Fig. 4.  Lipopolysaccharide-elicited preconditioning against ischemia-reperfusion (I/R) injury is MyD88-dependent, but interferon-β-mediated transcription factor (Trif)-independent. Wild-type C57BL/6J (WTBL/6), myeloid differentiation factor 88 knockout (MyD88^−/−), and TIR-domain-containing adaptor protein inducing interferon-β-mediated transcription-factor knockout (Trif^−/−) mice were treated with normal saline or 0.1 mg/kg lipopolysaccharide (LPS) intraperitoneally. Twenty-four hours later, mouse hearts were isolated and perfused in a Langendorff system. After 30 min of perfusion, the hearts were subjected to 30 min of no-flow global ischemia, followed by 60 min of reperfusion. (A)  Left ventricular developed pressure (LVDP). (B)  dP/dt^maxis expressed as percentage of the baseline. Each data point and error bar in A-B  represents the mean ± SE. The number of mice in each group is as follows: WTBL/6-saline: 10; WTBL/6-LPS: 11; Trif^−/−-saline: 6; Trif^−/−-LPS: 6; MyD88^−/−-Saline: 7; MyD88^−/−-LPS: 7. **P < 0.01, NS is not significant. (C)  Myocardial infarction (MI) size is expressed as the percentage of left ventricle area (LV). The long and short horizontal lines represent the mean ± SE. *P < 0.05, **P < 0.01, NS is not significant. (D)  Representative heart slices after triphenyltetrazolium chloride staining from Trif^−/−and MyD88^−/−mice. Viable myocardium was stained red, and infarcted myocardium appeared white.