Effects of green tea polyphenols on inflammation and iron status

Abstract

Background: Inflammation is an underlying problem for many disease states and has been implicated in iron deficiency (ID) and anemia through dysregulation of iron metabolism. Inflammation-induced ID is of great concern because it is associated with obesity, which continues to rise in both adults and children in the US. Cost-effective and safe dietary approaches such as the consumption of epigallocatechin-3-gallate (EGCG), a green tea extract, have been proposed to reduce inflammation and hence improve iron status, but data in this area is limited. Objective: the objective of this study was to determine whether iron status is affected in LPS-induced inflammation and to determine if it would improve by the mechanism of reduced inflammation by EGCG. Methods: Thirty-two male Sprague-Dawley rats were randomly divided into four groups (n = 8 each): positive control, negative control, treatment group with lipopolysaccharide (LPS) injections, and treatment group with LPS injections + EGCG mixed with the diet. Rats were administered LPS via intraperitoneal injection (0.5 mg/kg body weight) 3X weekly for three weeks. The EGCG diet was prepared by thoroughly mixing the EGCG powder with the diet (600 mg EGCG/kg diet). Iron status (hemoglobin, hematocrit, serum and tissue iron, hepcidin and inflammatory markers (C - reactive protein (CRP), serum amyloid A (SAA), and interleukin 6 (IL-6), were measured. Differences between groups were assessed using ANOVA with Tukey’s multiple comparison test against positive control and unpaired t-test between the two treatment groups. Results: There were no differences in treatment groups compared with control in CRP, hepcidin, and liver iron concentrations. Compared to the positive control, serum iron concentrations were significantly lower in the LPS (p=0.02) and the LPS+EGCG (p=0.01) but not the negative control. Compared to the positive control group, spleen iron concentrations were significantly lower in the negative control (p= <0.001) and significantly higher in the LPS (p=0.04) but no significant difference was found in the LPS+ EGCG group. Compared to the positive control group, SAA concentrations were significantly higher in LPS group (p= 0.048) but not the LPS + EGCG or negative control. However, SAA concentrations were significantly lower in LPS +EGCG when compared to LPS alone group. Compared to the positive control group, IL-6 concentrations were significantly higher in LPS+EGCG (p= 0.004) compared to LPS alone group may be due to anti-inflammatory response to EGCG treatment. Conclusion: EGCG reduced inflammation but had no effect on hepcidin or improving serum iron concentration or any other iron markers. These findings provide valuable information as we continue to confront disease states associated with chronic inflammation and iron deficiency. We can use this information to inform future public health programming interventions and opportunities.