Ergosta-7,9(11),22-trien-3β-ol Rescues AD Deficits by Modulating Microglia Activation but Not Oxidative Stress.
Hsin-Ping LiuYueh-Hsiung KuoJack ChengLi-Zhong ChangMeng-Shiun ChangLi-Wen SuTsai-Ni ChuangWei-Yong LinPublished in: Molecules (Basel, Switzerland) (2021)
Ergosta-7,9(11),22-trien-3β-ol (EK100) was isolated from the Taiwan-specific medicinal fungus Antrodia camphorata, which is known for its health-promotion and anti-aging effects in folk medicine. Alzheimer's disease (AD) is a major aging-associated disease. We investigated the efficacy and potential mechanism of ergosta-7,9(11),22-trien-3β-ol for AD symptoms. Drosophila with the pan-neuronal overexpression of human amyloid-β (Aβ) was used as the AD model. We compared the life span, motor function, learning, memory, oxidative stress, and biomarkers of microglia activation and inflammation of the ergosta-7,9(11),22-trien-3β-ol-treated group to those of the untreated control. Ergosta-7,9(11),22-trien-3β-ol treatment effectively improved the life span, motor function, learning, and memory of the AD model compared to the untreated control. Biomarkers of microglia activation and inflammation were reduced, while the ubiquitous lipid peroxidation, catalase activity, and superoxide dismutase activity remained unchanged. In conclusion, ergosta-7,9(11),22-trien-3β-ol rescues AD deficits by modulating microglia activation but not oxidative stress.
Keyphrases
- oxidative stress
- inflammatory response
- neuropathic pain
- dna damage
- ischemia reperfusion injury
- traumatic brain injury
- health promotion
- induced apoptosis
- signaling pathway
- transcription factor
- working memory
- spinal cord
- fatty acid
- hydrogen peroxide
- nitric oxide
- replacement therapy
- depressive symptoms
- combination therapy
- sleep quality
- induced pluripotent stem cells
- heat stress