摘要:Euglena gracilis is widely utilized as food or supplement to promote human and animal health, as it contains rich nutrients. In this study, we administered spray-dried powder of
E. gracilis and paramylon, β-glucan stored in
E. gracilis cells, to
A4gnt knockout (KO) mice.
A4gnt KO mice are a mutant mouse model that spontaneously develops gastric cancer through hyperplasia-dysplasia-adenocarcinoma sequence in the antrum of the stomach, and we observed the effects of
E. gracilis and paramylon on the early involvements of
A4gnt KO mice. Male and female 10-week-old
A4gnt KO mice and their age-matched wildtype C57BL/6J mice were orally administered with 50 mg of
E. gracilis or paramylon suspended in saline or saline as a control. After 3-week administration, animals were euthanatized and the stomach was examined histopathologically and immunohistochemically. Gene expression patterns of the stomach, which have been reported to be altered with
A4gnt KO, and IgA concentration in small intestine were also analyzed with real-time PCR and ELISA, respectively. Administration of
Euglena significantly reduced the number of stimulated CD3-positive T-lymphocytes in pyloric mucosa of
A4gnt KO mice and tend to reduce polymorphonuclear leukocytes infiltration.
Euglena administration further downregulated the expression of
Il11 and
Cxcl1 of
A4gnt KO mice.
Euglena administration also affected IgA concentration in small intestinal contents of
A4gnt KO mice. Paramylon administration reduced the number of CD3-positive lymphocytes in pyloric mucosa of
A4gnt KO mice, and downregulated the expressions of
Il11 and
Ccl2 of
A4gnt KO mice. Although we found no significant effects on gross and microscopic signs of gastric dysplasia and cell proliferation, the present study suggests that the administration of
Euglena and paramylon may ameliorate the early involvements of
A4gnt mice through the effects on inflammatory reactions in the gastric mucosa. The cancer-preventing effects should be studied with long-term experiments until actual gastric cancer formation.