INCLUSION OF QUERCETIN IN TREATMENT REDUCES THE LEVEL OF INTERLEUKIN 6 IN WOMEN WITH IRON DEFICIENCY ANEMIA AND OBESITY
According to the modern concepts of obesity (O), there is a condition of chronic low intensity inflammation with high content of proinflammatory cytokines, involving transcription factors, in particular nucleic Kb (NF-kB), which may be accompanied by a change in the concentration of iron in the serum. Quercetin is positioned as an anti-inflammatory agent with suppressive effects on NF-kB. The aim of the research was to determine the effect of quercetin inclusion on the systemic inflammatory markers in the comprehensive treatment of women with iron deficiency anemia (IDA) and O. Methods: 30 women with IDA and O participated in the study. Hemogram indicators, parameters of iron exchange (serum iron, ferritin, hepcidin, total iron binding capacity of serum, saturation of transferrin by iron) and inflammation markers were evaluated: C-reactive protein (CRP) and interleukin-6 (IL-6) in serum before and after treatment with iron sulfate. All patients were females of an average age of 40.3±7.59 years. In the distribution of patients based on the origin of the disease, the severity of IDA and basic indicators, there was no reliable difference between the groups (p>0.05). In the process of treatment, CRP and hepcidin had a significant difference in the comparison and study group (p<0.05), but in contrast, there was no difference between them on the 60th ± 3 days of treatment (p<0.05). IL-6 on the 60th ± 3 days of treatment revealed a significant decrease in the study group as opposed to the comparison group (p<0.05). In the course of treatment, ferritin had a significant difference between the comparison and study groups (p<0.05). Conclusion. Comprehensive treatment with inclusion of quercetin in female patients with IDA and O reduces the level of IL-6 and promotes the recovery of the iron depot.
2. Fadєєva G.A. Klіnіko-іmunologіchna efektivnіst' zastosuvannya kverzetinu u chvorich na bronchіal'nu astmu u poєdnannі іz vіszeral'nim ozhirіnnyam. Vіsnik Sums'kogo derzhavnogo unіversitetu. Serіya Medizina. 2009;2 (T.1): 162-167.
3. Bekri S., Gual P. Increased adipose tissue expression of hepcidin insevere obesity is independent from diabetes and NASH . Gastroenterology. 2006; 131: 788-796.
4. Cheng HL, Bryant CE, Rooney KB et al. Iron, hepcidin and inflammatory status of young healthy overweight and obese women in Australia. PloS One. 2013; 8(7):e68675. doi.org/10.1371/journal.pone.0068675
5. Egert S, Boesch-Saadatmandi C, Wolffram S, et al. Serum lipid and blood pressure responses to quercetin vary in overweight patients by apolipoprotein E genotype. J Nutr 2010;140:278-284.
6. Ganz T. Hepcidin, a key regulator of iron metabolism and mediator of anemia of inflammation. Blood. 2003; 102(3):783–788.
7. Greenberg AS, Obin MS. Obesity and the role of adipose tissue in inflammation and metabolism. Am J Clin Nutr. 2006; 83:461-465.
8. Kaĭdashev IP. NF-kB activation as a molecular basis of pathological process by metabolic syndrome. Fiziol Zh. 2012;58(1):93-101. Review. Ukrainian.
9. Karl JP, Lieberman HR, Cable SJ et al. Poor iron status is not associated with overweight or overfat in non-obese pre-menopausal women. J Am Coll Nutr. 2009; 28(1): 37–42.
10. Rogers JT: Ferritin translation by interleukin-1 and interleukin-6: the roleof sequences upstream of the start codons of the heavy and lightsubunit genes. Blood 1996; 87:2525-2537.
11. Sanad M, Osman M, Gharib A. Obesity modulate serum hepcidin and treatment outcome of iron deficiency anemia in children: A case control study. Italian Journal of Pediatrics. 2011;37:34. doi.org/10.1186/1824-7288-37-34
12. Yanoff LB, Menzie CM, Denkinger B, Sebring NG, McHugh T, Remaley AT, Yanovski JA: Inflammation and iron deficiency in the hypoferremia of obesity. Int J Obes (Lond) 2007; 31(9):1412-19.