nder normal conditions. These results suggest that Roscovitine web exposure to hypoxia causes substantial damage to the function of the rat intestinal barrier and bacterial translocation occurs by some means. TLR4 plays an important role in the innate intestinal immune system as the first part of the intestinal tract recognizing bacteria. It is not only an immune recognition receptor on the cell surface but also a transmembrane signal transduction molecule. During the development of enteric septicemia, LPS, a strong activator of TLR4 in the intestinal epithelium, specifically binds to TLR4. TLR4 then activates the MyD88-dependent and TRIF-dependent pathways and thereby activates intracellular signaling molecules such as the IRAKs, TRAFs, and TAK1. Thus, it ultimately forms the primary and secondary signal waves that activate NF-kB. NFkB induces the transcription and translation of inflammatory cytokines and leads to the massive release of inflammatory mediators. In local regions, these molecules can lead to apoptosis of intestinal mucosal epithelial cells and damage the tissues and organs of the intestinal tract. It can also act on distant organs and amplify systemic inflammatory reactions. Currently, studies on the role of TLR4 in intestinal immune function have not generated consistent results. Fukata et al. found that TLR4 could promote the proliferation of epithelial cells and inhibit intestinal bacterial translocation. However other studies showed that, compared to wild-type mice, intestinal epithelial damage caused by colitis was milder in TLR4-deficient mice. The infiltration of cytokines, macrophages, and neutrophils was reduced. These results suggest that TLR4 has different functions in different cellular events. The functions and mechanisms of TLR4 and NF-kB with respect to damage to the function of the intestinal barrier and to bacterial translocation under hypoxic conditions have not yet been reported. In this study, realtime fluorescent quantitative RT-PCR and western blot experiments showed that, in group H, the expression of TLR4 and NFkB was elevated in jejunal tissues, and these elevations were more substantial when LPS was added. These results suggest that hypoxia alone can upregulate TLR4 expression and activate the TLR4/NF-kB signaling pathway; hypoxia and infection can further aggravate such phenomena. TNF-a and IL-6 are important inflammatory factors located downstream from NFkB. They play important roles in various inflammatory reactions and are highly correlated with the severity of inflammation. In our study, by detecting TNF-a and IL-6, the degree of activation of this signaling pathway was found the TLR4/NF-kB to be consistent with changes in the rate of intestinal bacterial translocation, serum levels of endotoxin, and damage to the ultrastructure of the intestinal mucosa. Soares et al. proposed that TLR4 might play an important role in recruiting granulocytes after intestinal damage and in the inflammatory reaction caused by bacterial translocation. Therefore, we deduced that damage to the function of the intestinal barrier and bacterial translocation under hypoxic conditions might be closely related to the TLR4/NF-kB signaling pathway. PDTC is a specific inhibitor of NF-kB. It inhibits the nuclear translocation of the NF-kB p65 subunit by reducing IkB degradation; thus, it inhibits the expression of downstream cytokines. The current study also found that PDTC could significantly reduce TLR4 mRNA levels, possibly via positi