Neuroprotective effect of Da Chuanxiong Formula against cognitive and motor deficits in a rat controlled cortical impact model of traumatic brain injury

Autor: Clara Bik-San Lau, Chun-Hay Ko, Hoi Ting Shiu, Hing Lok Wong, Jinfang Zhang, Chun Fai Ng, Zhi Ke Liu, Wai Sang Poon, Wai Ching Chin, Ping Kuen Lam, Ping-Chung Leung
Rok vydání: 2018
Předmět:
Male
0301 basic medicine
Time Factors
Morris water navigation task
Brain Edema
Pharmacology
Rats
Sprague-Dawley

Cognition
0302 clinical medicine
Neural Stem Cells
Brain Injuries
Traumatic

Drug Discovery
Gait
Cerebral Cortex
Gastrodia
Behavior
Animal

Neural stem cell
Neuroprotective Agents
medicine.anatomical_structure
Blood-Brain Barrier
Microglia
medicine.symptom
Astrocyte
Traumatic brain injury
Neurogenesis
Brain damage
Motor Activity
Blood–brain barrier
Neuroprotection
Capillary Permeability
03 medical and health sciences
medicine
Animals
Maze Learning
Cell Proliferation
Dose-Response Relationship
Drug

business.industry
medicine.disease
Disease Models
Animal

030104 developmental biology
nervous system
Astrocytes
Rotarod Performance Test
Neuron
business
Rhizome
030217 neurology & neurosurgery
Apiaceae
Drugs
Chinese Herbal
Zdroj: Journal of Ethnopharmacology. 217:11-22
ISSN: 0378-8741
DOI: 10.1016/j.jep.2018.02.004
Popis: Ethnopharmacological relevance Da Chuanxiong Formula (DCXF) is one of the famous herb pairs that contains dried rhizomes of Ligusticum chuanxiong Hort. and Gastrodia elata Bl. in the mass ratio of 4:1. This classic representative traditional Chinese medicine has been widely used to treat brain diseases like headache and migraine caused by blood stasis and wind pathogen. However, the therapeutic effect of DCXF on traumatic brain injury (TBI) has not been reported yet. Aim of study The present study was performed to investigate the neuroprotective effects of DCXF and its underlying mechanisms in the controlled cortical impact (CCI)-induced TBI rat model. Materials and methods Male Sprague-Dawley rats were divided into four groups: Sham, TBI control, 1X DCXF (520.6 mg/kg) and 5X DCXF (2603.0 mg/kg). Two treatment groups (1X and 5X DCXF) were intragastrically administered daily for 7 days before CCI-induced TBI and then DCXF treatments were continued post-TBI until the animal behavioral tests, including Morris water maze test, acceleration rotarod motor test and CatWalk quantitative gait analysis test, were done. The brain water content and blood brain barrier (BBB) integrity were measured by wet-dry weight method and Evans blue method, respectively. The number of neuron cells, neural stem cells (NSCs), GFAP positive cells (astrocyte) as well as Iba-1 positive cells (microglia) were determined by histology and immunohistochemistry. Results Treatment with DCXF significantly improved the learning ability and memory retention in Morris water maze test, and remarkably enhanced motor performances in acceleration rotarod motor test and catwalk quantitative gait analysis test after TBI. Moreover, DCXF treatment was able to reduce BBB permeability, brain edema, microglia and astrocyte activation, improve the proliferation of NSCs and decrease neurons loss in the brain with TBI. Conclusions The present study demonstrated that DCXF treatment could decrease BBB leakage and brain edema, reduce neuron loss, microglia and astrocyte activation, and increase NSCs proliferation, which may contribute to the cognitive and motor protection of DCXF in the TBI rats. It is the first time to provide potentially underlying mechanisms of the neuroprotective effect of DCXF on TBI-induced brain damage and functional outcomes.
Databáze: OpenAIRE