Tanshinone IIA ameliorates lead (Pb)-induced cognitive deficits and oxidative stress in a rat pup model

Chronic lead (Pb) exposure affects the developing central nervous system, whereas Tanshinone IIA (TSA) improves cognitive deficits.

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.

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.

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).