Anti-Amnesia-like Effect of Pinus densiflora Extract by Improving Apoptosis and Neuroinflammation on Trimethyltin-Induced ICR Mice.
Min Ji GoJong Min KimHyo-Lim LeeTae Yoon KimSeung Gyum JooJu Hui KimHan Su LeeDae-Ok KimHo-Jin HeoPublished in: International journal of molecular sciences (2023)
This study was conducted to investigate the anti-amnestic property of Korean red pine bark extract (KRPBE) on TMT-induced cognitive decline in ICR mice. As a result of looking at behavioral function, the consumption of KRPBE improved the spatial work ability, short-term learning, and memory ability by Y-maze, passive avoidance, and Morris water maze tests. KRPBE suppressed antioxidant system damage by assessing the SOD activity, reduced GSH content, and MDA levels in brain tissue. In addition, it had a protective effect on cholinergic and synaptic systems by regulating ACh levels, AChE activity, and protein expression levels of ChAT, AChE, SYP, and PSD-95. Also, the KRPBE ameliorated TMT-induced mitochondrial damage by regulating the ROS content, MMP, and ATP levels. Treatment with KRPBE suppressed Aβ accumulation and phosphorylation of tau and reduced the expression level of BAX/BCl-2 ratio and caspase 3, improving oxidative stress-induced apoptosis. Moreover, treatment with KRPBE improved cognitive dysfunction by regulating the neuro-inflammatory protein expression levels of p-JNK, p-Akt, p-IκB-α, COX-2, and IL-1β. Based on these results, the extract of Korean red pine bark, which is discarded as a byproduct of forestry, might be used as an eco-friendly material for functional foods or pharmaceuticals by having an anti-amnesia effect on cognitive impairment.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- dna damage
- cognitive decline
- ischemia reperfusion injury
- cognitive impairment
- endoplasmic reticulum stress
- signaling pathway
- mild cognitive impairment
- high glucose
- cell death
- cell proliferation
- anti inflammatory
- type diabetes
- drug induced
- functional connectivity
- combination therapy
- lps induced
- heat shock
- resting state
- cerebrospinal fluid
- white matter
- protein kinase
- subarachnoid hemorrhage
- inflammatory response
- metabolic syndrome