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Systemic iron homeostasis dysregulation is primarily associated with inflammation- associated anemia (AI) due to hepcidin up-regulation. Tinospora cordifolia (TC) has shown remarkable anti-inflammatory properties and has been found useful in the treatment of inflammatory disorders. However, the effects and mechanisms of TC on AI have not been studied yet. We conducted in vivo and in vitro studies to evaluate the effect of TC on AI. HPLC studies were also carried out to find out active constituents in TC extract. Model system exhibiting AI was developed by repeated injections of HKBA in Wistar rats. TC treated groups showed significantly higher levels of Hb and RBC count compared to the inflammatory control group. TC treatment showed reduction in the expression of the HAMP (hepcidin) gene in the rat liver. TC extract also inhibited gene expression of inflammatory cytokines (TNF-α, IL-1β) and decreased NO production in RAW 264.7 cells. The HPLC analysis revealed the presence of tinosporaside, which could have synergistically contributed to the above findings. Overall results indicate that TC therapy was able to maintain circulating iron through reduction of inflammatory cytokines and expression of hepcidin in rats.

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A smartphone-based app for the accurate and sensitive measurement of hemoglobin was developed.

We investigated the association between iron status, B12, and inflammatory markers among 101 adolescent girls. We found that B12 showed significant negative association with tumor necrosis factor-alpha (TNF-α) (rs = -0.232, P = 0.020) and positive association with serum ferritin (SF) (rs = 0.209, P = 0.036) among girls. Our results showed that hepcidin discriminates anemic and non-anemic population under normal B12 conditions. The logistic regression analysis revealed that the risk of having higher TNF-α levels was 13.2 times higher in low B12 girls in the presence of anemia compared to the girls having normal hemoglobin and B12 levels.

Inflammatory bowel diseases (IBD) are complex disorders characterized by a cycle of inflammatory perpetuation. Iron accumulates in the inflamed tissue of IBD patients, yet neither a mechanism for the accumulation nor its implication on the course of inflammation are known. This study addresses the role of iron homeostasis in IBD using human biopsies, animal models and cellular systems. It demonstrates inflammation-mediated modifications of iron homeostasis, and an iron decoupled activation of the iron regulatory protein (IRP)1. To understand the role of IRP1 in the course of this inflammation-associated iron pattern, a novel cellular co-culture model was established, that reproduced the iron-pattern observed in vivo. Importantly, deletion of IRP1 from an IBD mouse model completely abolished mis-distribution of iron and intestinal inflammation, suggesting a central role of IRP1 in the coordination of inflammatory response in the intestinal mucosa. Thus, this work identifies IRP1 as a target for IBD treatment.

Rhodamine‐based reversible fluorescence turn‐on chemosensor appended with ‘N’ and ‘O’ donor atoms as chelating moieties has been synthesized for the selective detection of Fe3+ ion over other competitive metal ions in aqueous medium. Designed probe indicated color change to pink with lower limit of detection at 1.93×10−7 M exhibiting high sensitivity toward Fe3+ ion. Sensing mechanism was established by HRMS and NMR titration studies. The probe was successfully applied for the detection of Fe3+ ions in live MCF‐7 cells.

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