Objective To study the antitumor activity of Xerophilusin G on S180 cells,and Its mechanism.Methods Modified MTT assay was used to test the effect of Xerophilusin G on the proliferation of S180 tumor cell strain.The influences on tumor growth and immune organs of mice with transplanted sarcoma (S180) were observed.The cell cycle of S180 cell lines and mouse sarcoma (S180) was analyzed by flow cytometry.The lymphocyte proliferation activity of spleen stimulating was tested.The level of IL-2 in serum of mice with transplanted sarcoma (S180) was measured by ELISA.Results The IC50 of Xerophilusin G in S180 cell lines was 19.80 μg·mL-1,the LD50 in mouse for Xerophilusin G was 121.11 mg·kg-1 through intraperitoneal injection.The tumor inhibition rate of Xerophilusin G was 32.11％ and 41.60％,respectively at the doses of 3 and 6 mg · kg-1 (P ＜ 0.05).Compared with the control,the thymus,kidney and cardiac index were decreased.The cell proportion at G0/G1 phase of mouse sarcoma (S180) was increased.T and B cell proliferation activities in tumor-bearing mice were enhanced (P ＜ 0.05).As compared with control group,the serum level of IL-2 was decreased 90.9％ and 77.1％ in low-and medium-dose groups,respectively (P ＜ 0.05).Conclusion Xerophilusin G has remarkable effects in sarcoma (S180) bearing mice.The antitumor mechanism of Xerophilusin G might be related with G0/G1 phase arrest of mouse sarcoma (S180) cells and enhancing the activity of T and B cell but not related with increasing the secreting of IL-2.

Objective To investigate the role of nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome in hydrogen-rich saline-induced reduction of lipopolysaccharide (LPS)-caused damage to mitochondria in macrophages of mice.Methods Macrophage line RAW264.7 of mice were routinely cultured and divided into 4 groups (n=6 each) using a random number table method:control group (group C),group LPS,hydrogen-rich saline plus LPS group (group LPS+H2) and hydrogen-rich saline plus LPS plus ATP group (group LPS+ATP+H2).LPS was given at the concentration of 1 μg/ml,and the cells were then incubated for 30 min in group LPS.LPS at the concentration of 1 μg/ml and hydrogen-rich saline at the concentration of 0.6 mmol/L were simultaneously given,and the cells were then incubated for 30 min in LPS+H2 and LPS+ATP+H2 groups.ATP at the concentration of 1 nmol/L was then given,and the cells were incubated for 6 h in group LPS+ATP+H2.Mitochondrial membrane potential (MMP) was determined by JC-1 staining,and respiratory control ratio (RCR) was measured using a Clark-type electrode.The expression of NLRP3,caspase-1 and apoptosisassociated speck-like protein containing C-terminal caspase recruitment domain (ASC) was determined by Western blot.The concentrations of INTERLEUKIN-1 BETA (IL-1β),IL-18 and IL-6 in the supernatant were determined by enzyme-linked immunosorbent assay.Results Compared with group C,MMP and RCR were significantly decreased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were increased,and the expression of NLRP3,caspase-1 and ASC was up-regulated in group LPS (P＜0.05).Compared with group LPS,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-l8 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+H2 (P＜0.05).Compared with group LPS+H2,MMP and RCR were significantly increased,the concentrations of IL-1β,IL-18 and IL-6 in the supernatant were decreased,and the expression of NLRP3,caspase-1 and ASC was down-regulated in group LPS+ATP+H2 (P＜0.05).Conclusion Hydrogen-rich saline can reduce LPS-caused damage to mitochondria in macrophages of mice through inhibiting the activation of NLRP3 inflammasome.