TLR2 and Sepsis: The inhibition of HMGB1 secretion (Figure 2A,B), reduction of the quantity of expressed HMGB1 signal recipients, such as TLR2, TLR4, and RAGE (Figure 2C), and the HMGB1-induced excessive permeability (Figure 4A–C) through blocking the p38 biochemical modification (Figure 4D), along with its pathway by CN could influence the progression of HMGB1-induced sepsis.