The Effect Of Radix Hedysari Polysaccharide(HPS)on The Expression Of TRAF6 And TRIF During Endotoxin-induced Uveitis In Rats

Purpose: The aim of this study is to investigate the effect of Radix Hedysari Polysaccharide(HPS)on the expression of TRAF6 and TRIF in EIU and to study the inhibitory effect of HPS on the Endotoxin-induced Uveitis in Rats.Methods: Animal model of acute anterior uveitis was established by subcutaneous injection of male Wistar rats with 1mg/kg Cholera vibrio lipopolysaccharide(LPS).The Wistar rats were divided into four groups.HPS(400 mg/kg)or an equivalent volume of phosphate-buffered saline(PBS)was given through intraperitoneal injection 1h before the LPS induction in HPS treatment group and EIU group.HPS was also given by subcutaneous route to the Wistar rats in HPS control group.The clinical manifestation was observed and scored at 2h intervals using a slit microscope.The degree of inflammatory reaction was determined by routine histological examinations.Real-time RT-PCR was used to assess the effects of HPS on the expression of TRAF6 and TRIF m RNA.The protein expression levels of TRAF6 and TRIF were examined by western blot.The expression of NF-κB p65 m RNA and its nucleoprotein,as the marker of inflammation in EIU were also detected.Results: The animal model of acute anterior uveitis was successfully established.HPS treatment produced therapeutic results by significantly reducing the clinical severity of EIU as well as mild inflammatory reaction in the eye.The expression of NF-κB p65 which was the marker of EIU was consistent with the effect of HPS.The result of RT-PCR showed that HPS treatment decreased the m RNA expression of TRAF6.But the western blot result showed that the protein of TRAF6 was highly expressed.The effect of HPS on the expression of TRIF has no statistical significance.Conclusion: HPS can restrain the intraocular inflammation reaction in EIU by inhibiting the expression of TRAF6 m RNA and inhibiting TRAF6 protein from degradation.HPS inhibits EIU primarily through My D88 dependent pathway.