Astragaloside IV attenuates cadmium induced nephrotoxicity in rats by activating Nrf2 DOI Creative Commons
Yuchen Li, Jiayi Zhou, Tianxin Zhang

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 15, 2025

Acute kidney injury (AKI) has become a disease of global concern due to its high morbidity and mortality. This highlighted the need for renoprotective agents. Astragaloside IV (AS-IV) is saponin isolated from Astragalus membranaceus with good antioxidant, anti-inflammatory anti-tumor properties. In this study, HK2 cells rat model were utilized explore protective effect AS-IV against cadmium chloride-induced oxidative stress-induced apoptosis. CdCl2-induced apoptosis, ROS production, mitochondrial membrane potential alterations significantly inhibited in -treated cells. Expression mitochondria-associated apoptotic proteins Cleaved-Caspase3, Cleaved-Caspase9, Cleaved-PARP was reduced after intervention. addition, Rat weight loss also alleviated symptoms nephrotoxicity injury. Further experiments showed that suppresses heavy metal Cd-induced mitochondria-mediated apoptosis by regulating Nrf2/HO-1 pathway. conclusion, could protect metal-induced toxicity be used as nephroprotective agent.

Language: Английский

Astragaloside IV attenuates cadmium induced nephrotoxicity in rats by activating Nrf2 DOI Creative Commons
Yuchen Li, Jiayi Zhou, Tianxin Zhang

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 15, 2025

Acute kidney injury (AKI) has become a disease of global concern due to its high morbidity and mortality. This highlighted the need for renoprotective agents. Astragaloside IV (AS-IV) is saponin isolated from Astragalus membranaceus with good antioxidant, anti-inflammatory anti-tumor properties. In this study, HK2 cells rat model were utilized explore protective effect AS-IV against cadmium chloride-induced oxidative stress-induced apoptosis. CdCl2-induced apoptosis, ROS production, mitochondrial membrane potential alterations significantly inhibited in -treated cells. Expression mitochondria-associated apoptotic proteins Cleaved-Caspase3, Cleaved-Caspase9, Cleaved-PARP was reduced after intervention. addition, Rat weight loss also alleviated symptoms nephrotoxicity injury. Further experiments showed that suppresses heavy metal Cd-induced mitochondria-mediated apoptosis by regulating Nrf2/HO-1 pathway. conclusion, could protect metal-induced toxicity be used as nephroprotective agent.

Language: Английский

Citations

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