Antioxidant effect of mogrosides against oxidative stress induced by palmitic acid in mouse insulinoma NIT-1 cells

Xu, Qing; Chen, S.Y.; Deng, Lijuan; Feng, Leping; Huang, Liyingzi; Rao, Yu

doi:10.1590/1414-431x20133163

Cited by 21 publications

(9 citation statements)

References 18 publications

(22 reference statements)

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“… 29 Mogrosides were shown to exert an antioxidant effect in insulinoma cells by reducing the intracellular ROS level and regulating the expression of genes related to glucose metabolism under palmitic acid-induced oxidative stress. 30 A study on the antioxidant and anti-glycosylation activity of S. grosvenorii extracts showed that mogrosides are H 2 O 2 free radical scavengers that also exert strong effects on DPPH and ABTS. 31 …”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Mogroside V on Oxidative Stress Induced by H2O2 in Skin Fibroblasts

Mo¹,

Fu²,

Zhao³

et al. 2021

DDDT

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Purpose Damage caused by oxidative stress leads to the premature aging of cells. Mogrosides, the main active components of Siraitia grosvenorii , have strong antioxidant activity; however, it is unclear whether mogroside V (MV) exerts these effects in skin cells. This was investigated in the present study by evaluating the protective effects of MV against oxidative damage induced by hydrogen peroxide (H 2 O 2 ) in skin fibroblasts. Methods Mouse skin fibroblasts (MSFs) were treated with H 2 O 2 and cell viability, total antioxidant capacity, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and antioxidant enzyme activity were assessed. Results Treatment with MV reduced the ROS level and MDA content in MSFs treated with H 2 O 2 . This was accompanied by increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities. Conclusion MV reduces H 2 O 2 -induced oxidative stress and enhances endogenous antioxidant activity in skin fibroblasts. Thus, MV can potentially be used as an ingredient in anti-aging cosmetic products.

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Section: Discussionmentioning

confidence: 99%

Protective Effects of Mogroside V on Oxidative Stress Induced by H2O2 in Skin Fibroblasts

Mo¹,

Fu²,

Zhao³

et al. 2021

DDDT

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“…Saturated FAs treatment is associated with an increase in ROS in rodent β-cell lines [ 41 , 53 , 98 , 185 , 214 , 215 , 216 , 217 , 218 , 219 , 220 ] (not in a human β-cell line [ 15 ]), and ROS increase was found to be involved in PA-induced apoptosis in rat INS-1 β-cells [ 221 ]. OA treatment causes this effect only in experimental models, where it also results in cell death induction [ 53 , 56 , 222 , 223 ].…”

Section: Mechanisms Mediating Pro-apoptotic Effects Of Saturated Fatty Acidsmentioning

confidence: 99%

Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells

Šrámek

Němcová‐Fürstová

Kovář

2021

IJMS

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Pancreatic β-cell failure and death contribute significantly to the pathogenesis of type 2 diabetes. One of the main factors responsible for β-cell dysfunction and subsequent cell death is chronic exposure to increased concentrations of FAs (fatty acids). The effect of FAs seems to depend particularly on the degree of their saturation. Saturated FAs induce apoptosis in pancreatic β-cells, whereas unsaturated FAs are well tolerated and are even capable of inhibiting the pro-apoptotic effect of saturated FAs. Molecular mechanisms of apoptosis induction by saturated FAs in β-cells are not completely elucidated. Saturated FAs induce ER stress, which in turn leads to activation of all ER stress pathways. When ER stress is severe or prolonged, apoptosis is induced. The main mediator seems to be the CHOP transcription factor. Via regulation of expression/activity of pro- and anti-apoptotic Bcl-2 family members, and potentially also through the increase in ROS production, CHOP switches on the mitochondrial pathway of apoptosis induction. ER stress signalling also possibly leads to autophagy signalling, which may activate caspase-8. Saturated FAs activate or inhibit various signalling pathways, i.e., p38 MAPK signalling, ERK signalling, ceramide signalling, Akt signalling and PKCδ signalling. This may lead to the activation of the mitochondrial pathway of apoptosis, as well. Particularly, the inhibition of the pro-survival Akt signalling seems to play an important role. This inhibition may be mediated by multiple pathways (e.g., ER stress signalling, PKCδ and ceramide) and could also consequence in autophagy signalling. Experimental evidence indicates the involvement of certain miRNAs in mechanisms of FA-induced β-cell apoptosis, as well. In the rather rare situations when unsaturated FAs are also shown to be pro-apoptotic, the mechanisms mediating this effect in β-cells seem to be the same as for saturated FAs. To conclude, FA-induced apoptosis rather appears to be preceded by complex cross talks of multiple signalling pathways. Some of these pathways may be regulated by decreased membrane fluidity due to saturated FA incorporation. Few data are available concerning molecular mechanisms mediating the protective effect of unsaturated FAs on the effect of saturated FAs. It seems that the main possible mechanism represents a rather inhibitory intervention into saturated FA-induced pro-apoptotic signalling than activation of some pro-survival signalling pathway(s) or metabolic interference in β-cells. This inhibitory intervention may be due to an increase of membrane fluidity.

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“…Overload of lipids in nonadipose tissues that affects cellular functions, namely, lipotoxicity, could also induce cell hypertrophy or even cell death [ 2 ]. Evidence suggests that accumulation of PA, the major saturated fatty acids in blood, may give rise to lipotoxicity in cardiomyocytes by induction of oxidative stress [ 3 ] and persistent ER stress [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid

Zhao

Song

et al. 2016

Oxidative Medicine and Cellular Longevity

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Palmitic acid (PA) is known to cause cardiomyocyte dysfunction. Cardiac hypertrophy is one of the important pathological features of PA-induced lipotoxicity, but the mechanism by which PA induces cardiomyocyte hypertrophy is still unclear. Therefore, our study was to test whether necroptosis, a receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3-) dependent programmed necrosis, was involved in the PA-induced cardiomyocyte hypertrophy. We used the PA-treated primary neonatal rat cardiac myocytes (NCMs) or H9c2 cells to study lipotoxicity. Our results demonstrated that cardiomyocyte hypertrophy was induced by PA treatment, determined by upregulation of hypertrophic marker genes and cell surface area enlargement. Upon PA treatment, the expression of RIPK1 and RIPK3 was increased. Pretreatment with the RIPK1 inhibitor necrostatin-1 (Nec-1), the PA-induced cardiomyocyte hypertrophy, was attenuated. Knockdown of RIPK1 or RIPK3 by siRNA suppressed the PA-induced myocardial hypertrophy. Moreover, a crosstalk between necroptosis and endoplasmic reticulum (ER) stress was observed in PA-treated cardiomyocytes. Inhibition of RIPK1 with Nec-1, phosphorylation level of AKT (Ser473), and mTOR (Ser2481) was significantly reduced in PA-treated cardiomyocytes. In conclusion, RIPKs-dependent necroptosis might be crucial in PA-induced myocardial hypertrophy. Activation of mTOR may mediate the effect of necroptosis in cardiomyocyte hypertrophy induced by PA.

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Antioxidant effect of mogrosides against oxidative stress induced by palmitic acid in mouse insulinoma NIT-1 cells

Cited by 21 publications

References 18 publications

Protective Effects of Mogroside V on Oxidative Stress Induced by H2O2 in Skin Fibroblasts

Protective Effects of Mogroside V on Oxidative Stress Induced by H2O2 in Skin Fibroblasts

Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells

Inhibition of Receptor Interacting Protein Kinases Attenuates Cardiomyocyte Hypertrophy Induced by Palmitic Acid

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