2015•Zhongguo bingli shengli zazhiRequires access

Ulinastatin protects rat pulmonary tissues from paraquat-induced acute injury

D Chen

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Abstract

AIM: To investigate the protective effects of ulinastatin on the rats with paraquat-induced acute lung injury and its mechanisms. METHODS: The Wistar rats( n = 108) were randomly divided into control group,paraquat group and ulinastatin group. The rats in paraquat group and ulinastatin group were given paraquat by gavage,while the rats in control group were given sterile saline by gavage. The rats in ulinastatin group were also given ulinastatin treatment. The serum levels of MDA,SOD,IL-6,IL-10 and TNF-α were measured after 1 d,3 d,7 d,14 d,21 d and 28 d.The expression levels of p38 MAPK,MMP-2 and TIMP-1 in the lung were also measured. RESULTS: The levels of SOD in 1 d,3 d and 7 d in paraquat group and ulinastatin group were significantly lower than those in control group( P 0. 01). The level of SOD in ulinastatin group was significantly higher than that in paraquat group( P 0. 05). The levels of MDA,IL-6,IL-10 and TNF-α in 1 d,3 d and 7 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and those in ulinastatin group were significantly lower than those in paraquat group( P 0. 05).The levels of p38 MAPK and TIMP-1 in 1 d,3 d,7 d,14 d,21 d and 28 d in paraquat group and ulinastatin group were higher than those in control group( P 0. 01),and those in ulinastatin group was significantly lower than those in paraquat group( P 0. 05). The level of MMP-2 in 1 d,3 d,7 d,14 d and 21 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and that in ulinastatin group was significantly lower than that in paraquat group( P 0. 05). CONCLUSION: Ulinastatin protects the lung tissues of rats from paraquat-induced acute lung injury by inhibiting p38 MAPK signaling pathway and ameliorating inflammatory and oxidative responses.

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AIM: To investigate the protective effects of ulinastatin on the rats with paraquat-induced acute lung injury and its mechanisms. METHODS: The Wistar rats( n = 108) were randomly divided into control group,paraquat group and ulinastatin group. The rats in paraquat group and ulinastatin group were given paraquat by gavage,while the rats in control group were given sterile saline by gavage. The rats in ulinastatin group were also given ulinastatin treatment. The serum levels of MDA,SOD,IL-6,IL-10 and TNF-α were measured after 1 d,3 d,7 d,14 d,21 d and 28 d.The expression levels of p38 MAPK,MMP-2 and TIMP-1 in the lung were also measured. RESULTS: The levels of SOD in 1 d,3 d and 7 d in paraquat group and ulinastatin group were significantly lower than those in control group( P 0. 01). The level of SOD in ulinastatin group was significantly higher than that in paraquat group( P 0. 05). The levels of MDA,IL-6,IL-10 and TNF-α in 1 d,3 d and 7 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and those in ulinastatin group were significantly lower than those in paraquat group( P 0. 05).The levels of p38 MAPK and TIMP-1 in 1 d,3 d,7 d,14 d,21 d and 28 d in paraquat group and ulinastatin group were higher than those in control group( P 0. 01),and those in ulinastatin group was significantly lower than those in paraquat group( P 0. 05). The level of MMP-2 in 1 d,3 d,7 d,14 d and 21 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and that in ulinastatin group was significantly lower than that in paraquat group( P 0. 05). CONCLUSION: Ulinastatin protects the lung tissues of rats from paraquat-induced acute lung injury by inhibiting p38 MAPK signaling pathway and ameliorating inflammatory and oxidative responses.

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Available abstract

AIM: To investigate the protective effects of ulinastatin on the rats with paraquat-induced acute lung injury and its mechanisms. METHODS: The Wistar rats( n = 108) were randomly divided into control group,paraquat group and ulinastatin group. The rats in paraquat group and ulinastatin group were given paraquat by gavage,while the rats in control group were given sterile saline by gavage. The rats in ulinastatin group were also given ulinastatin treatment. The serum levels of MDA,SOD,IL-6,IL-10 and TNF-α were measured after 1 d,3 d,7 d,14 d,21 d and 28 d.The expression levels of p38 MAPK,MMP-2 and TIMP-1 in the lung were also measured. RESULTS: The levels of SOD in 1 d,3 d and 7 d in paraquat group and ulinastatin group were significantly lower than those in control group( P 0. 01). The level of SOD in ulinastatin group was significantly higher than that in paraquat group( P 0. 05). The levels of MDA,IL-6,IL-10 and TNF-α in 1 d,3 d and 7 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and those in ulinastatin group were significantly lower than those in paraquat group( P 0. 05).The levels of p38 MAPK and TIMP-1 in 1 d,3 d,7 d,14 d,21 d and 28 d in paraquat group and ulinastatin group were higher than those in control group( P 0. 01),and those in ulinastatin group was significantly lower than those in paraquat group( P 0. 05). The level of MMP-2 in 1 d,3 d,7 d,14 d and 21 d in paraquat group and ulinastatin group increased compared with control group( P 0. 01),and that in ulinastatin group was significantly lower than that in paraquat group( P 0. 05). CONCLUSION: Ulinastatin protects the lung tissues of rats from paraquat-induced acute lung injury by inhibiting p38 MAPK signaling pathway and ameliorating inflammatory and oxidative responses.

Key concepts: Ulinastatin, Paraquat, Saline, Lung, Medicine, Anesthesia, Internal medicine, Pharmacology

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