Exploring in vitro, in vivo metabolism of mogroside V and distribution of its metabolites in rats by HPLC-ESI-IT-TOF-MSn

Xu, Feng; Li, Dianpeng; Huang, Zhencong; Lu, Fushen; Wang, Lei; Huang, Yonglin; Wang, Rufeng; Liu, Guang-Xue; Shang, Ming‐Ying; Cai, Shao‐Qing

doi:10.1016/j.jpba.2015.07.024

Cited by 58 publications

(44 citation statements)

References 13 publications

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“…Also distribution in rat organs was studied: seven bioactive metabolites of mogroside V were identified, among which mogroside IIE was abundant in four organs (heart, liver, spleen and lung) collected from rats treated with mogroside V, suggesting that it may contribute to the bioactivity of mogroside V in vivo. Moreover, the 39% mass deficiency noted in the former study by Murata et al (2010) appears to be close to the proportion of metabolites found by Xu et al (2015) in the rat organs. After repeated dosing, mogroside V itself was also found throughout all analysed organs, in blood plasma and in urine.…”

Section: In Vivosupporting

confidence: 78%

“…After repeated dosing, mogroside V itself was also found throughout all analysed organs, in blood plasma and in urine. Thus, the study by Xu et al (2015) indicates absorption of mogroside V and systemic bioavailability along with its extensive conversion by digestive enzymes and the intestinal microbiota of rats. Luo et al (2016a,b) studied the kinetics of mogroside V in male Sprague-Dawley rats that were given a single dose of either 2 mg/kg bw by i.v.…”

Section: In Vivomentioning

confidence: 98%

“…Biotransformation of mogroside V and of mogroside III in the human intestine has been investigated in vitro. Xu et al (2015) incubated mogroside V under anaerobic conditions with the intestinal microbiota of a healthy Chinese man, and analyzed the biotransformation products by HPLC in tandem with an electrospray ionisation ion-trap time-of-flight multistage mass spectrometer (HPLC-ESI-IT-TOF-MS). Along with unchanged mogroside V, mainly siamenoside I, mogroside IVE, mogroside IIIE, mogroside IIIA1, and mogroside IIA were detected.…”

Section: In Vitromentioning

confidence: 99%

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Safety of use of Monk fruit extract as a food additive in different food categories

Flavourings¹,

Younes²,

Aquilina³

et al. 2019

EFS2

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The EFSA Panel on Food Additives and Flavourings (FAF) provides a scientific opinion on the safety of Monk fruit extract proposed for use as a new food additive in different food categories. Monk fruit extracts are prepared by water extraction of the fruits of Siraitia grosvenorii. Cucurbitane glycosides, mogrosides, are the main components of the S. grosvenorii fruit and mogroside V is the main mogroside in the Monk fruit extract. Mogroside V is absorbed to some extent and is systemically bioavailable. Monk fruit extract containing 25% and 55% mogroside V were negative in the bacterial reverse mutation assay and did not induce structural and/or numerical chromosomal damage. However, the Panel noted that the in vitro toxicity studies including study with metabolic activation were not sufficiently informative to evaluate the genotoxic potential of the metabolites generated after microbial metabolism, including the aglycone. The effects on the testis observed in a 90-day study with monk fruit extract-52% mogroside V cannot be dismissed and the adversity of these effects cannot be ruled out. No effects on parental, reproductive or development toxicity were observed in a reproductive and developmental screening study in rats. For male animals, the time of exposure did not cover the full length of spermatogenesis and, therefore, a longer term study at higher doses would be needed to clarify the effects on testes observed in the 90-day study. No maternal and developmental toxicity was observed. Considering the systemic availability of mogroside V, the effects observed in the rat subchronic study and following the principles of EFSA Guidance on food additives evaluation, data from chronic/carcinogenicity toxicity testing would have been warranted. Exposure to mogroside V was calculated based on the proposed use levels. The Panel concluded that toxicity database on Monk fruit extract is insufficient to conclude on the safety of the use of Monk fruit extract as a food additive.

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Section: In Vivosupporting

confidence: 78%

Section: In Vivomentioning

confidence: 98%

Section: In Vitromentioning

confidence: 99%

See 1 more Smart Citation

Safety of use of Monk fruit extract as a food additive in different food categories

Flavourings¹,

Younes²,

Aquilina³

et al. 2019

EFS2

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show abstract

“…Mogroside V and mogroside IVE were purified from this triperpene glycoside extract by column chromatography. Mogroside IIIE, mogroside IIE, mogroside IE and mogrol were prepared by the enzyme or acid hydrolysis of mogroside V [17, 26]. These compounds were purified at least 96% and dissolved in DMSO.…”

Section: Methodsmentioning

confidence: 99%

Mogrol Derived from Siraitia grosvenorii Mogrosides Suppresses 3T3-L1 Adipocyte Differentiation by Reducing cAMP-Response Element-Binding Protein Phosphorylation and Increasing AMP-Activated Protein Kinase Phosphorylation

Harada¹,

Ishihara²,

Horiuchi³

et al. 2016

PLoS ONE

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This study investigated the effects of mogrol, an aglycone of mogrosides from Siraitia grosvenorii, on adipogenesis in 3T3-L1 preadipocytes. Mogrol, but not mogrosides, suppressed triglyceride accumulation by affecting early (days 0–2) and late (days 4–8), but not middle (days 2–4), differentiation stages. At the late stage, mogrol increased AMP-activated protein kinase (AMPK) phosphorylation and reduced glycerol-3-phosphate dehydrogenase activity. At the early stage, mogrol promoted AMPK phosphorylation, inhibited the induction of CCAAT/enhancer-binding protein β (C/EBPβ; a master regulator of adipogenesis), and reduced 3T3-L1 cell contents (e.g., clonal expansion). In addition, mogrol, but not the AMPK activator AICAR, suppressed the phosphorylation and activity of the cAMP response element-binding protein (CREB), which regulates C/EBPβ expression. These results indicated that mogrol suppressed adipogenesis by reducing CREB activation in the initial stage of cell differentiation and by activating AMPK signaling in both the early and late stages of this process.

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“…It has been reported that mogrosides have various bioactivities, including antiinflammatory, anti-obesity, anti-diabetic, and anti-allergic effects as well as hepatoprotective effects (Chen et al, 2011;Di et al, 2011;Jin and Lee, 2012;Sun et al, 2012;Xiao et al, 2012;Xiao and Wang, 2013;Song et al, 2014). Recent research has shown that mogroside V (MGV) attenuated LPS-induced acute lung injury and inflammation (Suzuki et al, 2005;Shi et al, 2014;Xu et al, 2015); however, the anti-fibrotic effects of mogrosides on respiratory diseases have not been reported.…”

Section: Introductionmentioning

confidence: 99%

Mogroside IIIE, a Novel Anti-Fibrotic Compound, Reduces Pulmonary Fibrosis through Toll-Like Receptor 4 Pathways

Tao

Yang

Cao

et al. 2017

J Pharmacol Exp Ther

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Idiopathic pulmonary fibrosis is a progressive fibrotic lung disease, and eventually most patients develop respiratory failure with a median survival rate of 2 to 3 years after diagnosis due to the lack of clinically effective therapies. Mogroside IIIE (MGIIIE), a cucurbitane-type compound, was isolated from MGIIIE has shown the strongest inhibition of nitric oxide release, a crucial inflammatory factor, from lipopolysaccharide (LPS)-treated RAW264.7 cells compared with other mogrosides. In the pulmonary fibrosis mouse model induced by bleomycin, MGIIIE treatment attenuated pulmonary fibrosis, indicated as a reduction in myeloperoxidase activity, collagen deposition, and pathologic score. MGIIIE also significantly suppressed expression of several important fibrotic markers, e.g.,-smooth muscle actin, collagen I, transforming growth factor- (TGF-) signal, and metalloproteinases-9/tissue inhibitor of metalloproteinase-1. Furthermore, MGIIIE blocked tansdifferentiation of lung resident fibroblasts into myofibroblast-like cells induced by TGF- or LPS and subsequently inhibited collagen production in lung fibroblasts. These data indicate that MGIIIE is a potent inhibitor for pulmonary fibrosis. In vitro and in vivo mechanistic studies have shown that MGIIIE significantly decreased expression of toll-like receptor 4 (TLR4) and its downstream signals of myeloid differentiation factor 88 (MyD88)/mitogen-activated protein kinase (MAPK), an inflammatory signal essential for extracellular matrix (ECM) deposition in pulmonary fibroblasts. Taken together, these results demonstrate that MGIIIE significantly prevents pulmonary fibrosis by inhibiting pulmonary inflammation and ECM deposition through regulating TLR4/MyD88-MAPK signaling. Our study suggests that MGIIIE may have therapeutic potential for treating pulmonary fibrosis in clinical settings.

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Exploring in vitro, in vivo metabolism of mogroside V and distribution of its metabolites in rats by HPLC-ESI-IT-TOF-MSn

Cited by 58 publications

References 13 publications

Safety of use of Monk fruit extract as a food additive in different food categories

Safety of use of Monk fruit extract as a food additive in different food categories

Mogrol Derived from Siraitia grosvenorii Mogrosides Suppresses 3T3-L1 Adipocyte Differentiation by Reducing cAMP-Response Element-Binding Protein Phosphorylation and Increasing AMP-Activated Protein Kinase Phosphorylation

Mogroside IIIE, a Novel Anti-Fibrotic Compound, Reduces Pulmonary Fibrosis through Toll-Like Receptor 4 Pathways

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