Abstract
The aim of our study was to investigate the therapeutic efficacy of Morroniside (MR) in a chronic atrophic gastritis (CAG) rat model and its underlying mechanisms. Male Wistar rats were employed to induce CAG model. All animals were divided into six groups: control, model (CAG), positive (Vitacoenzyme tablets), MR low, middle and high three doses groups. Histopathology observation of gastric tissues was detected by hematoxylin and eosin (H&E) staining. The levels of gastrointestinal hormones and inflammatory factors in serum were measured by Enzyme-linked immunosorbent assay (ELISA). Apoptosis of gastric mucosa cell was detected using Terminal-deoxynucleoitidyl Transferase Mediated Nick End Labeling (TUNEL) assay. Protein expressions were evaluated by Western blotting. Obvious pathological injury and in the CAG model group were observed, which was improved after treatment with MR. The contents of serum gastrin (GAS) was increased whereas motilin (MTL) was decreased in a dose-dependent manner after MR treatment. MR markedly attenuated the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and interleukin-1 beta (IL-1β). Moreover, MR inhibited apoptosis of gastric mucosal cell as presented by TUNEL, coupled with an upregulation in Bcl-2 expression and a downregulation in Bax, cleaved caspase-3 and cleaved caspase-9 expression. Furthermore, the expression levels of phospho-NF-κB p65 (p-NF-κB p65) and p-IKKα/β proteins were reduced accompanied by an increase in IκB-α expression in the MR-treated groups. The study demonstrated that MR is able to protect against CAG via inhibiting inflammation and apoptosis, which might provide a stronger theoretical basis for the treatment of CAG.