Lycium barbarum polysaccharides alleviate cadmium-induced renal injury in ducks by activating the Nrf2-mediated antioxidant defense pathway.
4 affiliations
- 1College of Veterinary Medicine, Yangzhou University, Yangzhou, Jiangsu, China.
- 2Institute of Agricultural Science and Technology Development (Joint International Research Laboratory of Agriculture and Agri-Product Safety of the Ministry of Education of China), Yangzhou University, Yangzhou, Jiangsu, China.
- 3Jiangsu Co-Innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses, Yangzhou, Jiangsu, China.
- 4College of Animal Science and Technology, Xinyang Agriculture and Forestry University, Xinyang, Henan, China.
Abstract
Cadmium (Cd) is a widespread environmental contaminant related to renal immunosuppression and metabolic dysfunction. Lycium barbarum polysaccharides (LBPs) are active extracts of wolfberry and possess a variety of excellent properties. However, the specific mechanism of action for Cd and LBP remain unclear. In the present study, Shaoxing ducks were used to establish an in vivo model to elucidate the effects of combined Cd and LBP exposure on the kidneys and the underlying mechanisms. The ducks were exposed to CdCl2 (50 mg/kg) and/or LBP (50 mg/kg) for 30 days. We observed that Cd exposure increased the kidney index and the levels of the renal function indicators CREA and UA. Further research revealed that Cd exposure caused histopathological damage and ultrastructural alterations. In addition, Cd accumulation induced oxidative stress by disrupting ionic homeostasis and inhibiting the Nrf2-mediated antioxidant defense pathway. Finally, we found that Cd promoted lipid accumulation, disrupted lipid metabolism, and thereby induced renal immunosuppression. Notably, LBP effectively alleviated Cd-induced renal injury, suggesting beneficial effects against Cd-triggered nephrotoxicity.
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BibTeX
@article{wang2026lycium,
title = {{Lycium barbarum polysaccharides alleviate cadmium-induced renal injury in ducks by activating the Nrf2-mediated antioxidant defense pathway.}},
author = {Xueru Wang and Dongdi Liu and Yonggang Ma and Hui Zou and Xishuai Tong and Jiaqiao Zhu and Ruilong Song and Hongyan Zhao and Zongping Liu},
journal = {Frontiers in veterinary science},
year = {2026},
month = oct,
doi = {10.3389/fvets.2026.1998071},
url = {https://europepmc.org/article/MED/42953643},
note = {CC BY},
}
RIS
TY - JOUR
TI - Lycium barbarum polysaccharides alleviate cadmium-induced renal injury in ducks by activating the Nrf2-mediated antioxidant defense pathway.
AU - Xueru Wang
AU - Dongdi Liu
AU - Yonggang Ma
AU - Hui Zou
AU - Xishuai Tong
AU - Jiaqiao Zhu
AU - Ruilong Song
AU - Hongyan Zhao
AU - Zongping Liu
PY - 2026
DA - 2026/10/14
JO - Frontiers in veterinary science
DO - 10.3389/fvets.2026.1998071
UR - https://europepmc.org/article/MED/42953643
AB - Cadmium (Cd) is a widespread environmental contaminant related to renal immunosuppression and metabolic dysfunction. Lycium barbarum polysaccharides (LBPs) are active extracts of wolfberry and possess a variety of excellent properties. However, the specific mechanism of action for Cd and LBP remain unclear. In the present study, Shaoxing ducks were used to establish an in vivo model to elucidate the effects of combined Cd and LBP exposure on the kidneys and the underlying mechanisms. The ducks were exposed to CdCl2 (50 mg/kg) and/or LBP (50 mg/kg) for 30 days. We observed that Cd exposure increased the kidney index and the levels of the renal function indicators CREA and UA. Further research revealed that Cd exposure caused histopathological damage and ultrastructural alterations. In addition, Cd accumulation induced oxidative stress by disrupting ionic homeostasis and inhibiting the Nrf2-mediated antioxidant defense pathway. Finally, we found that Cd promoted lipid accumulation, disrupted lipid metabolism, and thereby induced renal immunosuppression. Notably, LBP effectively alleviated Cd-induced renal injury, suggesting beneficial effects against Cd-triggered nephrotoxicity.
SN - 2297-1769
ER -