Rannasangpei Is a Therapeutic Agent in the Treatment of Vascular Dementia.

Peng Wu,Xianda Hu,Huiyuan Xue,Lifang Zhen,Yuandai Luo,Ying Shang,Fukai Huang,Yinuo Liao,Wei Xiao

doi:10.1155/2016/2530105

Abstract

Rannasangpei (RSNP) is used as a therapeutic agent in the treatment of cardiovascular diseases, neurological disorders, and neurodegeneration in China; however, its potential use in the treatment of vascular dementia (VD) was unclear. In this study, our aim was to examine the neuroprotective effect of RSNP in a VD rat model, which was induced by permanent bilateral common carotid artery occlusion (2VO). Four-week administration with two doses of RSNP was investigated in our study. Severe cognitive deficit in the VD model, which was confirmed in Morris water maze (MWM) test, was significantly restored by the administration of RSNP. ELISA revealed that the treatments with both doses of RSNP could reinstate the cholinergic activity in the VD animals by elevating the production of choline acetyltransferase (ChAT) and reducing the acetylcholinesterase (AChE); the treatment of RSNP could also reboot the level of superoxide dismutase (SOD) and decrease malondialdehyde (MDA). Moreover, Western blot and quantitative PCR (Q-PCR) results indicated that the RSNP could suppress the apoptosis in the hippocampus of the VD animals by increasing the expression ratio of B-cell lymphoma-2 (Bcl-2) to Bcl-2-associated X protein (Bax). These results suggested that RSNP might be a therapeutic agent in the treatment of vascular dementia in the future.

Highlights

Vascular dementia (VD), which is caused by chronic cerebral hypoperfusion (CCH), hampers the intelligence of an individual, leading to the development of cognitive dysfunction syndrome [1, 2]
The Morris water maze (MWM) test was used to observe the effect of RSNP on the spatial learning and memory capability of VD rat model, which was induced by 2VO
These results indicated that both doses of RSNP improved the learning disability of VD animals, which was induced by 2VO; the medium dose of RSNP probably showed a better effect than the low dosage, and there was no significant difference in the recovery of learning ability of VD animals in RSNP-M group and EGB group

Summary

Introduction

Vascular dementia (VD), which is caused by chronic cerebral hypoperfusion (CCH), hampers the intelligence of an individual, leading to the development of cognitive dysfunction syndrome [1, 2]. Several evidences have indicated that CCH aggravates cerebrovascular pathological changes [5, 6], such as central cholinergic dysfunction, oxidative injury, and apoptosis in hippocampus [7]. It is a well-known fact that central cholinergic neurotransmission is closely associated with learning and memory in humans [8]; reactive oxygen species cause oxidative stress that activates various signal transduction pathways involved in apoptosis. Owing to the complicated etiology and pathology of VD, it is difficult to develop a single-target therapy for patients with VD

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Conclusion