Effect of Chicken Peptide-Ferrous Chelate on Iron Deficiency Anemia in Mice

This study systematically investigated the ameliorative effect of Chicken Peptide-Ferrous Chelate (CMP-Fe) on anemia symptoms in mice with iron deficiency anemia (IDA). The intervention effects were comprehensively evaluated through multiple dimensions, including changes in body weight, blood routine parameters, iron metabolism indicators, inflammatory responses, and tissue protection. The experimental results showed that, compared to the model group, all CMP-Fe dose groups (with low-dose, medium-dose, and high-dose administered at Fe 1.0, 2.0 and 3.0 mg/kg, respectively, based on mouse body weight) exhibited significant improvements in body weight, blood routine parameters (including red blood cell count RBC, hemoglobin HGB, hematocrit HCT, mean corpuscular volume MCV, mean corpuscular hemoglobin MCH, mean corpuscular hemoglobin concentration MCHC, and red blood cell distribution width-coefficient of variation RDW-CV), and serum iron metabolism markers (including serum iron SI, total iron-binding TIBC, transferrin receptor TRF, ferritin FER, transferrin saturation TSAT, and unsaturated iron-binding capacity UIBC), with the high-dose group demonstrating the most pronounced effects. The ameliorative effects of CMP-Fe on erythrocyte-related parameters such as RBC, HGB, and HCT were comparable to those of the positive control group and exhibited a clear dose-dependent trend (low, medium, and high dose gradients). In terms of inflammation regulation, CMP-Fe could suppress the production of serum and colonic pro-inflammatory factors (IL-6, TNF-α, and CRP), while elevating the levels of the anti-inflammatory factor IL-10 and the intestinal mucosal immune marker sIgA. Specifically, the levels of pro-inflammatory factors such as IL-6, TNF-α, and CRP in the colonic tissues of mice in the CMP-Fe group were significantly lower than those in the model control group (P < 0.05), suggesting that CMP-Fe effectively modulates the inflammatory response associated with IDA. Notably, under high-dose CMP-Fe intervention, the recovery of sIgA levels in mice outperformed that of the model control group (P < 0.05) and even exceeded that of the positive control group. Histopathological examination shows that CMP-Fe causes no significant pathological damage to organs such as the heart, lungs, spleen, and kidneys in mice, indicating its favorable biosafety. Meanwhile, this chelate also significantly alleviates pathological injuries in intestinal and liver tissues caused by iron deficiency. In conclusion, CMP-Fe effectively alleviates iron metabolism disorders, inhibits inflammatory responses, and mitigates intestinal and liver tissue damage in mice with IDA, while demonstrating good safety. As a promising novel organic iron supplement, it holds potential for application in the development of specialized pet foods and nutritional supplements for various animals such as cats and dogs.