Expressions of NF-κB p65 protein, TNF-α, IL-1β, IL-6 and NO in myocardial tissues, together with levels of cTnI in serum were significantly elevated rats, while inhibition of TLR4-NF-κB signaling pathway could lead to reduced levels of downstream inflammatory factors and a protective effect on myocardial depression caused by sepsis [25]. This evidence concerns the gene TNNI3 and Sepsis.