To explore the specific mechanism of the gastric protective effect of salvianolic acid B (Sal B) on precancerous lesions of the stomach (PLGC) in rats by regulating the microRNA (miR)-106b-5p/B-cell translocation gene 3 (BTG3) molecular axis.

Except for the NC group, the rat models of PLGC were established. The rats were randomly divided into the NC group (without any treatment, intragastric administration of normal saline), the model group (after successful modeling, intragastric administration of normal saline), the experimental group (intragastric administration of Sal B based on the model group), the NC mimic group (based on the experimental group, injection of NC mimic plasmid via the tail vein), the miR-106b-5p mimic group (based on the experimental group, injection of miR-106b-5p mimic plasmid via the tail vein), the pcDNA3.1-NC group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-NC plasmid) and the pcDNA3.1-BTG3 group (based on the miR-106b-5p mimic group, intraperitoneal injection of pcDNA3.1-BTG3 plasmid). Quantitative real-time polymerase chain reaction experiments were carried out to detect the mRNA expression levels of miR-106b-5p, BTG3 and inflammatory factors in the gastric mucosa tissues. Enzyme-linked immunosorbent assays were performed to detect the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA) and gastrin-17 (G-17) in the serum. Western blot experiments were used to detect the levels of proteins related to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway and mucin 2 (MUC2) in the gastric mucosa tissues.

The relative expression levels of miR-106b-5p in the NC group, the model group and the experimental group were 1.00±0.08, 1.76±0.35 and 1.33±0.26, respectively, and the relative expression levels of BTG3 mRNA were 1.00±0.05, 0.39±0.06 and 0.81±0.15, respectively. There were statistically significant differences in the above-mentioned indicators between the model group and the NC group, as well as between the experimental group and the model group (all P<0.05). The levels of SOD in the NC group, the model group, the experimental group, the NC mimic group, the miR-106b-5p mimic group, the pcDNA3.1-NC group and the pcDNA3.1-BTG3 group were (197.81±47.15), (118.54±20.49), (172.29±34.34), (176.78±35.57), (127.65±21.23), (119.41±20.50) and (158.28±31.07) U·mL^-1, respectively; the levels of MDA were (3.44±0.67), (8.08±1.32), (3.92±0.75), (3.84±0.70), (6.50±1.21), (6.34±1.17) and (4.22±0.79) nmol·mL^-1, respectively; the levels of G-17 were (221.57±40.26), (155.62±28.43), (201.13±37.35), (194.85±35.24), (162.72±31.65), (160.04±29.37) and (189.32±32.15) pg·mL^-1, respectively; the levels of PI3K were 1.00±0.14, 1.81±0.36, 1.23±0.21, 1.19±0.20, 1.65±0.32, 1.70±0.35 and 1.38±0.28, respectively; the ratios of phosphorylated AKT/AKT were 1.00±0.09, 1.94±0.39, 1.27±0.23, 1.21±0.18, 1.77±0.37, 1.73±0.33 and 1.42±0.26, respectively. There were statistically significant differences in the above-mentioned indicators between the miR-106b-5p mimic group and the NC mimic group, and between the pcDNA3.1-BTG3 group and the pcDNA3.1-NC group (all P<0.05).

Sal B may exert a gastric protective effect by down-regulating the targeted negative regulation of BTG3 expression by miR-106b-5p, inhibiting the activation of the PI3K/AKT signaling pathway, thereby alleviating the oxidative stress and inflammatory response in PLGC rats and improving the condition of the gastric mucosa.