Research on the Prophylactic Effect of Lactobacillus plantarum KSFY06 on HCl/Ethanol-induced Gastric Injury in Mice

The present study was conducted to determine the prophylactic effect of Lactobacillus plantarum
KSFY06 (LP-KSFY06) on HCl/ethanol-induced gastric injury in Kunming mice. The experimental mice
were allocated into six groups: the normal group, HCl/ethanol treated group, HCl/ethanol + ranitidine
treated group, HCl/ethanol + Lactobacillus delbrueckii subsp. Bulgaricus (LB) treated group,
HCl/ethanol + low concentration of Lactobacillus plantans KSFY06 (LP-KSFY06-L) treated group, and
HCl/ethanol + high concentration of Lactobacillus plantans KSFY06 (LP-KSFY06-H) treated group.
The changes in daily body weight and food intake of the mice in the HCl/ethanol + LP-KSFY06-H
treated group were the closest to those of the HCl/ethanol + ranitidine treated and normal groups. LPKSFY06
significantly inhibited the formation of gastric mucosal lesions, reduced the area of
gastric lesions, inhibited gastric-juice secretion, and increased pH compared with the HCl/ethanol
treated group. After the treatment, the serum interleukin-6 (IL)-6, IL-12, tumor necrosis factor-α
(TNF-α), and interferon-γ levels and the gastrictissue IL-6 and IL-12 levels in the LP-KSFY06
(including LP-KSFY06-L and LP-KSFY06-H) group decreased compared with those in the HCl/
ethanol treated group. The level of serum and gastric tissue malondialdehyde was lower and the nitric
oxide, total superoxide dismutase, and glutathione activities in the LP-KSFY06 treated mice were
higher than those in the HCl/ethanol treated mice. Quantitative polymerase chain reaction analysis
and western blot analysis showed that LP-KSFY06 increased the mRNA and protein expression
of the epidermal growth factor, epidermal growth factor receptor, vascular endothelial growth
factor, inhibitor kappaB-α, neuronal nitric oxide synthase, and endothelial NOS and reduced
the mRNA and protein expression of nuclear factor kappaB, inducible NOS, cyclooxygenase-2,
TNF-α, and IL-1β in gastric tissues compared with the HCl/ethanol treated mice. These experimental
results showed that a high concentration (1.0 × 109 CFU per kg B.W.) of LP-KSFY06 had a
stronger effect on preventing gastric injury than a low concentration (1.0 × 108 CFU per kg B.W.)
of LP-KSFY06. In conclusion, LP-KSFY06-H could significantly reduce HCl/ ethanol-induced
gastric injury in mice compared with LP-KSFY06-L. The positive effect probably was due to
ameliorating inflammation, oxidative stress and apoptosis, in addition to enhancing gastric mucin
secretion by increasing the mice daily body weight, food intake and the pH value of the gastric juice,
decreasing the gastric injury area and gastric juice secretion volume, reducing serum and gastrictissue
IL-6, IL-12, TNF-α, and IFN-γ levels and MDA activities, improving serum and gastric-tissue
NO, T-SOD, and GSH activities, increasing the mRNA expression and protein of EGF, EGFR, VEGF,
IκBα, nNOS, eNOS, TNF-α and IL-1β and abating the NF- κB, iNOS, and COX-2 activation in gastric
tissue. These results suggest that LP-KSFY06 has a potential probiotic effect in preventing gastric
injury.