Amentoflavone protects hippocampal neurons: anti-inflammatory, antioxidative, and antiapoptotic effects

Zhen Zhang; Tao Sun; Jian-Guo Niu; Zhen-Quan He; Yang Liu; Feng Wang

doi:10.4103/1673-5374.160109

Amentoflavone protects hippocampal neurons: anti-inflammatory, antioxidative, and antiapoptotic effects

Neural Regen Res. 2015 Jul;10(7):1125-33. doi: 10.4103/1673-5374.160109.

Authors

Zhen Zhang¹, Tao Sun¹, Jian-Guo Niu², Zhen-Quan He², Yang Liu³, Feng Wang¹

Affiliations

¹ Ningxia Key Laboratory of Cerebrocranial Disease, Incubation Base of National Key Laboratory, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China ; Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China.
² Ningxia Key Laboratory of Cerebrocranial Disease, Incubation Base of National Key Laboratory, Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China.
³ Department of Neurosurgery, General Hospital of Ningxia Medical University, Yinchuan, Ningxia Hui Autonomous Region, China.

Abstract

Amentoflavone is a natural biflavone compound with many biological properties, including anti-inflammatory, antioxidative, and neuroprotective effects. We presumed that amentoflavone exerts a neuroprotective effect in epilepsy models. Prior to model establishment, mice were intragastrically administered 25 mg/kg amentoflavone for 3 consecutive days. Amentoflavone effectively prevented pilocarpine-induced epilepsy in a mouse kindling model, suppressed nuclear factor-κB activation and expression, inhibited excessive discharge of hippocampal neurons resulting in a reduction in epileptic seizures, shortened attack time, and diminished loss and apoptosis of hippocampal neurons. Results suggested that amentoflavone protected hippocampal neurons in epilepsy mice via anti-inflammation, antioxidation, and antiapoptosis, and then effectively prevented the occurrence of seizures.

Keywords: NSFC grant; apoptosis; brain inflammation; brain injury; epilepsy; inducible nitric oxide synthase; interleukin-1 beta; interleukin-6; nerve regeneration; neural regeneration; neuroprotection; nitric oxide; nuclear factor-κB; prostaglandin E2.