Qing'e Pill extract attenuates vascular calcification and improves renal dysfunction in chronic kidney disease mice by modulating calcium-phosphorus homeostasis and downregulating the expression of Runx2/OCN.

ETHNOPHARMACOLOGICAL RELEVANCE: Chronic kidney disease (CKD) is a progressive renal disorder with vascular calcification (VC) as a major comorbidity that elevates cardiovascular mortality. As a classic traditional Chinese medicine compound widely used in clinical practice, Qing'e Pill (QP) has long been renowned for its remarkable efficacy in tonifying the kidney and strengthening bones. However, its potential therapeutic effects and underlying mechanism in the treatment of chronic kidney disease (CKD) and CKD-induced vascular calcification (CKD-VC) remain unclear to date.

AIM OF THE STUDY: The present study aimed to establish a murine model of CKD-associated VC, and to investigate the therapeutic potency and underlying molecular mechanisms of QP in the treatment of VC secondary to CKD.

MATERIALS AND

METHODS

The chemical profile of QP was characterized. Adenine-induced CKD mice were treated with QP for 15 weeks to evaluate its effects. During adenine feeding, mice were orally administered QP, and systematic assessments were performed on general status, renal metabolic parameters, renal and vascular histology, and the expression levels of key target proteins.

RESULTS

Total 49 constituents were identified in QP. QP treatment improved general status, restored renal excretory function, attenuated renal injury and fibrosis, and relieved oxidative stress in CKD mice. Furthermore, QP normalized serum calcium, phosphorus and parathyroid hormone levels, and consequently ‌downregulated‌ the expression of ‌key osteogenic markers‌, Runx2 and OCN in vascular tissues, thereby ‌reducing‌ the incidence and severity of VC.

CONCLUSION

QP improves renal excretory function, alleviates oxidative stress, and retards the progression of CKD, thereby reducing mortality. Moreover, QP effectively attenuates CKD-VC by correcting calcium-phosphorus metabolic disorders and downregulating the Runx2/OCN signaling pathway.