Regulatory Function Of Peroxiredoxin Ⅰ In Mice Inflammatory Response Induced By Lipopolysaccharide

Peroxiredoxins (Prxs) belong to an important superfamily of small nonseleno peroxidasesthat scavenge hydrogen peroxide and organic hydroperoxide, and are essential for maintainingreactive oxygen species (ROS) homeostasis. Over the past20years, extensive research revealsthat the PrxⅠprotein not only have peroxidase activity but also plays a role in cell proliferation,differentiation, apoptosis, aging, and cancer by interacting with numbers proteins. Recently, thefunction of PrxⅠin oncogenesis and cancer development has also been defined. But thepossible regulatory effect of PrxⅠin innate immune response has not been clear. In order tounderstand the function of PrxⅠin the process of innate immune response, the PrxⅠknockoutmice and the wild mice were used to investigate the regulatory effect of PrxⅠin the sepsisinduced by LPS.The influence of PrxⅠon the mortality was examined with the PrxⅠknockout and wildmice after treatment with LPS. The main damaged organs associated of dead mice were foundout using the H&E staining. Apoptosis proteins in the damaged liver cells were detected byWestern blot and inflammatory factors in the liver and serum were determined by ELISA. AfterLPS intraperitoneal injection, mortality of PrxⅠknockout mice significantly increasedcomparing with wild type mice and necrosis foci in the liver of PrxⅠknockout mice appearobvious comparing with wild type mice. ELISA results show that comparing with wild typemice, the level of IL-10significantly decreased in the serum of PrxⅠknockout mice and thelevel of TNF-a significantly increased in the liver of PrxⅠknockout mice after intraperitonealinjection of LPS. Expression of caspase3obviously increased and expression of ROSassociated protein SOD2, Catalase, GPx obviously increased in the liver tissue of Prx Iknockout mice after intraperitoneal injection of LPS.When the body receiving LPS attack, PrxⅠdeficiency will increase significantly themortality of mice, and because the PrxⅠdeficiency can cause high mortality concomiting withmassive apoptosis of liver cell and increase of ROS level in the liver. Therefore, Prx I, asantioxidant enzyme, probably protects the body from damage caused by oxidative stressthrough eliminating active oxygen levels in the liver, and PrxⅠcan be used as a soothingtargeted protein for sepsis treatment.