Data on metabolic profiling of healthy human subjects’ plasma before and after administration of the Japanese Kampo medicine maoto

Kitagawa, Hiroyuki; Ohbuchi, Katsuya; Munekage, Masaya; Fujisawa, Kazune; Kawanishi, Yuji; Namikawa, Tsutomu; Mutoh, T.; Shimobori, Chika; Nishi, Akinori; Sadakane, Chiharu; Watanabe, Junko; Yamamoto, Masahiro; Hanazaki, Kazuhiro

doi:10.1016/j.dib.2018.11.116

Cited by 9 publications

(8 citation statements)

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“…Clustering analysis of the kinetic time-course of metabolites can further improve the reliability of annotation. The time-course of four subjects was visualized as a heatmap using the normalized peak area (see Methods) and concentration of maoto components from a preceding research (Kitagawa et al 2019b). The time-course of maoto components in the untargeted analysis matched well with those in the targeted quantitative analysis (Fig.…”

Section: Confirmation Of Re-annotation Results Through the Kinetic Timentioning

confidence: 75%

“…Since the concept of the diagnosis is not fully elucidated, it The kinetic time course of maoto components and metabolites are represented by a heatmap. Regarding the blue-colored components, plasma concentration was used from a previous report (Kitagawa et al 2019b). The intensities of maoto-derived metabolites and concentrations of maoto components were auto-scaled across all experimental samples has been presumed to estimate the host's ability to absorb and metabolize Kampo compounds, which leads to identifying unknown biomarkers reflecting the reactivity to a specific Kampo medicine.…”

Section: Discussionmentioning

confidence: 99%

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Differential annotation of converted metabolites (DAC-Met): Exploration of Maoto (Ma-huang-tang)-derived metabolites in plasma using high-resolution mass spectrometry

et al. 2020

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Introduction Traditional herbal medicine (THM) contains a vast number of natural compounds with varying degrees of pharmacological activity. To elucidate the mode of action, comprehensive metabolite profiling in the plasma before and after administration of THM is essential. Objective The aim of this study was to explore and identify/annotate converted metabolites after administration of THM in humans. Methods We performed untargeted metabolome analysis of human plasma collected before and after administration of maoto (ma-huang-tang), a traditional Japanese Kampo medicine. Maoto-derived metabolites were then selected and annotated following the DAC-Met strategy, which is an annotation method that uses mass differences of major metabolic reactions among the detected peaks and a differential network analysis. Results About 80% of maoto-derived components were found to be converted forms. Following DAC-Met, the structures of 15 previously unidentified metabolites were determined, and five of these were later confirmed with authentic standards. Using published literature, we also reconstructed the metabolic pathway of maoto components in humans. A kinetic timecourse analysis revealed their diverse kinetic profiles. Conclusion The results demonstrated that time-resolved comprehensive metabolite profiling in plasma using the DAC-Met strategy is highly useful for elucidating the complex nature of THM.

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Section: Confirmation Of Re-annotation Results Through the Kinetic Timentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Differential annotation of converted metabolites (DAC-Met): Exploration of Maoto (Ma-huang-tang)-derived metabolites in plasma using high-resolution mass spectrometry

et al. 2020

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“…Hepatic hydrophilic metabolites and lipid mediators were measured by liquid chromatography–tandem mass spectrometry (LC–MS/MS) and gas chromatography–tandem mass spectrometry (GC–MS/MS). Analyses were conducted as previously described [ 14 ] using the Method Packages (Shimadzu, Kyoto, Japan), which contains a mass spectral library, method files specifying the analytical conditions, and data analysis parameters. A more detailed protocol is described in Supplementary Methods 1 .…”

Section: Methodsmentioning

confidence: 99%

Combination therapy of Juzentaihoto and mesenchymal stem cells attenuates liver damage and regresses fibrosis in mice

Iwasawa

Nojiri

Tsuchiya

et al. 2021

Regenerative Therapy

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Background Liver cirrhosis is an end-stage multiple liver disease. Mesenchymal stem cells (MSCs) are an attractive cell source for reducing liver damage and regressing fibrosis; additional therapies accompanying MSCs can potentially enhance their therapeutic effects. Kampo medicines exhibit anti-inflammatory and anti-oxidative effects. Here, we investigated the therapeutic effect of MSCs combined with the Kampo medicine Juzentaihoto (JTT) as a combination therapy in a carbon tetrachloride (CCl4)-induced cirrhosis mouse model. Methods C57BL/6 mice were administered JTT (orally) and/or MSCs (one time, intravenously). The levels of liver proteins were measured in the sera. Sirius Red staining and hydroxyproline quantitation of hepatic tissues and immune cells were conducted, and their associated properties were evaluated. Liver metabolomics of liver tissues was performed. Results JTT monotherapy attenuated liver damage and increased serum albumin level, but it did not effectively induce fibrolysis. JTT rapidly reduced liver damage, in a dose-dependent manner, after a single-dose CCl4 administration. Furthermore, JTT-MSC combination therapy attenuated liver damage, improved liver function, and regressed liver fibrosis. The combination increased the CD4+/CD8+ ratio. JTT had stronger effects on NK and regulatory T cell induction, whereas MSCs more strongly induced anti-inflammatory macrophages. The combination therapy further induced anti-inflammatory macrophages. JTT normalized lipid mediators, and tricarboxylic acid cycle- and urea cycle-related mediators effectively. Conclusions The addition of JTT enhanced the therapeutic effects of MSCs; this combination could be a potential treatment option for cirrhosis.

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“…The analysis was performed based on a previously described method. 30,31) The extracted samples were loaded onto an ion-exchange Solid Phase Extraction (SPE) cartridge and the target metabolites were retained in the SPE. Derivatization was performed using methoxyamine/ pyridine and N-methyl-N-(trimethylsilyl) trifluoroacetamide, which were sequentially added directly to the SPE.…”

Section: Measurement Of Xfp Extracellular Fluxmentioning

confidence: 99%

Role of Mitochondrial Dysfunction in the Pathogenesis of Cisplatin-Induced Myotube Atrophy

Matsumoto

Sekine

Nahata

et al. 2022

Biological & Pharmaceutical Bulletin

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Muscle atrophy is commonly observed during cisplatin chemotherapy, leading to a reduced QOL in cancer patients. Reduced skeletal muscle mass caused by cisplatin treatment results from the activation of ubiquitin ligases-Atrogin-1 and MuRF1, but the precise mechanisms are poorly understood. In this study, we investigated the possible involvement of mitochondrial dysfunction, including reactive oxygen species (ROS) generation and ATP production, in cisplatin-induced muscle atrophy. Skeletal C2C12 myotubes were treated with cisplatin, and gene and protein expression were evaluated. Mitochondrial mass, membrane potential, and ROS levels were measured using fluorescent dyes. Mitochondrial respiratory function, ATP production rates, and glycolytic capacity were also analyzed using an extracellular flux analyzer. Metabolomic analyses were performed using gas chromatography-tandem mass spectrometry. Cisplatin treatment reduced myosin heavy chain expression by activating the ubiquitin-proteasome system. Increased ROS production was observed after cisplatin treatment, followed by significant changes in apoptosis-related gene expression and decrease in mitochondrial mass, membrane potential, respiration, and ATP production. Glycolytic capacity and tricarboxylic acid (TCA) cycle metabolite levels were reduced with cisplatin treatment. Mitochondriatargeted antioxidant mitoquinone mesylate prevented up-regulation of Atrogin-1 gene expression and restored myosin heavy chain levels, accompanied by a decrease in ROS generation, but not mitochondrial ATP production. We concluded that cisplatin-induced myotube atrophy was associated with mitochondrial dysfunction. Reducing ROS generation, rather than promoting ATP production, could be a useful therapeutic strategy for preventing cisplatin-induced muscle atrophy.

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Data on metabolic profiling of healthy human subjects’ plasma before and after administration of the Japanese Kampo medicine maoto

Cited by 9 publications

References 3 publications

Differential annotation of converted metabolites (DAC-Met): Exploration of Maoto (Ma-huang-tang)-derived metabolites in plasma using high-resolution mass spectrometry

Differential annotation of converted metabolites (DAC-Met): Exploration of Maoto (Ma-huang-tang)-derived metabolites in plasma using high-resolution mass spectrometry

Combination therapy of Juzentaihoto and mesenchymal stem cells attenuates liver damage and regresses fibrosis in mice

Role of Mitochondrial Dysfunction in the Pathogenesis of Cisplatin-Induced Myotube Atrophy

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