Puyuan Wen1, Hao Luo2, Li Zhou3, Zhi Song4, Wenwen Li2, Jun Zhou1. 1. Department of Neurology, Medical Research Center, Third Xiangya Hospital, Xiangya Medical School, Central South University, Changsha 410013, China. 2. Department of Microbiology and Immunology, Xiangya Medical School, Central South University, Changsha 410013, China. 3. Medical Research Center, Third Xiangya Hospital, Xiangya Medical School, Central South University, Changsha 410013, China. 4. Department of Neurology, Xiangya Medical School, Central South University, Changsha 410013, China.
Abstract
OBJECTIVE: To observe the effects of tanshinone IIA (Tan IIA) on the expressions of serine/threonine kinase Akt, nuclear factor κB (NF-κB) and caspase-3 in the brain tissues of rat models of Alzheimer's disease (AD). METHODS: Thirty male Sprague-Dawley rats were randomized into three groups (n=10 per group): Sham group, AD group, Tan IIA treatment group. The models of AD were established by injecting β-amyloid (Aβ) into the hippocampus of rats. The location and expression level of Aβ1-16; was observed by immunofluorescence, the expression level of caspase-3 was detected by immunohistochemistry, and the expression levels of Akt and NF-κB were determined by immunohistochemistry and Western blotting. RESULTS: There was no Aβ1-16; detected in the control group, and the difference in the expression level of Aβ1-16; between AD group and Tan IIA treatment group was not significant statistically (P>0.05); The expression of Akt in AD group was lower than that in the control group and the Tan IIA treatment group, and the difference between AD group and the other two groups was of statistical significance (P<0.05). Conversely, compared with Tan IIA treatment group and sham group, the AD group was significantly higher in the expression levels of NF-κB and caspase-3 (P<0.05). CONCLUSION: Tan IIA can up-regulate the expression of Akt and inhibit the production of NF-κB and caspase-3 in the model rats with AD.
OBJECTIVE: To observe the effects of tanshinone IIA (Tan IIA) on the expressions of serine/threonine kinase Akt, nuclear factor κB (NF-κB) and caspase-3 in the brain tissues of rat models of Alzheimer's disease (AD). METHODS: Thirty male Sprague-Dawley rats were randomized into three groups (n=10 per group): Sham group, AD group, Tan IIA treatment group. The models of AD were established by injecting β-amyloid (Aβ) into the hippocampus of rats. The location and expression level of Aβ1-16; was observed by immunofluorescence, the expression level of caspase-3 was detected by immunohistochemistry, and the expression levels of Akt and NF-κB were determined by immunohistochemistry and Western blotting. RESULTS: There was no Aβ1-16; detected in the control group, and the difference in the expression level of Aβ1-16; between AD group and Tan IIA treatment group was not significant statistically (P>0.05); The expression of Akt in AD group was lower than that in the control group and the Tan IIA treatment group, and the difference between AD group and the other two groups was of statistical significance (P<0.05). Conversely, compared with Tan IIA treatment group and sham group, the AD group was significantly higher in the expression levels of NF-κB and caspase-3 (P<0.05). CONCLUSION: Tan IIA can up-regulate the expression of Akt and inhibit the production of NF-κB and caspase-3 in the model rats with AD.