The regenerating gene iα is overexpressed in atrophic gastritis rats with hypergastrinemia

Abstract

The role of gastrin on the development of atrophic gastritis (AG) and its relationship with the expression of RegIα in vivo remain unclear. We established experimental AG in rats by combination administration with sodium salicylate, alcohol, and deoxycholate sodium. The mean score of inflammation in gastric antrum in AG rats was significantly elevated (P < 0.05), while the number of glands dramatically decreased (P < 0.05). In addition, the cell proliferation in gastric glands was increased in experimental AG rats, as determined by immunohistochemistry staining of PCNA and GS II. The level of serum gastrin in AG rats was significantly elevated relative to that of normal rats (P < 0.01). Moreover, the expression of RegIα protein and its receptor mRNA was increased in gastric tissues in AG rats (P < 0.05). Taken together, we demonstrated that the overexpression of Reglα is related with hypergastrinemia in AG rats.

Figure 1

Pathological finding in rats with atrophic gastritis. (a) Gloss appearance of gastric mucosa. Flat with pale appearance and thin mucin on the gastric mucosa in atrophic gastritis group rats (right diagram) when compared with normal rats (left diagram). (b) H&E (×100) staining of gastric gland. Irregular arrangement and cystic dilation of gastric glands in atrophic gastritis (right diagram). (c) H&E (×200) staining showed that neutrophils and lymphocytes infiltrated into the gastric glands in rats with atrophic gastritis (right diagram). (d) The mean number of infiltrated inflammatory cells was calculated in each of 10 microscopic fields of gastric antrum glands. The mean inflammation score (mean ± s.d) was 1.95 ± 0.55 and 1.3 ± 0.34, respectively, in atrophic gastritis and normal rats. (e) The number of gastric glands in each of 1 mm area (mean ± SD) was randomly analyzed in 5 microscopic fields, which was 39.8 ± 4.59 and 44.2 ± 2.57, respectively, in atrophic gastritis and normal rats. Normal group: normal rats; Model group: atrophic gastritis rats. *P < 0.05.

Figure 2

Immunohistochemistry stains of PCNA and GSII in gastric glands. (a) Positive stain of PCNA in cellular nucleus, which are mainly localized in deep layer of gastric glands in normal rats (left diagram), while extended to whole glands in atrophic gastritis (right diagram). (b) GSII was moderately positive stained in the neck and deep layer of gastric glands in normal rats (left diagram). It showed of strong stain in the neck and upper areas in the gastric glands in rats with atrophic gastritis (right diagram). Control group: normal control rats; Model group: atrophic gastritis rats. *P < 0.05, **P < 0.01.

Figure 3

The RegIα protein and its receptor mRNA were overexpressed in atrophic gastritis rats with hypergastrinemia. (a) The average serum gastrin levels (ng/mL) in atrophic gastritis and normal rats were determined by ELISA assay. (b) Representative results of RegIα protein expression in gastric tissues from atrophic gastritis and normal rats (upper lane) were performed by immunoblot experiments. Band densities were quantified and protein levels were normalized to β-actin (lower diagram). (c) The expression of RegIα receptor mRNA was measured by quantity real-time PCR and calculated using the value of 2^−ΔΔCT. Relative fold change in atrophic gastritis group was compared with that of normal group, which was normalized as a reference value of 1.0. Control group: normal control rats; Model group: atrophic gastritis rats. *P < 0.05, **P < 0.01.