In vitro and in vivo, Lycium barbarum Polysaccharide Extracted from Water Inhibited Lipopolysaccharide and Heavy Metal Inflammation

A BSTRACT Background: The pharmacological activities of Lycium barbarum polysaccharide (LBP) are well established. In the study, in vitro and in vivo experiments were used to investigate the immunomodulatory effect of LBP on regulating the inflammatory response induced by lipopolysaccharide (LPS) and heavy metals (arsenic and lead). Aim: The objectives of this study were to evaluate the inhibitory effect of LBP on inflammatory mechanisms in vitro and the inhibitory efficacy of LBP on arsenic- and lead-induced inflammation in vivo . Methods: Traditional hot water extraction was used to extract crude polysaccharides, which were then purified using DEAE-Sephacel chromatography and size exclusion chromatography. This study uses the following methods, including cell viability assay, CM-H2DCFDA stain, RNA extraction and Reverse transcriptional polymerase chain reaction, and Real-time PCR. In the in vitro and in vivo test, TNF-α, IL-1β, TLR4, NF-κB of RAW264.7 cells and animal organs were measured. Results: The results showed that LBP inhibited the gene expression of IL-1β and TNF-α and reduced the gene expression of NF-κB and TLR4 in LPS-induced RAW264.7 cells. TNF-α gene expression increased in organs (liver, colon, pancreas, bladder, and testicle) of animals exposed to lead in in vivo studies. LBP inhibited the increase in TNF- gene expression in organs exposed to lead. TNF-α gene expression was significantly increased in the brain and heart after arsenic exposure. Following LBP administration, TNF-α gene expression was significantly reduced in arsenic-exposed brain and heart. Conclusions: LBP can inhibit the inflammatory response induced by LPS and reduce inflammatory factor production by inhibiting the gene expression of TNF-α, IL-1β, TLR4 and NF-κB in RAW264.7 cells. LBP inhibited TNF-α, which suppressed lead and arsenic-induced inflammation, and thus had an anti-inflammatory effect on heavy metal-induced inflammation.