Home Bratislava Medical Journal 2017 Bratislava Medical Journal Vol.118, No.4, p.196-201, 2017

Journal info


 


Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.564

 

Aims and Scope
Editorial Info
Submission Guidelines

Select Journal







Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Bratislava Medical Journal Vol.118, No.4, p.196-201, 2017

Title: Tanshinone IIA ameliorates lead (Pb)-induced cognitive deficits and oxidative stress in a rat pup model
Author: L. M. Tang, L. X. Wang, Z. Y. Wang, L. F. Sun, X. D. PAN, G. Q. Pan

Abstract: OBJECTIVE: Chronic lead (Pb) exposure affects the developing central nervous system, whereas Tanshinone IIA (TSA) improves cognitive deficits.
METHODS: In this study, we investigated the effects of TSA against lead-induced neurotoxicity in a rat pup model. A total of thirty two healthy male Wistar rats were randomly divided into four groups: lead-treated group, lead plus TSA-treated 1 group, lead plus TSA-treated 2 group, and controls. After a 4-week lead exposure, memory function was determined using Morris water maze and the concentration of lead was measured in blood. Total superoxide dismutase (T-SOD), glutathione (GSH), malonaldehyde (MDA) and brain-derived neurotrophic factor (BDNF) activities were determined in hippocampus samples.
RESULTS: Lead exposure causes decrease of body weight; increase of the blood lead concentration; decrease of antioxidant activities and BDNF content. However, co-administration of TSA with lead ameliorated the weight loss. Furthermore, TSA inhibited neurotoxicity as evidenced by decreased latency period and increase in percentage of time spent in the target quadrant. Administration of TSA also improved antioxidant activities by increased T-SOD, GSH, and decreased MDA activities compared to lead-treated group.
CONCLUSION: This study provides evidence of that TSA has a neuroprotective effect against lead-induced cognitive deficit by enhancing antioxidant activities in the brain (Tab. 2, Fig. 3, Ref. 27).

Keywords: lead exposure, Tanshinone IIA, memory, oxidative stress, neurotoxicity
Published online: 02-May-2017
Year: 2017, Volume: 118, Issue: 4 Page From: 196, Page To: 201
doi:10.4149/BLL_2017_039


download file



© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.