The antioxidant, taurine reduced lipopolysaccharide (LPS)-induced generation of ROS, and activation of MAPKs and Bax in cultured pneumocytes.

Lipopolysaccharide (LPS) can cause damage to the epithelia of the respiratory tract. However, taurine can protect the lung tissue from such oxidant-induced inflammation. This study examined the effects of a LPS treatment on the intracellular calcium levels ([Ca(2+)]i) as well as the specific mechanisms of LPS-induced cell death in pneumocytes. In addition, the effects of taurine on the LPS-induced increase in the accumulation of reactive oxygen species (ROS) in pneumocytes were investigated. The [Ca(2+)]i in cultured pneumocytes was determined using microfluorescence techniques. The level of activation of the mitogen-activated protein kinases (MAPKs) and Bax protein were measured by Western blotting. LPS at 10 and 100 ng/ml induced cell death and decreased the viability of MRC-5 cells. Moreover, the intracellular Ca(2+) and ROS levels were increased by LPS. The LPS treatment led to the phosphorylation of ERK1/2, JNK and the activation of Bax. A pretreatment with 20 mM taurine reduced the LPS-induced production of ROS and MARK activity. These results show that a LPS treatment induces cell death in MRC-5 cells by increasing the intracellular ROS and Ca(2+) levels. The increase in the intracellular level of ROS promotes MAPKs activation and Bax translocation. Overall, LPS induces lung cell death by activating MAPKs. Furthermore, taurine decreased the LPS-induced generation of ROS and activation of MAPK and Bax.