, reduction of acetylcholine (ACh) content, elevation of malondialdehyde (MDA), and decreased superoxide dismutase (SOD) in brain tissue. However, administration of EFLF significantly improved these changes. In the analysis of protein, EFLF treatment significantly increased brain-derived neurotrophic factor (BDNF) expression and AMP-activated protein kinase (AMPK) phosphorylation, enhanced the insulin signaling pathway, and inhibited the mitochondrial apoptotic signaling pathway. Finally, quercetin-3-O-galactoside, 3,4-O-dicaffeoylquinic acid, and 3,5-O-dicaffeoylquinic acid and acetylated quercetin of 3-O-galactoside as phenolic compounds of EFLF were identified using a UPLC-QTOF/MS system.

In conclusion, the results suggest that EFLF improves cognitive function in streptozotocin (STZ)-induced diabetic cognitive impairment by preventing neuronal apoptosis via the insulin signaling pathway in diabetic mice.


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