Xiao Hu1, Yuanyuan Liang1, Hongyu Zhao1, Min Zhao2. 1. Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, China. 2. Department of Emergency Medicine, Shengjing Hospital of China Medical University, Shenyang 110004, China. Electronic address: zhaom@sj-hospital.org.
Abstract
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.
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.
Authors: Hong Luan; Chuanxiao Wang; Jianping Sun; Long Zhao; Lin Li; Bin Zhou; Shihong Shao; Xuefei Shen; Yan Xu Journal: Front Physiol Date: 2020-04-03 Impact factor: 4.566