Background Pre-administration of probiotic Lactobacilli attenuates ethanol-induced gastric mucosal injury (GMI). The underpinning mechanisms remain to be elucidated. We speculated that lactate, the main metabolite of Lactobacillus that can be safely used as a common food additive, mediated the gastroprotective effect. This study aimed to gain experimental evidence to support our hypothesis and to shed lights on its underlying mechanisms. Methods Lactate was orally administrated to mice at different doses 30 min prior to the induction of GMI. Gastric tissue samples were collected and underwent histopathological and immunohistochemical assessments, enzyme-linked immunosorbent assay, quantitative polymerase chain reaction (qPCR) and western blot analyses. Results Pretreatment with lactate at 1–3 g/kg significantly curtailed the severity of ethanol-induced GMI, as shown by morphological and histopathological examinations of gastric tissue samples. Significantly lower level of cytokines indicative of local inflammation were found in mice receiving lactate treatment prior to ethanol administration. Western-blot, immunohistochemical analysis and qPCR suggested that gastroprotective properties of lactate were mediated by its modulatory effects on the expression of the apoptosis regulator gene Bax, the apoptotic executive protein gene Casp3, and genes critical for gastric mucosal integrity, including those encoding tight junction proteins Occludin, Claudin-1, Claudin-5, and that for lactate receptor GPR81. Conclusion Lactate mitigates ethanol-induced GMI by curtailing local gastric inflammatory response, down-regulating the expression of the apoptosis regulator and executor genes Bax and Casp3, and up-regulating the expression of genes encoding tight junction proteins Occludin, Claudin-1, and Claudin-5 and the lactate receptor GPR81.

Aims To observe the therapeutic effects of vaginal infusion of probiotic Clostridium butyricum WZ001 on bacterial vaginosis (BV) in mice. Methods and Results Female ICR mice were used to establish the model of BV by infecting oestrogen‐treated mice with Escherichia coli, and then treated with high‐ and low dose of C. butyricum. Clinical indexes of mice in the C. butyricum‐treated groups were significantly improved and comparable to those in the antibiotic group. Pap staining showed that neutrophil count was significantly increased after modelling and largely decreased after C. butyricum treatment (P < 0·01). Dynamic observation of E. coli and Lactobacillus showed that the number of E. coli significantly decreased in the C. butyricum‐treated groups or in the antibiotic group with prolonged treatment (P < 0·01). Besides, the number of E. coli in the low‐dose C. butyricum group was higher than that in either its high‐dose counterpart or the antibiotic group respectively (P < 0·01). The number of Lactobacillus decreased evidently in the antibiotic group (P < 0·01), while that in the C. butyricum groups remained consistent. Moreover, C. butyricum inhibited the proliferation of E. coli by the experiment in vitro. The phosphorylation of nuclear factor‐kappa B (NF‐κB) p65 in vaginal tissue and the serum levels of inflammatory cytokines, IL‐1β, TNF‐α and IL‐6, increased after modelling and significantly decreased after treated with C. butyricum (P < 0·01), with no difference found when compared with the antibiotic group. Conclusion Clostridium butyricum inhibits the growth of pathogenic bacteria as well as the inflammatory response induced by E. coli and promotes the growth of Lactobacillus to maintain the vaginal micro‐ecological balance. Significance and Impact of the Study Our results suggest that probiobitc C. butyricum WZ001 has a great potential in the clinical treatment of BV.