Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2026
Paeoniflorin alleviates cadmium-induced kidney injury by inhibiting ferroptosis through suppressing P2X7 receptor/NLRP3 signaling pathway.
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Li Zihe, Liu Siqi, Geng Huafeng, Ye Cong, Wang Chunxi, Zhang Yue
Аннотация
BACKGROUND: Paeoniflorin (PF), a naturally occurring glucoside isolated from Paeonia lactiflora, has anti-inflammatory and antioxidant activities.
AIMS: The purpose of this study was to investigate whether PF could protect against cadmium (Cd)-induced kidney injury in mice.
METHODS: Cd-induced kidney injury model was induced by giving 5 mg/kg body weight of Cd chloride (CdCl2, dissolve in saline) once daily for seven days. PF (25, 50, 100 mg/kg) were given intraperitoneally 1 h prior to CdCl₂ administration, once daily for 7 days. Pathological changes in kidney tissues were detected by H&E staining. The levels of GSH, SOD, iron and MDA were measured in this study. Furthermore, the levels of TNF-α, IL-1β and IL-6 in kidney tissues were detected by ELISA. The level of protein expression was detected by western blot analysis.
RESULTS: Our results showed that Cd resulted in kidney injury, showing histological changes of kidney and increases in serum blood urea nitrogen (BUN) and creatinine. However, these changes were significantly attenuated by treatment of PF. Additionally, compared with Cd-exposed mice, PF administration inhibited Cd-induced increases in MDA content, iron accumulation, and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in kidney tissues, while restoring the reduced levels of SOD and GSH. At the protein level, PF up-regulated GPX4 expression and down-regulated PTGS2 expression in Cd-exposed mice. Moreover, PF significantly suppressed Cd-induced overexpression of P2X7 receptor, as well as activation of NF-κB and NLRP3 in kidney tissues.
CONCLUSIONS: Taken together, our results indicated that PF inhibited Cd-induced kidney injury by inhibiting inflammation and ferroptosis through suppressing P2X7 receptor/NLRP3 signaling pathway.
AIMS: The purpose of this study was to investigate whether PF could protect against cadmium (Cd)-induced kidney injury in mice.
METHODS: Cd-induced kidney injury model was induced by giving 5 mg/kg body weight of Cd chloride (CdCl2, dissolve in saline) once daily for seven days. PF (25, 50, 100 mg/kg) were given intraperitoneally 1 h prior to CdCl₂ administration, once daily for 7 days. Pathological changes in kidney tissues were detected by H&E staining. The levels of GSH, SOD, iron and MDA were measured in this study. Furthermore, the levels of TNF-α, IL-1β and IL-6 in kidney tissues were detected by ELISA. The level of protein expression was detected by western blot analysis.
RESULTS: Our results showed that Cd resulted in kidney injury, showing histological changes of kidney and increases in serum blood urea nitrogen (BUN) and creatinine. However, these changes were significantly attenuated by treatment of PF. Additionally, compared with Cd-exposed mice, PF administration inhibited Cd-induced increases in MDA content, iron accumulation, and pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) in kidney tissues, while restoring the reduced levels of SOD and GSH. At the protein level, PF up-regulated GPX4 expression and down-regulated PTGS2 expression in Cd-exposed mice. Moreover, PF significantly suppressed Cd-induced overexpression of P2X7 receptor, as well as activation of NF-κB and NLRP3 in kidney tissues.
CONCLUSIONS: Taken together, our results indicated that PF inhibited Cd-induced kidney injury by inhibiting inflammation and ferroptosis through suppressing P2X7 receptor/NLRP3 signaling pathway.