Thymol in Trachyspermum ammi seed extract exhibits neuroprotection, learning, and memory enhancement in scopolamine-induced Alzheimer's disease mouse model.
Binod TimalsinaMd Nazmul HaqueHo Jin ChoiRaju DashIl Soo MoonPublished in: Phytotherapy research : PTR (2023)
Several reports have stated the neuroprotective and learning/memory effects of Tachyspermum ammi seed extract (TASE) and its principal component thymol; however, little is known about its underlying molecular mechanisms and neurogenesis potential. This study aimed to provide insights into TASE and a thymol-mediated multifactorial therapeutic approach in a scopolamine-induced Alzheimer's disease (AD) mouse model. TASE and thymol supplementation significantly reduced oxidative stress markers such as brain glutathione, hydrogen peroxide, and malondialdehyde in mouse whole brain homogenates. Tumor necrosis factor-alpha was significantly downregulated, whereas the elevation of brain-derived neurotrophic factor and phospho-glycogen synthase kinase-3 beta (serine 9) enhanced learning and memory in the TASE- and thymol-treated groups. A significant reduction in the accumulation of Aβ 1-42 peptides was observed in the brains of TASE- and thymol-treated mice. Furthermore, TASE and thymol significantly promoted adult neurogenesis, with increased doublecortin positive neurons in the subgranular and polymorphic zones of the dentate gyrus in treated-mice. Collectively, TASE and thymol could potentially act as natural therapeutic agents for the treatment of neurodegenerative disorders, such as AD.
Keyphrases
- oxidative stress
- hydrogen peroxide
- mouse model
- cerebral ischemia
- diabetic rats
- high glucose
- rheumatoid arthritis
- brain injury
- white matter
- resting state
- adipose tissue
- high fat diet induced
- signaling pathway
- type diabetes
- newly diagnosed
- protein kinase
- multiple sclerosis
- blood brain barrier
- drug induced
- functional connectivity
- ischemia reperfusion injury
- induced apoptosis
- anti inflammatory
- skeletal muscle
- adverse drug
- heat shock protein
- combination therapy
- endoplasmic reticulum stress