Pretreatment with Lactobacillus fermentum XY18 Relieves Gastric Injury Induced by HCl/Ethanol in Mice via Antioxidant and Anti-Inflammatory Mechanisms

Abstract

Lactobacillus fermentum XY18 (LF-XY18) is a bacterial strain with satisfactory antioxidant properties in vitro that we previously isolated from Xinjiang yogurt. This article will explore the preventive effect of LF-XY18 on acute gastric injury and provide the basis for the innovative development and application of lactic acid bacteria (LAB). Methods: Kunming mice underwent gastric injury induced by hydrochloric acid and ethanol. LF-XY18 isolated from yogurt in Xinyuan County in the Yili region of Xinjiang was subsequently administered intragastrically to mice for 2 weeks to explore the mechanism of LF-XY18 in preventing gastric injury via its antioxidant effects. Results: There was decreased gastric juice volume, gastric injury area, and formation of gastric mucosal lesions in the LF-XY18 mice as compared to those in the control mice, while LF-XY18 prevented the decrease in the gastric juice pH value in mice. Compared with the gastric injury model group mice, LF-XY18 reduced the serum levels of motilin, substance P, interleukin-6, interleukin-12, tumor necrosis factor-α, and interferon-γ but increased the serum levels of somatostatin and vasoactive intestinal peptide. The activities of superoxide dismutase, glutathione peroxidase, glutathione, and nitric oxide were increased in the gastric tissue of the LF-XY18 mice compared with the control mice, but malondialdehyde activity was decreased in the LF-XY18 mice. Quantitative polymerase chain reaction analysis illustrated that in the gastric tissue of LF-XY18 mice, the messenger RNA (mRNA) expression of occludin, epidermal growth factor (EGF), EGF receptor, vascular EGF, inhibitor kappa-B-α, neuronal nitric oxide synthase, endothelial nitric oxide synthase, cuprozinc superoxide dismutase, manganese superoxide dismutase, and catalase was stronger than that in the control mice, but the mRNA expression of activated B cells (NF-κB), inducible nitric oxide synthase, and cyclooxygenase-2 was weaker than in the control mice. Conclusion:These results indicate that LF-XY18 has a potential role in the prevention of gastric injury through antioxidant effects, and a high concentration (1.0 × 10 9 CFU/kg b.w.) of LF-XY18 has a stronger anti-gastric injury effect than a low concentration (1.0 × 10 8 CFU/kg b.w.).

Preventive effect of Lactobacillus plantarum HFY15 on carbon tetrachloride (CCl4)‐induced acute liver injury in mice

“…Then, 2% of the inoculum amount was taken, and the overnight cultured bacteria solution was inoculated in an MRS-THIO medium (MRS medium containing 0.2% sodium thioacetate [Shanghai Macklin Biochemical Co., Ltd., Shanghai, China]) containing 0.0% and 0.3% bovine bile salt. After incubating for 24 h at 37 • C, with a blank medium (uninoculated MRS-THIO medium) as the control, the absorbance at 600 nm was measured with a microplate reader (Thermo Fisher Scientific, Waltham, MA, USA), and the tolerance to bile salts was calculated using the following formula: Growth efficiency (%) = (Bile salt medium OD600)/(Blank medium OD600) × 100 (Wang et al, 2020).…”

Preventive Effect of Lactobacillus Plantarum HFY15 on Oxidative Damage and Acute Liver Injury Induced by Carbon Tetrachloride (CCl 4 ) in Mice

“…Then, 2% of the inoculum amount was taken, and the overnight cultured bacteria solution was inoculated in an MRS-THIO medium (MRS medium containing 0.2% sodium thioacetate (Shanghai Macklin Biochemical Co., Ltd., Shanghai, China) containing 0.0% and 0.3% bovine bile salt. After incubating for 24 h at 37°C, with a blank medium (uninoculated MRS-THIO medium) as the control, the absorbance at 600 nm was measured with a microplate reader (Thermo Fisher Scienti c, Waltham, MA, USA), and the tolerance to bile salts was calculated using the following formula: Growth e ciency (%)=(Bile salt medium OD 600 )/(Blank medium OD 600 )×100 [54].…”

Involvement of microRNA/cystine/glutamate transporter in cold-stressed gastric mucosa injury

“…The gastric injury involves an imbalance in mucous defense and injury. Gastric ulcers induced by Helicobacter pylori infection and nonsteroidal anti-inflammatory drugs (NSAIDS) are related to the increase in some inflammatory factors ( Wang et al, 2020 ), cytokines, and reactive oxygen species ( Wang et al, 2021 ), which can impair gastric mucous ( Ren et al, 2021 ). Further, these gastric ulcers can also contribute to decreased secretion of endogenous substances such as nitric oxide ( Dejban et al, 2020 ), prostaglandins ( Wang et al, 2021 ), and glutamate ( Akhigbe et al, 2022 ), which have protective effects on the stomach.…”