Jian-Pi-Yi-Shen formula restores iron metabolism from dysregulation in anemic rats with adenine-induced nephropathy

Li C, Huang H, Wang R, Zhang C, Huang S, Wu J, Mo P, Yu H, Li S, Chen J · Journal of Ethnopharmacology · 2023 August

DOI 10.1016/j.jep.2023.116526

Objective

To investigate the impact of Jian-Pi-Yi-Shen (JPYS), a herbal decoction, on renal anemia and iron metabolism in chronic kidney disease (CKD) through network pharmacology, chemical profiling, and in vivo experiments.

Conclusions

Jian-Pi-Yi-Shen (JPYS) reduces hepcidin levels by inhibiting JAK2-STAT3 signaling, thereby improving iron metabolism and alleviating renal anemia in CKD rats. Experimental results demonstrated improvements in renal function, histopathological damage, and hematological parameters following JPYS treatment.

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Insights

The herbal decoction Jian-Pi-Yi-Shen reduces symptoms of chronic kidney disease and anaemia by improving iron metabolism and inhibiting the JAK2-STAT3 signaling pathway.

Methodology used included an analysis of network pharmacology, chemical profiling, and in vivo experiments on the effect of Jian-Pi-Yi-Shen (JPYS) on renal anemia and chronic kidney disease (CKD). The active compounds in JPYS were detected in in vivo experiment, and their potential targets were predicted by network pharmacology. An animal model of CKD-related anemia was developed using adenine-feeding for further analysis. The estimation of renal injury was conducted using blood tests, histopathological examinations, and fibrosis degree assessment while the levels of JAK2, STAT3 and iron metabolism-related factors were measured through various techniques. Discussion of the results reveals that 164 active ingredients, including prototypes and metabolites in JPYS, were discovered and 21 core targets were identified. Many of these core targets were associated with the JAK2-STAT3 signaling pathways. Experimental results demonstrated that JPYS treatment significantly improved hematological parameters and iron metabolism in CKD rats, decreased certain indicators of renal damage, and suppressed the expression of JAK2 and STAT3.