51 research outputs found

    Optimal extraction parameters of Theabrownin from Sichuan Dark Tea

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    Background: Sichuan Dark Tea is a popular beverage with hypolipidemic and lifting greasy properties in the minority neighborhoods of Sichuan and Tibet regions. The theabrownin, an important pigment of dark tea, has been proven for the role of the hypolipidemic property in Sichuan Dark Tea. The objective of the study investigated the extraction process of theabrownin.Materials and Methods: Theabrownin was extracted from Sichuan Dark Tea with water and organic solvents. The quadratic regression orthogonally rotational combinational design experiment was performed to obtain the optimal extraction parameters.Results: The extraction yield of theabrownin was significantly influenced by both water extraction temperature and solid-liquid ratio, and the contribution of these factors on theabrownin yield was as follows: water temperature﹥solid-liquid ratio﹥organic solvent temperature. Moreover, the polynomial regression model established could predict the experimental value accurately.Conclusion: The optimum extraction process of theabrownin from Sichuan Dark Tea was established, which water temperature at 65.69-77.88℃, organic solvent temperature at 13.65-17.48℃ and a solid liquid ratio of 1:43.58-1:50.75(g/mL).Keywords: theabrownin; extraction; optimization; Sichuan Dark TeaAbbreviations list: SDT: Sichuan Dark Tea; TB: Theabrowni

    Dimethyloxalylglycine Prevents Bone Loss in Ovariectomized C57BL/6J Mice through Enhanced Angiogenesis and Osteogenesis

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    <div><p>Hypoxia-inducible factor 1-α (HIF-1α) plays a critical role in angiogenesis-osteogenesis coupling during bone development and bone regeneration. Previous studies have shown that 17β-estradiol activates the HIF-1α signaling pathway and that mice with conditional activation of the HIF-1α signaling pathway in osteoblasts are protected from ovariectomy (OVX)-induced bone loss. In addition, it has been shown that hypoxia facilitates the osteogenic differentiation of mesenchymal stem cells (MSCs) and modulates Wnt/β-catenin signaling. Therefore, we hypothesized that activation of the HIF-1α signaling pathway by hypoxia-mimicking agents would prevent bone loss due to estrogen deficiency. In this study, we confirmed the effect of dimethyloxalylglycine (DMOG), a hypoxia-mimicking agent, on the HIF-1α signaling pathway and investigated the effect of DMOG on MSC osteogenic differentiation and the Wnt/β-catenin signaling pathway. We then investigated the effect of DMOG treatment on OVX-induced bone loss. Female C57BL/6J mice were divided into sham, OVX, OVX+L-DMOG (5 mg/kg/day), and OVX+H-DMOG (20 mg/kg/day) groups. At sacrifice, static and dynamic bone histomorphometry were performed with micro computed tomography (micro-CT) and undecalcified sections, respectively. Bone strength was assessed with the three-point bending test, and femur vessels were reconstructed and analyzed by micro-CT. Serum vascular endothelial growth factor (VEGF), osteocalcin, and C-terminal telopeptides of collagen type(CTX) were measured by ELISA. Tartrate-resistant acid phosphatase staining was used to assess osteoclast formation. Alterations in the HIF-1α and Wnt/β-catenin signaling pathways in the bone were detected by western blot. Our results showed that DMOG activated the HIF-1α signaling pathway, which further activated the Wnt/β-catenin signaling pathway and enhanced MSC osteogenic differentiation. The micro-CT results showed that DMOG treatment improved trabecular bone density and restored the bone microarchitecture and blood vessels in OVX mice. Bone strength was also partly restored in DMOG-treated OVX mice. Dynamic bone histomorphometric analysis of the femur metaphysic revealed that DMOG increased the mineralizing surface, mineral apposition rate, and bone formation rate. The serum levels of VEGF and osteocalcin were higher in DMOG-treated OVX mice. However, there were no significant differences in serum CTX or in the number of tartrate-resistant acid phosphatase-stained cells between DMOG-treated OVX mice and OVX mice. Western blot results showed that DMOG administration partly rescued the decrease in HIF-1α and β-catenin expression following ovariectomy. Collectively, these results indicate that DMOG prevents bone loss due to ovariectomy in C57BL/6J mice by enhancing angiogenesis and osteogenesis, which are associated with activated HIF-1α and Wnt/β-catenin signaling pathways.</p></div

    Activation of HIFa Pathway in Mature Osteoblasts Disrupts the Integrity of the Osteocyte/Canalicular Network

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    <div><p>The hypoxia-inducible factors (HIFs), HIF-1α and HIF-2α, are the central mediators of the homeostatic response that enables cells to survive and differentiate in low-oxygen conditions. Previous studies indicated that disruption of the von Hippel-Lindau gene (<i>Vhl</i>) coincides with the activation of HIFα signaling. Here we show that inactivation of <i>Vhl</i> in mature osteoblasts/osteocytes induces their apoptosis and disrupts the cell/canalicular network. VHL-deficient (ΔVHL) mice exhibited a significantly increased cortical bone area resulting from enhanced proliferation and osteogenic differentiation of the bone marrow stromal cells (BMSCs) by inducing the expression of β-catenin in the BMSC. Our data suggest that the VHL/HIFα pathway in mature osteoblasts/osteocytes plays a critical role in the bone cell/canalicular network and that the changes of osteocyte morphology/function and cell/canalicular network may unleash the bone formation, The underlying mechanism of which was the accumulation of β-catenin in the osteoblasts/osteoprogenitors of the bone marrow.</p></div

    Bone quality of the femur as measured by the three-point bending test.

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    <p>The groups designated with an asterisk shown significant differences with Sham group (<i>P<0.05</i>), the groups designated with a pound sign shown significant differences with OVX group (<i>P<0.05</i>).</p><p>Bone quality of the femur as measured by the three-point bending test.</p

    Osteoclast numbers assayed by tartrate-resistant acid phosphatase staining of femoral sections.

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    <p>(A)Osteoclast counting results showed that DMOG treatment had no obvious effect on OVX-enhanced osteoclast formation. Original magnification, ×100. <b>Dynamic bone formation illustrated by double tetracycline labeling.</b> (B) DMOG administration promoted bone formation, as evidenced by improved MS/BS, MAR, and BFR/BS. Original magnification, ×200. <i>P</i><0.05 for comparisons among the groups designated with an asterisk.</p

    Biochemical markers of bone in serum as measured by ELISA.

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    <p>The groups designated with an asterisk shown significant differences with Sham group (<i>P<0.05</i>), the groups designated with a pound sign shown significant differences with OVX group (<i>P<0.05</i>).</p><p>Biochemical markers of bone in serum as measured by ELISA.</p

    HIF-1α, VEGF, and β-catenin expression in bone samples detected by western blot.

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    <p>(A) HIF-1α, VEGF, and β-catenin expression was lower in OVX mice than in sham mice. However, DMOG treatment increased HIF-1α, VEGF, and β-catenin expression relative to expression in the OVX group. <b>Effects of DMOG administration on tibial ALP, osteocalcin, RUNX-2, and RANKL/OPG mRNA expression in OVX mice assessed by real-time PCR.</b> (B) ALP/β-actin ratio. (C) Osteocalcin/β-actin ratio. (D) RUNX-2/β-actin ratio. (E) RANKL/OPG/β-actin ratio. <i>P</i><0.05 for comparisons among the groups designated with an asterisk.</p

    Effect of DMOG on MSC osteogenic differentiation and Wnt/β-catenin signaling.

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    <p>(A) ALP and alizarin red S staining. (B) DMOG promoted RUNX-2 and osterix mRNA expression. (C) DMOG increased β-catenin mRNA and protein expression. (D) DMOG increased nuclear β-catenin, LEF-1, TCF-1, and HIF-1α protein expression. These effects were attenuated by YC-1. <i>P</i><0.05 for comparisons among the groups designated with an asterisk.</p
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