International immunopharmacology · 2018
Effects of AT-RvD1 on paraquat-induced acute renal injury in mice.
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Hu Xiao, Liang Yuanyuan, Zhao Hongyu, Zhao Min
Аннотация
OBJECTIVE: To investigate the effects of aspirin-triggered resolvin D1 (AT-RvD1) on paraquat-induced acute renal injury (ARI) in mice.
METHODS: The ARI mouse model was established by administering 28 mg/kg paraquat to C57BL/6J mice by intraperitoneal injection. The mice received 10 or 100 ng AT-RvD1 by intravenous injection in the tail vein 2 h after toxication. The mice were euthanized 6, 24, or 72 h post-paraquat injection to collect blood and renal tissues. The samples were used to evaluate the pathological changes, renal function, inflammation and oxidative stress in the renal tissues.
RESULTS: Compared with those of the PQ group, AT-RvD1 administration mitigated the pathological changes and improved renal function, activated Nrf2 and upregulated the expression of its downstream antioxidant genes (NQO1, HO-1, SOD1 and GPx1), and decreased the MDA and protein carbonyls content in renal tissues. Treatment also reduced the expression of P-selectin in renal tissues, the percentage of Ly-6G+ CD41+ cells in the peripheral blood and infiltration of neutrophils in renal tissues. Furthermore, AT-RvD1 inhibited the activation of NF-κB and reduced IL-1β and TNF-α serum levels.
CONCLUSION: The administration of AT-RvD1 can effectively suppress paraquat-induced oxidative stress injury and the inflammatory reaction, and alleviate paraquat-induced ARI.
METHODS: The ARI mouse model was established by administering 28 mg/kg paraquat to C57BL/6J mice by intraperitoneal injection. The mice received 10 or 100 ng AT-RvD1 by intravenous injection in the tail vein 2 h after toxication. The mice were euthanized 6, 24, or 72 h post-paraquat injection to collect blood and renal tissues. The samples were used to evaluate the pathological changes, renal function, inflammation and oxidative stress in the renal tissues.
RESULTS: Compared with those of the PQ group, AT-RvD1 administration mitigated the pathological changes and improved renal function, activated Nrf2 and upregulated the expression of its downstream antioxidant genes (NQO1, HO-1, SOD1 and GPx1), and decreased the MDA and protein carbonyls content in renal tissues. Treatment also reduced the expression of P-selectin in renal tissues, the percentage of Ly-6G+ CD41+ cells in the peripheral blood and infiltration of neutrophils in renal tissues. Furthermore, AT-RvD1 inhibited the activation of NF-κB and reduced IL-1β and TNF-α serum levels.
CONCLUSION: The administration of AT-RvD1 can effectively suppress paraquat-induced oxidative stress injury and the inflammatory reaction, and alleviate paraquat-induced ARI.