Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study

Abstract 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...

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Main Authors: Yingpeng Huang, Jiali Zhang, Renjie Dong, Xiawei Ji, Yusha Jiang, Jianke Cen, Zhihuai Bai, Kairui Hong, Huihui Li, Jiajing Chen, Jinhui Zhou, Fanyu Qian, Fangyan Wang, Yue Qu, Yan Zhou
Format: Article
Language:English
Published: BMC 2021-01-01
Series:BMC Complementary Medicine and Therapies
Subjects:
Online Access:https://doi.org/10.1186/s12906-020-03198-7
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spelling doaj-fb6372a02bbb4b18ad5fd2403d5baadb2021-01-17T12:25:18ZengBMCBMC Complementary Medicine and Therapies2662-76712021-01-0121111010.1186/s12906-020-03198-7Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo studyYingpeng Huang0Jiali Zhang1Renjie Dong2Xiawei Ji3Yusha Jiang4Jianke Cen5Zhihuai Bai6Kairui Hong7Huihui Li8Jiajing Chen9Jinhui Zhou10Fanyu Qian11Fangyan Wang12Yue Qu13Yan Zhou14The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityThe Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityWenzhou Key Laboratory of Sanitary Microbiology, Key Laboratory of Laboratory Medicine, Ministry of Education, China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical UniversityThe Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Pathophysiology, School of Basic Medical Science, Wenzhou Medical UniversityDepartment of Microbiology, Biomedicine Discovery Institute, Monash UniversityWenzhou Key Laboratory of Sanitary Microbiology, Key Laboratory of Laboratory Medicine, Ministry of Education, China, School of Laboratory Medicine and Life Sciences, Wenzhou Medical UniversityAbstract 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.https://doi.org/10.1186/s12906-020-03198-7LactateEthanolGastric mucosal injuryInflammationApoptosisTight junction proteins
collection DOAJ
language English
format Article
sources DOAJ
author Yingpeng Huang
Jiali Zhang
Renjie Dong
Xiawei Ji
Yusha Jiang
Jianke Cen
Zhihuai Bai
Kairui Hong
Huihui Li
Jiajing Chen
Jinhui Zhou
Fanyu Qian
Fangyan Wang
Yue Qu
Yan Zhou
spellingShingle Yingpeng Huang
Jiali Zhang
Renjie Dong
Xiawei Ji
Yusha Jiang
Jianke Cen
Zhihuai Bai
Kairui Hong
Huihui Li
Jiajing Chen
Jinhui Zhou
Fanyu Qian
Fangyan Wang
Yue Qu
Yan Zhou
Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
BMC Complementary Medicine and Therapies
Lactate
Ethanol
Gastric mucosal injury
Inflammation
Apoptosis
Tight junction proteins
author_facet Yingpeng Huang
Jiali Zhang
Renjie Dong
Xiawei Ji
Yusha Jiang
Jianke Cen
Zhihuai Bai
Kairui Hong
Huihui Li
Jiajing Chen
Jinhui Zhou
Fanyu Qian
Fangyan Wang
Yue Qu
Yan Zhou
author_sort Yingpeng Huang
title Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
title_short Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
title_full Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
title_fullStr Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
title_full_unstemmed Lactate as a metabolite from probiotic Lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
title_sort lactate as a metabolite from probiotic lactobacilli mitigates ethanol-induced gastric mucosal injury: an in vivo study
publisher BMC
series BMC Complementary Medicine and Therapies
issn 2662-7671
publishDate 2021-01-01
description Abstract 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.
topic Lactate
Ethanol
Gastric mucosal injury
Inflammation
Apoptosis
Tight junction proteins
url https://doi.org/10.1186/s12906-020-03198-7
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