Ocimum sanctum Linn. Extract Improves Cognitive Deficits in Olfactory Bulbectomized Mice via the Enhancement of Central Cholinergic Systems and VEGF Expression

Xoan Thi Le; Hien Thu Nguyen; Tai Van Nguyen; Hang Thi Nguyet Pham; Phuong Thi Nguyen; Khoi Minh Nguyen; Ba Van Nguyen; Kinzo Matsumoto

doi:10.1155/2021/6627648

Ocimum sanctum Linn. Extract Improves Cognitive Deficits in Olfactory Bulbectomized Mice via the Enhancement of Central Cholinergic Systems and VEGF Expression

Evid Based Complement Alternat Med. 2021 Jun 30:2021:6627648. doi: 10.1155/2021/6627648. eCollection 2021.

Authors

Xoan Thi Le¹, Hien Thu Nguyen¹, Tai Van Nguyen², Hang Thi Nguyet Pham¹, Phuong Thi Nguyen¹, Khoi Minh Nguyen², Ba Van Nguyen³, Kinzo Matsumoto^{4

5}

Affiliations

¹ Department of Pharmacology and Biochemistry, National Institute of Medicinal Materials, Hanoi 10000, Vietnam.
² Department of Phytochemistry, National Institute of Medicinal Materials, Hanoi 10000, Vietnam.
³ Oncology Center of 103 Military Hospital, Vietnam Military Medical University, Hanoi 10000, Vietnam.
⁴ Center for Supporting Pharmaceutical Education, Daiichi University of Pharmacy, Fukuoka 815-8511, Japan.
⁵ Graduate School of Pharmaceutical Sciences, Daiichi University of Pharmacy, Fukuoka 815-8511, Japan.

Abstract

This study aimed to clarify the antidementia effects of ethanolic extract of Ocimum sanctum Linn. (OS) and its underlying mechanisms using olfactory bulbectomized (OBX) mice. OBX mice were treated daily with OS or a reference drug, donepezil (DNP). Spatial and nonspatial working memory performance was measured using a modified Y maze test and a novel object recognition test, respectively. Brain tissues of the animals were subjected to histochemical and neurochemical analysis. OS treatment attenuated OBX-induced impairment of spatial and nonspatial working memories. OBX induced degeneration of septal cholinergic neurons, enlargement of the lateral ventricles, and suppression of hippocampal neurogenesis. OS and DNP treatment also depressed these histological damages. OS administration reduced ex vivo activity of acetylcholinesterase in the brain. OBX diminished the expression levels of genes coding vascular endothelial growth factor (VEGF) and VEGF receptor type 2 (VEGFR2). Treatment with OS and DNP reversed OBX-induced decrease in VEGF gene and protein expression levels without affecting the expression of the VEGFR2 gene. These results demonstrate that the administration of OS can lessen the cognitive deficits and neurohistological damages of OBX and that these actions are, at least in part, mediated by the enhancement of central cholinergic systems and VEGF expression.