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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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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