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111 results for “Saponins”
Figure 2 in Afrosymetric method for quantifying saponins in Chenopodium Quinoa Willd. from Colombia
Figure 2. Percentage of saponin from quinoa materials in each Afrosymetric method. Different letters indicate significant differences according to the Fisher's mean comparison test (LSD) (p≤0.05). Vertical bars indicate standard error (n=3).
Figure 1 in Afrosymetric method for quantifying saponins in Chenopodium Quinoa Willd. from Colombia
Figure 1. Foam column in quinoa materials for each Afrosymetric method. (A) Standard Afrosymetric Method (MAE); (B) modified afrosymetric method (MAM); (C) Rapid Afrosymetric Method (MAR).
Figure 3 in Afrosymetric method for quantifying saponins in Chenopodium Quinoa Willd. from Colombia
Figure 3. Dendrogram of five quinoa materials, grouped by the saponin content in the seeds.
Impact of saponin on detached leaves under different Cd stress treatments
<p>Cd-0, Cd-10, Cd-100, and Cd-1000 represent detached leaves exposed to Cd2+ treatment, respectively. S-0, S-10, and S-20 represent leaves incubated with distilled water, 10 mg/ L saponin, and 100 mg/ L saponin. </p>
Fig. 5 in Acylated saponins and flavonoid glycosides from the fruits of Stewartia koreana
Fig. 5. Effect of compound 15 on PCSK9 and LDLR in the HepG2 human hepatocellular carcinoma cell line. (A) Expression of PCSK9 was assayed by qRTPCR in cells treated with compound 15 (2, 10 and 50 μM), and berberine (Ber10, 10 μM) for 24 h. (B) Expression of PCSK9 and LDLR were assayed by western blot in cells treated with compound 15 (10, 40 and 50 μM), and berberine (Ber20, 20 μM) for 24 h *p <0.05.
Fig. 4 in Acylated saponins and flavonoid glycosides from the fruits of Stewartia koreana
Fig. 4. Effect of compounds from S. koreana on PCSK9 and LDLR in the HepG2 human hepatocellular carcinoma cell line. (A) Expression of PCSK9 mRNA was assayed by qRT-PCR in cells treated with compounds (50 μM), and berberine (Ber20, 20 μM) for 24 h. (B) Expression of LDLR mRNA was assayed by qRTPCR in cells treated with compounds (50 μM), and berberine (Ber20, 20 μM) for 24 h.
Fig. 2 in Acylated saponins and flavonoid glycosides from the fruits of Stewartia koreana
Fig. 2. (A) Key HMBC (from H to C) and 1H–1H COSY correlations for compounds 1–3. (B) ROESY correlations of aglycone of compound 1.
Fig. 4 in Dammarane-type saponins with proprotein convertase subtilisin/kexin type 9 inhibitory activity from Gynostemma pentaphyllum
Fig. 4. Effects of compounds 1–11 on cell viabilities and PCSK9 inhibitory activities in HepG2 cells. (A–B) The cell viability assay of compounds 1–11 with different concentrations (5, 10, 20, 40, and 80 μM) in HepG2 cells. (C) Effect of compounds 1–11 (20 μM) and BBR (berberine, 10 μM) on the expression of PCSK9 in HepG2 cells. (D) Effect of compounds 1–11 (10 μM) and BBR (berberine, 10 μM) on the expression of PCSK9 in HepG2 cells. (E) Effect of compounds 2, 5 (5 μM) and BBR (berberine, 10 μM) on the expression of PCSK9 in HepG2 cells. The expression of PCSK9 was assayed by ELISA in HepG2 cells treated with compounds 1–11 and BBR (berberine) for 24 h. The results were calculated as the means ± SD of three independent experiments. ###p <0.001 vs control group; *p <0.05, **p <0.01, ***p <0.001 vs model group.
Fig. 8 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 8. Effect of furoasparoside D (4) and furoasparoside E (5) on blood glucose levels of the STZ-induced diabetic rats. After injecting STZ, animals were treated with either compounds at 100 mg/kg or metformin at 300 mg/kg dose and blood glucose levels were monitored at various time intervals. Shown are the glycemic response curves (a) and incremental AUC at 5 h (b) in diabetic rats after treatment. Data are expressed as the mean ± S.E.M., n = 5. *P <0.05, **P <0.01 relative to diabetic control (DC).
Fig. 4. GLUT4 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 4. GLUT4 translocation stimulatory potential of the ethanolic (A001) and butanolic (F004) extracts of A. racemosus in L6-GLUT4myc myotubes. Data are mean ± SEM, n = 4, *P <0.05, **P <0.01, ***P <0.001, ****P <0.0001 compared to control.
Fig. 7 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 7. Effect of furoasparoside E (5) and metformin on cell viability of L6 cells. Cells were treated with increasing concentrations of 5 and metformin for 24 h and cytotoxic effect was monitored by MTT assay.
Fig. 1 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 1. Structures of undescribed furostanol saponins, furoasparoside A-E (1–6) isolated from Asparagus racemosus.
Fig. 6 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 6. Effect of furoasparoside E (5) on Akt (Ser- 473) phosphorylation (a & b) and AMPK (Thr-172) phosphorylation (c & d) in L6 myotubes. (a and b) Cells we treated overnight with compound 5 (10 μM) with final 3 h in serum free medium and stimulated (Insulin) or not (Basal) with insulin (100 nM or 10 min) and subjected to western analysis. (c and d) Cells were treated overnight with increasing concentrations of furoasparoside E (5) and subjected to western analysis as described in methods section. Shown are representative immunoblots (a and c) and densitometric quantification of phospho-Akt relative to total Akt (b) and phospho-AMPKα relative to total AMPK (d). Results of three independent experiments are presented as mean ± S.E.M. **P <0.01 relative to control condition.
Fig. 9 in Furostanol saponins from Asparagus racemosus as potential hypoglycemic agents
Fig. 9. Effect of furoasparoside E (5) and metformin on blood glucose levels of the db/db mice. Mice were treated daily with compound 5 (100 mg/kg) or metformin (300 mg/kg) for 21 consecutive day and blood glucose levels were monitored daily and OGGT at day 15 and day 21. Shown are the data of body weight (a), blood glucose (b) and glycemic response curve and AUC during OGTT at day 15 (c and d) and day 21 (e and f) in db/db mice during compound 5 treatment. Data are expressed as the mean ± S.E.M., n = 5. *P <0.05 relative to control animals.
Fig. 3. A in Phytochemical and biological diversity of triterpenoid saponins from family Sapotaceae: A comprehensive review
Fig. 3. A) Cumulative histogram plotting the number of annually reported saponins (1990–2021), B) Percentage of the major triterpene aglycone of which the total identified saponins in family Sapotaceae were reported.
Fig. 1 in Phytochemical and biological diversity of triterpenoid saponins from family Sapotaceae: A comprehensive review
Fig. 1. Chemical structure of the major triterpenoid aglycones identified in family Sapotaceae, 1: protobassic acid, 38: 16-α-hydroxyprotobassic acid, 81: oleanolic acid, 84: bayogenin.
Fig. 6 in Undescribed glucosylceramide, flavonol triglycoside, and oleanane saponin from the halophyte Agathophora alopecuroides: Promising candidates for stimulating ceramide synthesis
Fig. 6. Effect of isolated compounds (1–11) and methanol extract of A. alopecuroides (12) on mRNA expression levels of CerS3 involved in ceramide synthesis in HaCaT cells. HaCaT cells were cultured in the presence or absence of tested samples at 10–400 μg/mL for 24 h. RT-PCR analysis was performed as described in Material and methods part. Data are expressed as means ± SD of at least three independent experiments; *p <0.05, **p <0.01.
Fig. 5 in Undescribed glucosylceramide, flavonol triglycoside, and oleanane saponin from the halophyte Agathophora alopecuroides: Promising candidates for stimulating ceramide synthesis
Fig. 5. Effect of extract and isolated compounds on viability of HaCaT cells. A: Compounds 1–3; B: Compounds 4–6; C: Compounds 7–9; D: Compounds 10–11 and methanol extract (12). Cell viability was measured by MTT assay. HaCaT cells (1 105 cells/well) were seeded to a 96-well plate and incubated overnight. The cell × viability was performed after treatment with extract and isolated compounds (1–400 μg/mL) for 24 h. Values are expressed as the mean ± SD of three wells; *p <0.05, **p <0.01.
Fig. 2 in Transcriptome analysis of Paris polyphylla var. yunnanensis illuminates the biosynthesis and accumulation of steroidal saponins in rhizomes and leaves
Fig. 2. Genes involved in Paris saponin biosynthesis. (a) Genes participated in the MVA and MEP pathways. (b) Genes participated in the downstream of saponin backbone biosynthesis.
Fig. 4 in Transcriptome analysis of Paris polyphylla var. yunnanensis illuminates the biosynthesis and accumulation of steroidal saponins in rhizomes and leaves
Fig. 4. An overview of DEG expression patterns and GO enrichments. (a) Heatmap of expression values for all DEGs. (b) GO enrichments of DEGs, with displaying the top fifteen subcategories for each category.
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