Apigenin Ameliorates Scopolamine-Induced Cognitive Dysfunction and Neuronal Damage in Mice
Yeojin Kim1,2, Jihyun Kim1, Meitong He1
1Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Korea.
Molecules (Basel, Switzerland)
|September 10, 2021
Summary
Apigenin, a natural compound, significantly improved learning and memory in mice with scopolamine-induced cognitive impairment. It works by reducing brain cell damage and regulating key molecular pathways involved in memory.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Scopolamine injection induces cognitive deficits and memory dysfunction in mice.
- Understanding the molecular mechanisms behind cognitive impairment is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of apigenin against scopolamine-induced cognitive impairments.
- To elucidate the underlying mechanisms of apigenin's action on cognitive and memory functions.
Main Methods:
- A scopolamine-induced mouse model of cognitive impairment was used.
- Apigenin was administered at doses of 100 and 200 mg/kg/day.
- Behavioral tests (T-maze, novel object recognition, Morris water maze) and Western blot analysis were employed.
Main Results:
- Apigenin administration significantly improved cognitive abilities in mice.
- Apigenin attenuated scopolamine-induced lipid peroxidation and regulated apoptosis markers (Bax/Bcl-2 ratio, caspase-3, PARP cleavage).
- Apigenin modulated amyloidogenesis (BACE1, PS1, PS2) and promoted neurotrophic factors (insulin-degrading enzyme, BDNF, TrkB).
Conclusions:
- Apigenin demonstrates significant potential in improving cognitive and memory functions.
- Apigenin exerts its protective effects by regulating apoptosis, amyloidogenesis, and the BDNF/TrkB signaling pathway.
