Dataset Information

Carbon Nanoparticles Inhibit ?-Glucosidase Activity and Induce a Hypoglycemic Effect in Diabetic Mice.

ABSTRACT: New, improved therapies to reduce blood glucose are required for treating diabetes mellitus (DM). Here, we investigated the use of a new nanomaterial candidate for DM treatment, carbon nanoparticles (CNPs). CNPs were prepared by carbonization using a polysaccharide from Arctium lappa L. root as the carbon source. The chemical structure and morphology of the CNPs were characterized using Fourier-transform infrared spectroscopy, X-ray photoelectron spectroscopy, elemental analysis, and transmission electron microscopy. CNPs were spherical, 10-20 nm in size, consisting of C, H, O, and N, and featuring various functional groups, including C=O, C=C, C-O, and C-N. In vitro, the as-prepared CNPs could inhibit ?-glucosidase with an IC50 value of 0.5677 mg/mL, which is close to that of the reference drug acarbose. Moreover, in vivo hypoglycemic assays revealed that the CNPs significantly reduced fasting blood-glucose levels in mice with diabetes induced by high-fat diet and streptozocin, lowering blood glucose after intragastric administration for 42 days. To the best of our knowledge, this is the first report of CNPs exhibiting ?-glucosidase inhibition and a hypoglycemic effect in diabetic mice. These findings suggest the therapeutic potential of CNPs for diabetes.

SUBMITTER: Shao T

PROVIDER: S-EPMC6767295 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature

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Carbon Nanoparticles Inhibit Α-Glucosidase Activity and Induce a Hypoglycemic Effect in Diabetic Mice.

Shao Taili T Yuan Pingchuan P Zhu Lei L Xu Honggang H Li Xichen X He Shuguang S Li Ping P Wang Guodong G Chen Kaoshan K

Molecules (Basel, Switzerland) 20190906 18

New, improved therapies to reduce blood glucose are required for treating diabetes mellitus (DM). Here, we investigated the use of a new nanomaterial candidate for DM treatment, carbon nanoparticles (CNPs). CNPs were prepared by carbonization using a polysaccharide from <i>Arctium lappa</i> L. root as the carbon source. The chemical structure and morphology of the CNPs were characterized using Fourier-transform infrared spectroscopy, X-ray photoelectron spectroscopy, elemental analysis, and tran ...[more]

PMID: 31500170

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Project description:BackgroundHonokiol is one of the main bioactive constituents of the traditional Chinese herbal drug Magnolia bark (Cortex Magnoliae officinalis, Hou Po). The aim of this study was to probe its anti-type 2 diabetes mellitus effects and the underlying mechanism.MethodsType 2 diabetic mouse model was established by intraperitoneally injecting with streptozotocin. Fasting blood glucose, body weight, and lipid profile were measured. The subcutaneous adipose tissue, skeletal muscle, and liver were isolated as well as homogenized. The phospho-insulin receptor β-subunit (IRβ), IRβ, phospho-AKT, AKT, phospho-ERK1/2, ERK1/2, phosphotyrosine, and actin were examined by Western blot assay. Cell viability or cytotoxicity was analyzed by using MTT method. The inhibitory potencies of honokiol on the protein tyrosine phosphatase 1B (PTP1B) activity were performed in reaction buffer. Molecular docking and dynamic simulation were also analyzed.ResultsIn in vivo studies, oral treatment with 200 mg/kg honokiol for 8 weeks significantly decreases the fasting blood glucose in type 2 diabetes mellitus mice. The phosphorylations of the IRβ and the downstream insulin signaling factors including AKT and ERK1/2 significantly increase in adipose, skeletal muscle, and liver tissue of the honokiol-treated mice. Moreover, honokiol enhanced the insulin-stimulated phosphorylations of IRβ, AKT, and ERK1/2 in a dose-dependent manner in C2C12 myotube cells. Meanwhile, honokiol enhanced insulin-stimulated GLUT4 translocation. Importantly, honokiol exhibited reversible competitive inhibitory activity against PTP1B with good selectivity in vitro and in vivo. Furthermore, using molecular docking and dynamic simulation approaches, we determined the potential binding mode of honokiol to PTP1B at an atomic level.ConclusionThese findings indicated the hypoglycemic effects of honokiol and its mechanism that honokiol improved the insulin sensitivity by targeting PTP1B. Therefore, our study may highlight honokiol as a promising insulin sensitizer for the therapy of type 2 diabetes.

Project description:Carbon black nanoparticles (CBNP) are the most widely produced nanomaterial and are thus a concern for occupational exposures. CBNPs are known to cause inflammation upon inhalation; however, detailed time course data to evaluate the changing nature of inflammatory responses have not been evaluated. In this study, we investigate the short- and longer-term effects of CBNP following a single intratracheal exposure. Female C57BL/6BomTac mice were exposed to CBNPs (printex 90) via a single intratracheal instillation of 162 µg/mouse alongside vehicle controls. Mice were examined 3 hours (hrs), and 1, 2, 3, 4, 5, 14, and 42 days (d) post-exposure. Global gene expression was assessed using DNA microarrays in parallel with analysis of pulmonary inflammation assessed as bronchoalveolar lavage (BAL) cell counts and DNA strand breaks assessed by the comet assay. Pulmonary inflammation in terms of increased neutrophil influx was obverved at all time points. Increased levels of DNA strand breaks were observed in BAL cells 3 hrs post exposure and in lung tissue 2-5 d post exposure. Approximately 2600 significant differentially expressed genes (±1.5 fold; p ≤0.05) across all of the time-points in the lungs of exposed mice were identified upon comparison to time-matched controls. Transcriptional alterations were enriched for genes involved in common respiratory infectious diseases. The perturbed biological processes and pathways were primarily related to immune-inflammatory responses and acute phase responses, consistent with the BAL inflammatory profiles. Gene and pathway analysis revealed a biphasic inflammatory response, with changes occurring as early as 3 hrs post-exposure and declining to base-levels by 3 d post-exposure, but with inflammatory pathways increasing in response again at 14 d and persisting to 42 d post-exposure. Other perturbed pathways included DNA repair and apoptosis, cell cycle regulation, and muscle contraction. Single CBNP exposure induced a biphasic inflammatory response that lasted until 42 d post-exposure. Such persistent inflammatory response raises concerns over the chronic effects of CBNP exposure since the administered dose corresponds to pulmonary deposition in mice during nine 8-hour working days at the current occupational exposure limit for carbon black.

Dataset Information

Carbon Nanoparticles Inhibit ?-Glucosidase Activity and Induce a Hypoglycemic Effect in Diabetic Mice.

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Carbon Nanoparticles Inhibit Α-Glucosidase Activity and Induce a Hypoglycemic Effect in Diabetic Mice.

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