Neuroprotective Effect of ent-Kaur-15-en-17-al-18-oic Acid on Amyloid Beta Peptide-Induced Oxidative Apoptosis in Alzheimer's Disease.
Caiyun ZhangXingming ZhaoShiqi LinFangyuan LiuJiahui MaZhuo HanFujuan JiaWei-Dong XieQian ZhangXia LiPublished in: Molecules (Basel, Switzerland) (2019)
ent-Kaur-15-en-17-al-18-oic acid, extracted from the Chinese well known folk herb Leontopodium longifolium, performed a significantly neuroprotective effect on amyloid beta peptide 25-35 (Aβ25-35)-induced SH-SY5Y cells neurotoxicity in Alzheimer's disease. The results demonstrated that this compound maintained oxidative stress balance, reduced levels of reactive oxygen species (ROS), malondialdehyde (MDA), and improved contents of glutathione (GSH) and superoxide dismutase (SOD) without obvious cytotoxicity. This compound also obviously relieved oxidative stress-induced apoptosis associated with p53 and nuclear factor κB (NF-κB) pathways accompanied by upregulating B-cell lymphoma-2 (bcl-2) and downregulating p53, nuclear factor κB (NF-κB), Bax, Cleaved-caspase 3, and Cytochrome C protein expressions further. Briefly, ent-kaur-15-en-17-al-18-oic acid protected cells from oxidative apoptosis associated with p53 and NF-κB pathways.
Keyphrases
- induced apoptosis
- nuclear factor
- oxidative stress
- diabetic rats
- endoplasmic reticulum stress
- toll like receptor
- signaling pathway
- reactive oxygen species
- dna damage
- cell cycle arrest
- ischemia reperfusion injury
- pi k akt
- high glucose
- cell death
- cognitive decline
- immune response
- drug induced
- cerebral ischemia
- heat shock
- binding protein
- nitric oxide
- inflammatory response
- small molecule
- subarachnoid hemorrhage
- fluorescent probe