Evidence for Quercetin as a Dietary Supplement for the Treatment of Cardio-Metabolic Diseases in Pregnancy: A Review in Rodent Models
Abstract
:1. Introduction
2. Quercetin
3. Quercetin Intervention in Rodents during Pregnancy and Lactation
4. Quercetin Intervention in Gestational Diabetes Mellitus
4.1. GDM: A Pregnant Disorder Linked to Oxidative Stress and Inflammation
4.2. Quercetin Supplementation in Rodent Models of GDM
5. Quercetin Intervention in Gestational Undernutrition
5.1. Gestational Undernutrition: A Pregnant Disorder Linked to Oxidative Stress and Inflammation
5.2. Quercetin Supplementation in Rodent Models of Gestational Undernutrition
6. Quercetin Supplementation in High-Fat Diet Rodent Models Inducing Maternal Overweight and Dyslipidemia
7. Quercetin Supplementation in Rodent Models of Pregnancy Hypertension Syndromes
8. Conclusions and Future Perspectives
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Acknowledgments
Conflicts of Interest
Abbreviations
References
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Reference | Type of Study | Dose | Duration | Maternal Outcomes | Embryonic, Fetal, and Neonatal Outcomes |
---|---|---|---|---|---|
Cao et al., 2016 [24] | Experimental (mice) | 100 mg/kg | Embryonic period: 7.5 to 10.5. | No difference in maternal glucose. | ↓ Decreased the neural tube defects rate; ↓ Apoptosis in the dorsal neural tube of the embryos and levels of Caspase-3; ↓ Nos2 level in the neural tissues of the embryos; ↓ Levels of protein S nitrosylation in the neural tube; ↑ Enzyme levels of SOD1 and SOD2; ↓ Levels of 4-HNE and MDA; ↑ Expression of redox regulating and DNA damage; There was the presence of quercetin metabolites in the embryo. |
Tan et al., 2018 [39] | Experimental (mice) | 100 mg/kg | Embryonic period: 6.5 to 9.5. | The authors did not evaluate maternal outcomes. | ↓ Neural tube defects; ↓ The apoptotic signals were lower in the neural tube regions; ↓ Nos2 expression in the embryos. ↑ The levels of Sod1 in the embryos; ↓ Nitrosative and oxidative stresses in the endoplasmic reticulum (ER); ↓ The expression of p65. |
Bolouki et al., 2020 [40] | Experimental (mice) | 30 mg/kg | 4 weeks before conception. | ↓ Levels of blood glucose; ↑ The number of embryos per mouse; ↑ Levels of serum 17β-estradiol; ↑ Estradiol/progesterone ratio. | ↑ The embryo morphological distribution to the well-developed stages; ↑ IGF1r, integrin αvβ3, and Cox2 mRNA express these genes in the blastocyst; ↓ Expression of the Caspase3 gene; Can activate the nuclear Wnt-β-catenin signaling pathway. |
Mahabady et al., 2021 [41] | Experimental (rats) | 75 mg/kg | On 0, 7, 14, and 20 days of gestation. | The authors did not evaluate maternal outcomes. | ↓ LIM thickness; ↓ Mean the number of glycogen cells; ↑ Increased placental adiponectin expression; ↓ Placental expression of AdipoR1 and AdipoR2. |
Reference | Type of Study | Dose | Duration | Maternal Outcomes | Embryonic, Fetal, and Neonatal Outcomes | Adulthood Outcomes |
---|---|---|---|---|---|---|
Anachuna et al., 2020 [10] | Experimental (rats) | 50, 100 and 200 mg/kg | 21–22 days—during pregnancy e/or 22 days during weaning. | The authors did not evaluate maternal outcomes. | ↓ Stillbirths; ↑ Nose-tail lenghts at P1 and P22. | ↓ Onset puberty. |
Anachuna et al., 2020 [54] | Experimental (rats) | 50, 100 and 200 mg/kg | 21–22 days—during pregnancy e/or 22 days during weaning. | ↑ Maternal weight. | ↑ Body weight undernourished rats until weaning | ↓ Body weight; ↑ Leptin levels; ↓ Ghrelin levels; ↓ Brain oxidative stress. |
Sato et al., 2013 [55] | Experimental (rats) | 80–110 mg/day | 10 to 22 postnatal days. | The authors did not evaluate maternal outcomes. | ↓ TG blood level; ↑ AMPK. | ↑ Body weight; ↑ Adiponectin; ↑ AMPK. |
Reference | Type of Study | Dose | Duration | Maternal Outcomes | Embryonic, Fetal and Neonatal Outcomes | Adulthood Outcomes |
---|---|---|---|---|---|---|
Adeyemi et al., 2021 [60] | Experimental (rats subjected to HFD contained 45% of fat) | 150 mg/kg | From the beginning of gestation to gestational day 19. | The authors did not evaluate maternal outcomes. | ↓ MDA and NO concentration in the placenta and liver tissues in neonate male rats; ↓ SOD concentration in the placenta and liver tissues in neonatal rats; ↑ Total antioxidant capacity of the liver in neonates. | The authors did not evaluate adulthood outcomes. |
Adeyemi et al., 2021 [61] | Experimental (rats subjected to HFD contained 45% of fat) | 150 mg/kg | From the beginning of gestation to gestational day 19. | The authors did not evaluate maternal outcomes. | ↓ Expression of mRNA of TNF-α and IL-1β in placenta and hypothalamus of neonatal rats; ↑ NF-κB mRNA level in placenta. | The authors did not evaluate adulthood outcomes. |
Liang et al., 2009 [62] | Experimental (mice subjected to HFD contained 60% of fat) | 66 mg/kg | For 4 weeks before breeding. | The authors did not evaluate maternal outcomes. | The authors did not evaluate embryonic, fetal, and neonatal outcomes. | ↓ Blood glucose and plasma insulin levels of 6- and 12-month offspring; ↓ Systolic and diastolic blood pressure of 6- and 12-month offspring. |
Takashima et al., 2021 [11] | Experimental (mice subjected to HFD contained 30% of fat) | 1.0% | Before breeding, throughout gestation, lactation until 13 weeks of postnatal days. | ↑ Body weight; ↑ Liver weight. | ↑ Total CHO, non-HDL-C, and HDL-C levels of pups; ↓ Gastric inhibitory polypeptide levels of pups. | The authors did not evaluate adulthood outcomes. |
Wu et al., 2014 [59] | Experimental (rats subjected to HFD contained about 42% of fat) | 50, 100 or 200 mg/kg | Throughout gestation and lactation. | Did not change body weight and blood glucose levels; Improved lipid profile (↓ TG, CHO, and ↑ HDL-C levels). | The authors did not evaluate embryonic, fetal, and neonatal outcomes. | ↓ Blood glucose and insulin levels in adult rats; Improved lipid profile (↓ TG, CHO) in adult rats; ↓ Expression of TNF-α, IL-6 in adult rats; ↓ Endoplasmic reticulum stress in liver and adipose tissues; ↓ In p-JNK and NF-κB protein expression. |
Reference | Type of Study | Dose | Duration | Maternal Outcomes | Embryonic, Fetal and Neonatal Outcomes |
---|---|---|---|---|---|
Li et al., 2020 [12] | Experimental (rats subjected to preeclampsia model) | The authors did not inform the dose of treatment. | The authors did not inform the duration of treatment. | ↓ Systolic blood pressure; ↓ Proteinuria. | Reversed imbalance of angiogenic factors production in the placenta; ↓ Placental growth factor; ↓ Placental expression of TNF-α, IL-6, and MCP-1 levels; ↓ Placental MDA; ↑ Placenta weight; ↓ Reabsorbed fetuses %; ↑ Pups weight; ↑ Placenta weight. |
Sun et al., 2020 [68] | Experimental (rats subjected to gestational hypertension) | 10 mg/kg, 20 mg/kg, or 50 mg/kg. | From gestational day 14 to gestational day 21. | ↓ Systolic and diastolic blood pressure; ↓ Plasma level of ET-1, sFLT1; ↑ Plasma level of VEGF; ↓ Plasma levels of TNF-α and IL-6, and ↑ IL-10. | ↓ ET-1, ETAR expression in placenta tissue; ↑ Fetal weight; Did not change placental weight; ↑ Fetal weight/ Placenta weight; ↓ Reabsorbed fetuses %. |
Tanir et al., 2005 [23] | Experimental (rats subjected to preeclampsia model) | 10 mg/kg | Single administration at gestational day 17. | Did not change blood pressure;↓ Plasma MDA levels; ↓ Erythrocyte CAT and SOD levels; ↓ Proteinuria. | Did not change the birth weight of pups; ↑ Neonatal survival (higher percentages of liveborn pups and lower rates of dead pups). |
Yang et al., 2019 [67] | Experimental (rats subjected to preeclampsia model) | 2 mg/kg | From gestational day 4 to gestational day 19. | ↓ Proteinuria; ↓ Plasma MDA levels; Did not change TNF-α; ↓ Plasma levels of IL-6. | Did not change placental MDA; Did not change placental expression of TNF-α and IL-6; Did not change relative mRNA expression of uterus VEGF and sFlt-1. |
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Costa, P.C.T.d.; de Souza, E.L.; Lacerda, D.C.; Cruz Neto, J.P.R.; Sales, L.C.S.d.; Silva Luis, C.C.; Pontes, P.B.; Cavalcanti Neto, M.P.; de Brito Alves, J.L. Evidence for Quercetin as a Dietary Supplement for the Treatment of Cardio-Metabolic Diseases in Pregnancy: A Review in Rodent Models. Foods 2022, 11, 2772. https://doi.org/10.3390/foods11182772
Costa PCTd, de Souza EL, Lacerda DC, Cruz Neto JPR, Sales LCSd, Silva Luis CC, Pontes PB, Cavalcanti Neto MP, de Brito Alves JL. Evidence for Quercetin as a Dietary Supplement for the Treatment of Cardio-Metabolic Diseases in Pregnancy: A Review in Rodent Models. Foods. 2022; 11(18):2772. https://doi.org/10.3390/foods11182772
Chicago/Turabian StyleCosta, Paulo César Trindade da, Evandro Leite de Souza, Diego Cabral Lacerda, José Patrocínio Ribeiro Cruz Neto, Ludmilla Christine Silva de Sales, Cristiane Cosmo Silva Luis, Paula Brielle Pontes, Marinaldo Pacífico Cavalcanti Neto, and José Luiz de Brito Alves. 2022. "Evidence for Quercetin as a Dietary Supplement for the Treatment of Cardio-Metabolic Diseases in Pregnancy: A Review in Rodent Models" Foods 11, no. 18: 2772. https://doi.org/10.3390/foods11182772