Soyghurt Potentially Controls the Level of sFlt1 and PLGF in Preeclampsia Maternal Serum-Induced Placental Trophoblast Cell in vitro.

Purpose: To observe the effect of soya yoghurt (Soyghurt), which is high in flavonoid substance, on the expression of preeclampsia biomarkers (sFLT-1 and PLGF) on preeclampsia serum-induced trophoblast primary cell culture isolated from placental tissue. Methods: The trophoblast primary culture was induced by preeclampsia serum (10%). The Soyghurt treatment was performed with 2.5%, 5%, and 7.5% Soyghurt supernatant concentrations in culture media. The expression of preeclampsia markers, sFLT-1 and PLGF, were evaluated using ELISA. Results: Expression of sFLT-1 on preeclampsia-induced cell culture treated with Soyghurt was significantly lowered compared to the untreated group (p<0.01). However, no significant difference was observed in the PLGF levels of all groups induced by preeclampsia serum (p>0.05). Conclusion: This study demonstrates the potential effect of Soyghurt's in balancing preeclampsia marker expression by inhibiting the expression of sFLT-1 in preeclampsia serum -induced trophoblast cells.

Anthocyanin-Containing Purple Sweet Potato (Ipomoea batatas L.) Synbiotic Yogurt Inhibited 3T3-L1 Adipogenesis by Suppressing White Adipocyte-Specific Genes.

Purpose: We unravel the effect of anthocyanin-containing purple sweet potato synbiotic yogurt (PSPY) on 3T3-L1 adipocyte differentiation and its fundamental molecular mechanisms. Methods: Molecular docking simulation was performed to observe and identify the affinity and interaction between bioactive compounds and targeted proteins. MDI (isobutylmethylxanthine, dexamethasone, and insulin)-containing medium, a cocktail that stimulates adipogenesis, was used in this study. The toxic effect possibility of the yogurt product was evaluated using 3-[4, 5-dimethylthiazol-2-yl]-2.5 diphenyl tetrazolium bromide (MTT) assay. A 0.25%, 0.5%, 1%, and 5% (v/v) plain or purple sweet potato yogurt supernatant was given to 3T3-L1 preadipocyte culture medium from 24 h after seeding until day 11 of MDI-induced differentiation. The mRNA expression and lipid accumulation were analyzed using RT-qPCR and Oil red O staining, respectively, on day 11 after differentiation induction. Results: In silico study suggested that anthocyanin-derived compounds have the potential to inhibit peroxisome proliferator activated receptor gamma (PPAR-γ), a master regulator for white adipogenesis. Anthocyanin-containing PSPY significantly suppressed the expression of Pparg, Adipoq, Slc2a4, and Pgc1a. PSPY significantly suppressed Pparg with 1% and 5% concentrations, while with a concentration of 0.25%, PSPY significantly suppressed Adipoq expression as compared to control. Significant inhibition of Slc2a4 and Pgc1a was observed starting from a 0.25% concentration of PSPY. The suppression of adipogenic genes was also observed with the treatment of plain yogurt; however, the effects were relatively lower than the PSPY. The group treated with 1% and 5% of PSPY also showed inhibition effects on lipid accumulation. Conclusion: This study demonstrated PSPY inhibition effect on white adipocyte differentiation through suppression of Pparg and its downstream genes, Adipoq and Slc2a4, indicating the potential of this yogurt as a functional food for obesity management and prevention.

Acute and sub-chronic oral toxicity study of purple sweet potato (Ipomoea batatas [L.] Lam) yogurt in mice (Mus musculus).

Background and Aim: Food safety is an important aspect to be evaluated in preventing any potentially harmful side effects of food product such as yogurt. The purple sweet potato yogurt product was developed to combine the benefits of probiotic activities in yogurt and the bioactive effects of anthocyanin in purple sweet potato. This study was performed to investigate acute and sub-chronic oral toxicity of purple sweet potato yogurt (PSPY) in mice. Materials and Methods: Acute oral toxicity was evaluated by a 14-day observation for any clinical sign of toxicity on fifteen female balb/c mice following a single dosage of PSPY (nil, 2 or 5 g/kg body weight). The sub-chronic oral toxicity study was conducted by feeding PSPY to four groups of mice with the dose of 0, 12, 20, and 40 g/kg body weight for 28 days, and another group of mice receiving 40 g/kg body weight purple sweet potato for 14 days longer to observe any delayed toxicity effect. Body weight and clinical signs of toxicity were observed daily. Liver and kidney macroscopy and relative organ weight, liver histology, liver enzyme, and hematology profile analyses were done at the end of the study. Results: There were no signs of toxicity observed from the acute toxicity study and no abnormality in body weight, relative organ weight, and gross organ examination. In the sub-chronic toxicity study, there were no clinical signs of toxicity, no significant differences in body weight, relative liver weight, liver enzymes, hematology profile, or abnormality in gross and histological examination of the liver. Conclusion: This study shows that oral administration of PSPY in mice up to 5 g/kg body weight did not result in acute toxicity, while the dosage up to 40 g/kg body weight did not lead to sub-chronic toxicity.