Korean Red Ginseng extract treatment prevents post-antibiotic dysbiosis-induced bone loss in mice

Kang, Hyeon Hui; Chargo, Nicholas J.; Chennupati, Soumya; Neugebauer, Kerri A.; Cho, Jae Youl; Quinn, Robert A.; McCabe, Laura R.; Parameswaran, Narayanan

doi:10.1016/j.jgr.2022.08.006

Cited by 4 publications

(8 citation statements)

References 34 publications

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“…Our lab and others have identified gut barrier function as integral in both the pathogenesis and treatment of osteoporosis in several models, including a subcutaneous pellet model of GIO. ( 16,19,27,28,38,39 ) The link has been supported by correlations between gut permeability (serum levels of endotoxin and/or oral FITC‐dextran) and trabecular bone volume fraction. Importantly, an intestinal barrier enhancer prevents bone loss in conditions such as post‐ABX, GIO, and bacterial challenge, demonstrating the link between gut barrier and bone health.…”

Section: Discussionmentioning

confidence: 96%

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Chargo,

Schepper,

Rios‐Arce

et al. 2023

JBMR Plus

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Glucocorticoids (GCs) are commonly used anti‐inflammatory medications with significant side effects, including glucocorticoid‐induced osteoporosis (GIO). We have previously demonstrated that chronic subcutaneous GC treatment in mice leads to gut barrier dysfunction and trabecular bone loss. We further showed that treating with probiotics or barrier enhancers improves gut barrier function and prevents GIO. The overall goal of this study was to test if probiotics could prevent GC‐induced gut barrier dysfunction and bone loss in a clinically relevant oral‐GC model of GIO. Eight‐week‐old male CD‐1 mice were treated with vehicle or corticosterone in the drinking water for 4 weeks and administered probiotics Lactobacillus reuteri ATCC 6475 (LR 6475) or VSL#3 thrice weekly via oral gavage. As expected, GC treatment led to significant gut barrier dysfunction (assessed by measuring serum endotoxin levels) and bone loss after 4 weeks. Serum endotoxin levels significantly and negatively correlated with bone volume. Importantly, LR 6475 treatment effectively prevented both GC‐induced increase in serum endotoxin and trabecular bone loss. VSL#3 had intermediate results, not differing from either control or GC‐treated animals. GC‐induced reductions in femur length, cortical thickness, and cortical area were not affected by probiotic treatment. Taken together, these results are the first to demonstrate that LR 6475 effectively prevents the detrimental effects of GC treatment on gut barrier, which correlates with enhanced trabecular bone health in an oral mouse model of GIO. © 2023 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research.

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Section: Discussionmentioning

confidence: 96%

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Chargo,

Schepper,

Rios‐Arce

et al. 2023

JBMR Plus

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“…We have previously shown that chronic GC treatment impairs intestinal barrier integrity in mice as demonstrated by increased serum endotoxin levels due to leaky gut ( Schepper et al, 2020 ; Chargo et al, 2023 ). Another method to assess barrier integrity is by measuring serum levels of FITC-Dextran, a method our lab and others have used extensively ( Schepper et al, 2019 ; Behera et al, 2021 ; Kang et al, 2023 ). Here, we show that 4-weeks of GC treatment in growing male CD-1 mice increased barrier permeability ( p = 0.0216) compared to vehicle control as assessed by FITC-Dextran flux into the serum ( Figure 3A ).…”

Section: Resultsmentioning

confidence: 99%

“…Whole intestinal permeability was assessed using 4kD fluorescein isothiocyanate dextran (FITC-dextran) as previously described ( Schepper et al, 2019 ; Kang et al, 2023 ). Briefly, mice were gavaged with 300 mg/kg FITC dissolved in sterile PBS at least 4 h prior to time of death.…”

Section: Methodsmentioning

confidence: 99%

“…Recent studies from our lab and others have shown that gut microbiota plays a critical role in regulating bone health in several etiologies of bone loss ( Sjögren et al, 2012 ; McCabe et al, 2015 ; Weaver, 2015 ; Hernandez, 2017 ; Quach and Britton, 2017 ; Wallace et al, 2017 ; Ohlsson and Sjögren, 2018 ; Pacifici, 2018 ; Cooney et al, 2020 ; Jeyaraman et al, 2023 ). We demonstrated that the microbiota composition is altered and linked with bone loss in several mouse models including GIO, post-antibiotic dysbiosis, type-1 diabetes, estrogen deficiency, and obesity ( Britton et al, 2014 ; McCabe et al, 2019 ; Schepper et al, 2019 ; 2020 ; Rios-Arce et al, 2020 ; Kang et al, 2023 ). Importantly, in these mouse models of bone loss, treatment with probiotics, particularly Lactobacillus reuteri 6475 significantly prevented bone loss.…”

Section: Introductionmentioning

confidence: 99%

“…Recently we showed that Korean Red Ginseng (KRG, Panax Ginseng Meyer, Araliaceae) extract was effective at preventing bone loss in a post-antibiotic dysbiosis model in mice ( Kang et al, 2023 ). We also demonstrated that KRG extract treatment altered gut microbiota composition as well as improved gut barrier function in the dysbiosis model.…”

Section: Introductionmentioning

confidence: 99%

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Korean red ginseng extract prevents bone loss in an oral model of glucocorticoid induced osteoporosis in mice

Chargo,

Kang,

Das

et al. 2024

Front. Pharmacol.

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The gut microbiota and barrier function play important roles in bone health. We previously demonstrated that chronic glucocorticoid (GC)-induced bone loss in mice is associated with significant shifts in gut microbiota composition and impaired gut barrier function. Korean Red Ginseng (KRG, Panax Ginseng Meyer, Araliaceae) extract has been shown to prevent glucocorticoid-induced osteoporosis (GIO) in a subcutaneous pellet model in mice, but its effect on gut microbiota and barrier function in this context is not known. The overall goal of this study was to test the effect of KRG extract in a clinically relevant, oral model of GIO and further investigate its role in modulating the gut-bone axis. Growing male mice (CD-1, 8 weeks) were treated with 75 μg/mL corticosterone (∼9 mg/kg/day) or 0.4% ethanol vehicle in the drinking water for 4 weeks. During this 4-week period, mice were treated daily with 500 mg/kg/day KRG extract dissolved in sterile water or an equal amount of sterile water via oral gastric gavage. After 4 weeks of treatment, we assessed bone volume, microbiota composition, gut barrier integrity, and immune cells in the bone marrow (BM) and mesenteric lymph nodes (MLNs). 4 weeks of oral GC treatment caused significant distal femur trabecular bone loss, and this was associated with changes in gut microbiota composition, impaired gut barrier function and altered immune cell composition. Importantly, KRG extract prevented distal femur trabecular bone loss and caused significant alterations in gut microbiota composition but had only modest effects on gut barrier function and immune cell populations. Taken together, these results demonstrate that KRG extract significantly modulates the gut microbiota-bone axis and prevents glucocorticoid-induced bone loss in mice.

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Quercetin ameliorates bone loss in OVX rats by modulating the intestinal flora-SCFAs-inflammatory signaling axis

Feng,

Wang,

et al. 2024

International Immunopharmacology

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Korean Red Ginseng extract treatment prevents post-antibiotic dysbiosis-induced bone loss in mice

Cited by 4 publications

References 34 publications

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Lactobacillus Reuteri 6475 Prevents Bone Loss in a Clinically Relevant Oral Model of Glucocorticoid‐Induced Osteoporosis in Male CD‐1 Mice

Korean red ginseng extract prevents bone loss in an oral model of glucocorticoid induced osteoporosis in mice

Quercetin ameliorates bone loss in OVX rats by modulating the intestinal flora-SCFAs-inflammatory signaling axis

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