Steroid-Enriched Fraction of Achyranthes bidentata Protects Amyloid β Peptide 1-40-Induced Cognitive Dysfunction and Neuroinflammation in Rats.
Li-Wei LinFan-Hsuan TsaiWan-Cheng LanYih-Dih ChengSheng-Chi LeeChi-Rei WuPublished in: Molecular neurobiology (2019)
The roots of Achyranthes bidentata Blume (AB) is commonly used in the treatment of osteoporosis and dementia in traditional Chinese medicine. Pharmacological reports evidenced that AB possessed anti-osteoarthritis effects. However, there is little literature about the anti-dementia activities of AB. The present study was designed to prepare steroid-enriched fraction of AB (ABS) and investigate whether ABS can protect from cognitive dysfunction and neuroinflammation against Aβ 1-40-induced Alzheimer's disease (AD) model in rats. ABS only contained 135.11 ± 4.28 mg of ecdysterone per gram. ABS (50 mg/kg) reversed the dysfunction of exploratory activity and memory function on plus-maze and Morris water maze caused by Aβ 1-40 in rats. ABS (50 mg/kg) also decreased amyloid deposition, neurofibrillary tangle, neural damage, activated astrocyte, and microglial caused by Aβ 1-40. Furthermore, ABS reversed the phenomenon of neural oxidative damage and neuroinflammation, including the higher levels of MDA and cytokines, and the lower activities of antioxidant enzymes and GSH levels caused by Aβ 1-40 in rat cortex and hippocampus. Finally, ABS restored the activation of ERK pathway and decreased NF-κB phosphorylation and translocation altered by Aβ 1-40. ABS alone (50 mg/kg) promoted cognitive function, activated brain antioxidant defense system, and decreased brain TNF-α levels in sham group. Therefore, ABS has the cognition-promoting and antidementia potential. Steroids especial ecdysterone are major active components of AB. The action mechanism is due to decreasing oxidative stress and neuroinflammation through modulating ERK pathway, NF-κB phosphorylation, and translocation in Aβ 1-40-induced AD rat model.
Keyphrases
- oxidative stress
- diabetic rats
- lps induced
- signaling pathway
- cognitive impairment
- cerebral ischemia
- lipopolysaccharide induced
- traumatic brain injury
- high glucose
- mild cognitive impairment
- rheumatoid arthritis
- pi k akt
- ischemia reperfusion injury
- inflammatory response
- drug induced
- induced apoptosis
- systematic review
- anti inflammatory
- multiple sclerosis
- clinical trial
- immune response
- subarachnoid hemorrhage
- bone mineral density
- brain injury
- blood brain barrier
- gram negative
- resting state
- postmenopausal women
- multidrug resistant
- electronic health record
- cell death
- adverse drug