Suggesting kaempferol and CXCR4 Agonist drug kaempferide do not influence cell viability of OA-treated HepG2

March 9, 2023

Suggesting kaempferol and CXCR4 Agonist drug kaempferide do not influence cell viability of OA-treated HepG2 cells.Int. J. Mol. Sci. 2021, 22,5 ofFigure three. Adjustments in viability of HepG2 cells soon after incubation with kaempferol and kaempferide. (a) Chemical structure of kaempferol. (b) Chemical structure of kaempferide. (c) HepG2 cell viability after incubation with kaempferol. (d) HepG2 cell viability soon after incubation with kaempferide. (e) No transform in HepG2 cell viability by co-incubation of OA and kaempferol for 48 h. (f) No adjust in HepG2 cell viability by co-incubation of OA and kaempferide for 48 h. Data have been expressed as Mean SD of 3 independent experiments (n = 3). p 0.01, compared with vehicle-treated control.2.3. Kaempferol and Kaempferide Suppressed Lipid Accumulation in OA-Treated HepG2 Cells To investigate no matter whether kaempferol and kaempferide influence intracellular lipid accumulation, oil red O staining was performed. 0.five mM OA brought on prominent increase lipid droplets accumulation in HepG2 cells, compared using the handle group (Figure 4a,b). Noticeably, incubation with kaempferol and kaempferide for 48 h cIAP-1 Inhibitor drug Decreased the accumulation of intracellular lipid droplets in a dose-dependent manner, compared with OA group. Moreover, kaempferide lowered the intracellular TG levels at concentration of 10 and 20 (p 0.01), compared using the OA group (Figure 4c). Kaempferol therapy induced a trend of reduction in TG content, but statistical significance was not accomplished. The results suggest that kaempferol and kaempferide attenuate OA-induced lipid accumulation in HepG2 cells.Int. J. Mol. Sci. 2021, 22,6 ofFigure 4. Kaempferol and kaempferide suppressed lipid accumulation in OA-induced HepG2 cells. HepG2 cells had been incubated with unique concentrations of kaempferol or kaempferide inside the presence of 0.5 mM OA for 48 h. (a) Oil red O staining inside the cultured HepG2 cells. (b) Visualization of intracellular lipid droplets in HepG2 cells beneath microscope (100magnification). (c) Quantification of intracellular TG contents in HepG2 cells. Data were expressed as mean SD of 3 independent experiments (n = 3). ## p 0.01, compared with vehicle-treated handle cells (Con); p 0.01, compared with OA-treated cells (OA).two.4. Kaempferol and Kaempferide Decreased Expression of SREBP1, FAS and SCD-1 in OA-Treated HepG2 Cells To identify the underlying mechanism for the inhibitory effect of kaempferol and kaempferide on lipid accumulation, expression of lipogenesis-related proteins, SREBP1, FAS and SCD-1 had been analyzed by western blot. As shown in Figure five, kaempferide dosedependently reduced the expression of SREBP1 in HepG2 cells (p 0.01), compared with OA group. Reduction was also observed in expression of FAS and SCD-1 (p 0.01), which was regulated by SREBP1. In contrast, treatment with kaempferol showed little impact on expression of SREBP1, FAS and SCD-1 (Figure 5). These findings recommend kaempferide may possibly decrease lipid accumulation in OA-treated HepG2 cells by way of decreasing the expression of lipogenic proteins.Int. J. Mol. Sci. 2021, 22,7 ofFigure five. Kaempferol and kaempferide reduced expression of SREBP1, FAS and SCD-1 in OA-treated HepG2 cells. HepG2 cells had been treated with different concentrations of kaempferol or kaempferide within the presence of 0.five mM OA for 48 h followed by western blot analysis of expression of SREBP1, FAS and SCD-1. (a) Representative blots. (b) Quantification benefits of the expression of FAS. (c) Quantification results in the expressio.