The Protective Effects and the Involved Mechanisms of Tanshinone IIA on Sepsis-Induced Brain Damage in Mice.

Abstract

To evaluate the protective effect of tanshinone IIA on sepsis using a mouse model as well as to preliminarily explore the mechanism behind its application. The mouse model of sepsis was established using the cecal ligation and puncture (CLP) method. Eighty mice were randomly divided into four groups: Sham operation group (Sham group), model group (CLP group), tanshinone IIA group (DS group), and dexamethasone group (DEX group). ELISA method was used to detect the levels of TNF-α and IL-6 in the hippocampal tissue of mouse. Western blot method was used to detect the expression levels of PSD-95, SYP, and Iba-1 in the hippocampus tissue. Immunohistochemistry was used to detect the expression level and distribution of astrocytes (GFAP antibody). Morris water maze test was used to determine the ability of learning and memory in mice. Tanshinone IIA could improve the postoperative survival and 7-day survival rate in the septic mice after operation, which shortens the escape latency and increases the number of crossing platform in the septic mice. It also reduces the expression of TNF-α, IL-6, and Iba-1 in the peripheral blood/hippocampus and the number of astrocytes in hippocampal CA3 area after 7days of sepsis in mice. However, tanshinone IIA increases the expression levels of SYP and PSD-95 in the hippocampus of septic mice on the seventh day after operation. Tanshinone IIA has a protective effect on the nerve of septic mice, and its mechanism may be related to the anti-inflammatory effects of the peripheral and hippocampal parts as well as inhibiting the over-activation of astrocytes and microglia.