scholarly journals Evaluation of the Effect of a Grape Seed Tannin Extract on Wine Ester Release and Perception Using In Vitro and In Vivo Instrumental and Sensory Approaches

Foods ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 93
Author(s):  
Carolina Muñoz-González ◽  
Celia Criado ◽  
María Pérez-Jiménez ◽  
María Ángeles Pozo-Bayón
Keyword(s):  
Grape Seed ◽  
Stir Bar Sorptive Extraction ◽  
Gas Chromatography Mass Spectrometry ◽  
Dependent Manner ◽  
Tannin Extract ◽  
Ethyl Hexanoate ◽  
In Vivo Experiments ◽  
Ethyl Decanoate

This study aimed to systematically evaluate the effect of a commercial grape seed tannin extract (GSE) fully characterized (53% monomers, 47% procyanidins) on wine ester release and perception using a global approach. The behavior of two esters (ethyl hexanoate, ethyl decanoate) was studied in a control wine or in the same wine supplemented with the GSE in preconsumption (in vitro headspace-stir bar sorptive extraction-gas chromatography mass spectrometry (HS-SBSE-GC/MS) and orthonasal perception) and consumption (intraoral-HS-SBSE-GC/MS and dynamic retronasal perception) conditions. For the compound ethyl hexanoate, no significant differences (p > 0.05) among wines were observed in the in vitro analyses while they were observed in the three in vivo experiments (p < 0.05). Thus, the wine supplemented with the GSE showed lower (35%) in vivo release and ortho (36%) and retronasal (16%) perception scores than the control wine. Overall, this suggests that components of the GSE could interact with this compound, directly and/or through complexes with oral components, affecting its release and conditioning its perception. However, perceptual interactions and effects of polyphenols on oral esterases cannot be discarded. On the contrary, the compound ethyl decanoate was not significantly affected by the addition of GSE. In conclusion, the addition of tannin extracts to wines can modulate aroma perception in a compound-dependent manner.

Levosimendan prevents doxorubicin-induced cardiotoxicity in time- and dose-dependent manner: implications for inotropy

2019 ◽  
Vol 116 (3) ◽  
pp. 576-591 ◽  
Author(s):  
Panagiotis Efentakis ◽  
Aimilia Varela ◽  
Evangelia Chavdoula ◽  
Fragiska Sigala ◽  
Despina Sanoudou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Female Breast Cancer ◽  
Bolus Administration ◽  
Dependent Manner ◽  
In Vivo Experiments ◽  
Doxorubicin Cardiotoxicity ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Abstract Aims Levosimendan (LEVO) a clinically-used inodilator, exerts multifaceted cardioprotective effects. Case-studies indicate protection against doxorubicin (DXR)-induced cardiotoxicity, but this effect remains obscure. We investigated the effect and mechanism of different regimens of levosimendan on sub-chronic and chronic doxorubicin cardiotoxicity. Methods and results Based on preliminary in vivo experiments, rats serving as a sub-chronic model of doxorubicin-cardiotoxicity and were divided into: Control (N/S-0.9%), DXR (18 mg/kg-cumulative), DXR+LEVO (LEVO, 24 μg/kg-cumulative), and DXR+LEVO (acute) (LEVO, 24 μg/kg-bolus) for 14 days. Protein kinase-B (Akt), endothelial nitric oxide synthase (eNOS), and protein kinase-A and G (PKA/PKG) pathways emerged as contributors to the cardioprotection, converging onto phospholamban (PLN). To verify the contribution of PLN, phospholamban knockout (PLN−/−) mice were assigned to PLN−/−/Control (N/S-0.9%), PLN−/−/DXR (18 mg/kg), and PLN−/−/DXR+LEVO (ac) for 14 days. Furthermore, female breast cancer-bearing (BC) mice were divided into: Control (normal saline 0.9%, N/S 0.9%), DXR (18 mg/kg), LEVO, and DXR+LEVO (LEVO, 24 μg/kg-bolus) for 28 days. Echocardiography was performed in all protocols. To elucidate levosimendan’s cardioprotective mechanism, primary cardiomyocytes were treated with doxorubicin or/and levosimendan and with N omega-nitro-L-arginine methyl ester (L-NAME), DT-2, and H-89 (eNOS, PKG, and PKA inhibitors, respectively); cardiomyocyte-toxicity was assessed. Single bolus administration of levosimendan abrogated DXR-induced cardiotoxicity and activated Akt/eNOS and cAMP-PKA/cGMP-PKG/PLN pathways but failed to exert cardioprotection in PLN−/− mice. Levosimendan’s cardioprotection was also evident in the BC model. Finally, in vitro PKA inhibition abrogated levosimendan-mediated cardioprotection, indicating that its cardioprotection is cAMP-PKA dependent, while levosimendan preponderated over milrinone and dobutamine, by ameliorating calcium overload. Conclusion Single dose levosimendan prevented doxorubicin cardiotoxicity through a cAMP-PKA-PLN pathway, highlighting the role of inotropy in doxorubicin cardiotoxicity.

scholarly journals Radioprotective Effect of Grape Seed Proanthocyanidins In Vitro and In Vivo

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Yijuan Huang ◽  
Hainan Zhao ◽  
Kun Cao ◽  
Ding Sun ◽  
Yanyong Yang ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
White Blood Cells ◽  
Survival Rates ◽  
Grape Seed ◽  
Dependent Manner ◽  
Grape Seed Proanthocyanidins ◽  
Speed Up ◽  
Dna Strand

We have demonstrated that grape seed proanthocyanidins (GSPs) could effectively scavenge hydroxyl radical (•OH) in a dose-dependent manner. Since most of the ionizing radiation- (IR-) induced injuries were caused by•OH, this study was to investigate whether GSPs would mitigate IR-induced injuries in vitro and in vivo. We demonstrated that GSPs could significantly reduce IR-induced DNA strand breaks (DSBs) and apoptosis of human lymphocyte AHH-1 cells. This study also showed that GSPs could protect white blood cells (WBC) from IR-induced injuries, speed up the weight of mice back, and decrease plasma malondialdehyde (MDA), thus improving the survival rates of mice after ionizing radiation. It is suggested that GSPs have a potential as an effective and safe radioprotective agent.

scholarly journals miR-30e targets GLIPR-2 to modulate diabetic nephropathy: in vitro and in vivo experiments

2017 ◽  
Vol 59 (2) ◽  
pp. 181-190 ◽  
Author(s):  
Dong Zhao ◽  
Jinhua Jia ◽  
Hong Shao
Keyword(s):  
High Glucose ◽  
Luciferase Reporter ◽  
Dependent Manner ◽  
Luciferase Reporter Gene ◽  
Related Factors ◽  
Qrt Pcr ◽  
In Vivo Experiments ◽  
Renal Tubular

The objectives of this study are to investigate the effect of miR-30e targeting GLIPR-2 on the pathological mechanism of DN. The renal tissues of db/db and db/m mice at different age of weeks were stained with PAS. qRT-PCR was applied to detect the expression of miR-30e and GLIPR-2, not only in the renal tissues of mice but also in the renal tubular epithelial cells (RTECs). By luciferase reporter gene assays, we found the 3′-UTR of the GLIPR-2 mRNA as a direct target of miR-30e. The RTECs cultured in high glucose were divided into blank control, NC, miR-30e mimics, miR-30e inhibitors, miR-30e inhibitor + si-GLIPR-2 and si-GLIPR-2 groups. MTT and flow cytometry were utilized to measure the proliferation and apoptosis of RTECs, while qRT-PCR and Western blot to detect the expression of GLIPR-2- and EMT-related factors. The following results were obtained: In the renal tissues of over 8-week-old db/db mice and the RTECs cultured for 6 h in high glucose, miR-30e was downexpressed while GLIPR-2 was upregulated in a time-dependent manner. Besides, overexpression of miR-30e and si-GLIPR-2 can not only greatly improve the proliferation of RTECs cultured in high glucose, but also downregulate the apoptosis rate of RTECs and the expressions of GLIPR-2, vimentin, α-SMA, Col-I and FN and upregulate E-cadherin. Moreover, si-GLIPR-2 can reverse the proliferation reduction, GLIPR-2 and EMT occurrence caused by the downexpression of miR-30e in RTECs. In conclusion, miR-30e is downregulated in DN, and the overexpression of miR-30e can inhibit GLIPR-2, promote the proliferation of RTECs and inhibit EMT, ultimately avoid leading to renal fibrosis in DN.

scholarly journals Identification of Sake Extract as a New Anti-melanogenic Ingredient by in vitro and Clinical Trials

2013 ◽  
Vol 8 (11) ◽  
pp. 1934578X1300801
Author(s):  
Jeong-Ah Hwang ◽  
Myeong-Jin Goh ◽  
Eun-Joo Kim ◽  
Myong-Ryul Lee ◽  
Nok-Hyun Park ◽  
...  
Keyword(s):  
Skin Diseases ◽  
Alcoholic Beverage ◽  
Human Keratinocytes ◽  
Equivalent Model ◽  
Dependent Manner ◽  
Melanin Production ◽  
In Vivo Experiments ◽  
Skin Hyperpigmentation

Overproduction of melanin is the cause of skin hyperpigmentation, which is related to several skin diseases and cosmetic concerns. Sake is a Japanese alcoholic beverage produced from rice and water by fermentation, but is little known for its effect on melanogenesis. To identify the effect of sake extract on melanin synthesis, a melanin assay was performed in melan-A murine melanocytes. Sake extract treatment significantly inhibited melanin production in a dose-dependent manner, and tyrosinase, the rate-limiting enzyme of melanogenesis, decreased significantly at the protein level. Further investigations were performed with multiple assay systems; a sake extract reduced melanin production in melan-A/SP-1 murine cell co-culture, and also in MelanoDermTM, a skin equivalent model of human keratinocytes-melanocytes. Finally, subjects were treated with a formula containing the sake extract. Topical application of the sake extract product improved skin lightness (L*) significantly within 7 days. We identified sake extract as a new anti-melanogenic ingredient through in vitro and in vivo experiments. These results suggest that a sake extract can be used to improve skin hyperpigmentation.

scholarly journals The fate of methylmercury through the formation of bismethylmercury sulfide as an intermediate in mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yumi Abiko ◽  
Yusuke Katayama ◽  
Wenyang Zhao ◽  
Sawako Horai ◽  
Kenji Sakurai ◽  
...  
Keyword(s):  
Ex Vivo ◽  
Intraperitoneal Administration ◽  
Distal Colon ◽  
The Body ◽  
Gas Chromatography Mass Spectrometry ◽  
Dependent Manner ◽  
Free System ◽  
A Cell

AbstractA previous study by our group indicated that methylmercury (MeHg) is biotransformed to bismethylmercury sulfide [(MeHg)2S)] by interaction with reactive sulfur species (RSS) produced in the body. In the present study, we explored the transformation of MeHg to (MeHg)2S in the gut and the subsequent fate of (MeHg)2S in vitro and in vivo. An ex vivo experiment suggested the possibility of the extracellular transformation of MeHg to (MeHg)2S in the distal colon, and accordingly, the MeHg sulfur adduct was detected in the intestinal contents and feces of mice administered MeHg, suggesting that (MeHg)2S is formed through reactions between MeHg and RSS in the gut. In a cell-free system, we found that (MeHg)2S undergoes degradation in a time-dependent manner, resulting in the formation of mercury sulfide and dimethylmercury (DMeHg), as determined by X-ray diffraction and gas chromatography/mass spectrometry, respectively. We also identified DMeHg in the expiration after the intraperitoneal administration of (MeHg)2S to mice. Thus, our present study identified a new fate of MeHg through (MeHg)2S as an intermediate, which leads to conversion of volatile DMeHg in the body.

scholarly journals LY900009 Regulates RANKL-Induced Osteoclast Formation and LPS-Induced Bone Resorption

2020 ◽  
Author(s):  
Tao Huang ◽  
Congyun Zhao ◽  
Yi Zhao ◽  
Yuan Zhou ◽  
Lei Wang ◽  
...  
Keyword(s):  
Bone Resorption ◽  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Osteoclast Formation ◽  
Dependent Manner ◽  
In Vivo Experiments ◽  
Secretase Inhibitor ◽  
Formation Number

Abstract To investigate the suppressive function of LY900009, a potent-secretase inhibitor, on RANKL-induced osteoclastogenesis. The cytotoxicity of LY900009 was evaluated. The suppressive effect and possible molecular mechanism of LY900009 on RANKL-induced osteoclastogenesis was evaluated both in vitro and in vivo. The IC50 of LY900009 was 2.93 mM. LY900009 treatment at different doses (100 nM, 200 nM, and 400 nM) effectively reduced osteoclast formation (number and arear) in a dose-dependent manner. The qPCR result shows that LY900009 attenuates RANKL-induced osteoclast formation and NFATc1 protein expression. The in vivo experiments demonstrated the inhibitory effect of LY900009 on LPS-induced bone resorption. LY900009 could potently inhibit osteoclastogenesis and bone resorption by down-regulating Notch/MAPK/Akt - mediated NFATc1 reduction in vitro. In accordance with the in vitro observations, we confirmed that LY900009 attenuated LPS-induced osteolysis in mice. In conclusion, our findings indicate that Notch was a potential therapeutic target which could be used for osteolytic diseases treatment.

Vitamin D as a Regulator of Adipocyte Differentiation Effects in vivo and in vitro

2018 ◽  
Vol 69 (3) ◽  
pp. 731-734
Author(s):  
Alin Constantin Pinzariu ◽  
Teodor Oboroceanu ◽  
Florin Zugun Eloae ◽  
Ioana Hristov ◽  
Victor Vlad Costan ◽  
...  
Keyword(s):  
Vitamin D ◽  
Adipocyte Differentiation ◽  
Dependent Manner ◽  
Omental Adipose Tissue ◽  
In Vivo Experiments ◽  
Dose Dependent ◽  
Stromal Stem Cells

The age-associated adiposity and the effect of long-term vitamin D was studied in vitamin D deficient rats. In in vivo experiments, the influence of a 9 months of vitamin D treatment (weekly oral gavage with 0.125 mg vitamin D3 (5000 IU)/100g body weight) on the adipocyte precursors from the omental adipose tissue was examinated. In in vitro experiment, rat adipose-derived mesenchymal stromal/stem cells (ASCs) were induced to differentiate into adipocytes in the presence or absence of 25(OH)D3 (0.25, 25, and 2500 nmol/L). ASCs derived from vitamin D-treated animals showed an increase adipogenic potential as compared to vitamin D-deficient rats. The addition of 25(OH)D3 inhibits the adipocyte differentiation and lipid deposition in a dose dependent manner.

Involvement of capsaicin-sensitive primary afferent fibers in regulation of jejunal alanine absorption

1995 ◽  
Vol 268 (4) ◽  
pp. G695-G699 ◽  
Author(s):  
C. F. Nassar ◽  
K. A. Barada ◽  
L. E. Abdallah ◽  
W. S. Hamdan ◽  
A. M. Taha ◽  
...  
Keyword(s):  
Inhibitory Effect ◽  
Dependent Manner ◽  
Primary Afferent ◽  
In Vivo Experiments ◽  
Afferent Fibers ◽  
Cervical Vagotomy ◽  
Primary Afferent Fibers

Capsaicin-sensitive primary afferent fibers (CSPA) in the small intestine regulate many functions through the release of peptides and neurotransmitters. This study was undertaken to assess the role of CSPA in the regulation of jejunal alanine absorption in the rat. In a series of in vivo experiments, the effects of the sensory neurotoxin capsaicin on small intestinal alanine absorption were evaluated. In vitro experiments were also done to study its effects on alanine uptake by isolated jejunal strips and mucosal scrapings. Jejunal alanine absorption was reduced by 27% when capsaicin (160 and 800 microM) was perfused intraluminally and by 21% when it was applied topically to the cervical vagi. On the other hand, bilateral cervical vagotomy and reversible block of vagal CSPA increased alanine absorption by 29 and 41%, respectively. In vitro, capsaicin reduced alanine uptake by intestinal strips in a dose-dependent manner. Maximal inhibition (36.5%) occurred at 400 microM with the mean ineffective concentration at 87 microM. Alanine uptake by jejunal mucosal scrapings, however, was decreased only by 6.7% when incubated with 1,600 microM capsaicin. These data suggest that vagal CSPA exerts a tonic inhibitory effect on alanine absorption and that capsaicin's inhibitory effect on alanine absorption is mediated largely by the capsaicin-sensitive afferent fibers.

scholarly journals Grape Seed Procyanidins Inhibit the Growth of Breast Cancer MCF-7 Cells by Down-Regulating the EGFR/VEGF/MMP9 Pathway

2021 ◽  
Vol 16 (2) ◽  
pp. 1934578X2199169
Author(s):  
Fan-ting Kong ◽  
Chen-xi He ◽  
Fan-lei Kong ◽  
Su-fen Han ◽  
Xiang-shun Kong ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cell Apoptosis ◽  
Growth Factor Receptor ◽  
Grape Seed ◽  
Dependent Manner ◽  
Flow Cytometric Data ◽  
Mcf 7

Breast cancer is the most common invasive cancer in women and the second leading cause of cancer death in women. However, it is not clear about its effective treatments. As a potential anticancer agent, grape seed procyanidins (GSPs) have been shown to inhibit the proliferation of various cancer cells in vitro and in vivo. In this study, it was shown that GSPs significantly inhibit MCF-7 cell proliferation in a concentration/time-dependent manner. The flow cytometric data clearly demonstrated that GSPs cause cell cycle arrest in the G2/M phase, followed by cell apoptosis. Moreover, it also confirmed that growth inhibition mediated by treatment with GSPs is related to the induction of apoptosis due to p53 elevation, purportedly by inhibition of the epidermal growth factor receptor (EGFR)/vascular endothelial growth factor (VEGF)/matrix metalloproteinase 9 (MMP9) pathway. Taken together, these findings suggest that GSPs inhibit MCF-7 cells proliferation and induce cell apoptosis by suppressing EGFR/VEGF/MMP9 pathway.

scholarly journals Atom-Precise Fluorescent Copper Cluster for Tumor Microenvironment Targeting and Transient Chemodynamic Cancer Therapy

2021 ◽  
Author(s):  
Zhenzhen Yang ◽  
Anli Yang ◽  
Wang Ma ◽  
Kai Ma ◽  
Ya-Kun Lv ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Therapy ◽  
Dependent Manner ◽  
Metal Nanoclusters ◽  
Concentration Dependent Manner ◽  
In Vivo Experiments ◽  
Low Cytotoxicity ◽  
High Cytotoxicity

Abstract Background: Reactive oxygen species (ROS) have been widely studied for cancer therapy. Nevertheless, instability and aspecific damages to cellular biomolecules limited the application effect. Recently, significant research efforts have been witnessed in the flourishing area of metal nanoclusters (NCs) with atomically precise structures for targeted release of ROS but few achieved success towards targeting tumor microenvironment.Results: In this work, we reported an atomically precise nanocluster Cu6(C4H3N2S)6 (Cu6NC), which could slowly break and generate ROS once encountered with acidic. The as-prepared Cu6NC demonstrated high biological safety and efficient chemodynamic anti-tumor properties. Moreover, Cu6NC enabled transient release of ROS and contained targeting behavior led by the tumor microenvironment. Both in vitro and in vivo experiments confirmed that Cu6NC demonstrated a low cytotoxicity for normal cells, while presented high cytotoxicity for tumor cells with a concentration-dependent manner.Conclusions: This work not only reported a promising candidate for chemodynamic cancer therapy, but also paved the route to address clinical issues at the atomic level.

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