Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways
Jingfan Deng,1 Jiao Feng,1 Tong Liu,1 Xiya Lu,1 Wenwen Wang,1 Ning Liu,2 Yang Lv,1 Qing Liu,1 Chuanyong Guo,1 Yingqun Zhou1 1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, People’s Republic of China; 2Depa...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Dove Medical Press
2018-11-01
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| Series: | Drug Design, Development and Therapy |
| Subjects: | |
| Online Access: | https://www.dovepress.com/beraprost-sodium-preconditioning-prevents-inflammation-apoptosis-and-a-peer-reviewed-article-DDDT |
| _version_ | 1818178404320542720 |
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| author | Deng J Feng J Liu T Lu X Wang W Liu N Lv Y Liu Q Guo C Zhou Y |
| author_facet | Deng J Feng J Liu T Lu X Wang W Liu N Lv Y Liu Q Guo C Zhou Y |
| author_sort | Deng J |
| collection | DOAJ |
| description | Jingfan Deng,1 Jiao Feng,1 Tong Liu,1 Xiya Lu,1 Wenwen Wang,1 Ning Liu,2 Yang Lv,1 Qing Liu,1 Chuanyong Guo,1 Yingqun Zhou1 1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, People’s Republic of China; 2Department of Gastroenterology, Shanghai Tenth People’s Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, People’s Republic of China Objective: The goal of this study was to determine the effects of beraprost sodium (BPS) preconditioning on hepatic ischemia-reperfusion (IR) injury and its underlying mechanisms of action. Materials and methods: Mice were randomly divided into sham, IR, IR+BPS (50 µg/kg), and IR+BPS (100 µg/kg) groups. Saline or BPS was given to the mice by daily gavage for 1 week before the hepatic IR model was established. Liver tissues and orbital blood were collected at 2, 8, and 24 hours after reperfusion for the determination of liver enzymes, inflammatory mediators, apoptosis- and autophagy-related proteins, key proteins in P38 and c-Jun N-terminal kinase (JNK) cascades, and evaluation of liver histopathology. Results: BPS preconditioning effectively reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, improved pathological damage, ameliorated production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and affected expressions of Bax, Bcl-2, Caspase-3, Caspase-8, and Caspase-9, microtubule-associated protein 1 light chain 3 (LC3), Beclin-1, and P62. The protective effects of BPS preconditioning were associated with reduced P38 and JNK phosphorylation. Conclusion: BPS preconditioning ameliorated hepatic IR injury by suppressing inflammation, apoptosis, and autophagy, partially via inhibiting activation of the P38 and JNK cascades. Keywords: liver injury, beraprost sodium, inflammation, apoptosis, autophagy, MAPK pathway |
| first_indexed | 2024-12-11T20:47:26Z |
| format | Article |
| id | doaj.art-01aaeeb76a2c429db847bec1efe08301 |
| institution | Directory Open Access Journal |
| issn | 1177-8881 |
| language | English |
| last_indexed | 2024-12-11T20:47:26Z |
| publishDate | 2018-11-01 |
| publisher | Dove Medical Press |
| record_format | Article |
| series | Drug Design, Development and Therapy |
| spelling | doaj.art-01aaeeb76a2c429db847bec1efe083012022-12-22T00:51:20ZengDove Medical PressDrug Design, Development and Therapy1177-88812018-11-01Volume 124067408242707Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathwaysDeng JFeng JLiu TLu XWang WLiu NLv YLiu QGuo CZhou YJingfan Deng,1 Jiao Feng,1 Tong Liu,1 Xiya Lu,1 Wenwen Wang,1 Ning Liu,2 Yang Lv,1 Qing Liu,1 Chuanyong Guo,1 Yingqun Zhou1 1Department of Gastroenterology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, People’s Republic of China; 2Department of Gastroenterology, Shanghai Tenth People’s Hospital, School of Clinical Medicine of Nanjing Medical University, Shanghai 200072, People’s Republic of China Objective: The goal of this study was to determine the effects of beraprost sodium (BPS) preconditioning on hepatic ischemia-reperfusion (IR) injury and its underlying mechanisms of action. Materials and methods: Mice were randomly divided into sham, IR, IR+BPS (50 µg/kg), and IR+BPS (100 µg/kg) groups. Saline or BPS was given to the mice by daily gavage for 1 week before the hepatic IR model was established. Liver tissues and orbital blood were collected at 2, 8, and 24 hours after reperfusion for the determination of liver enzymes, inflammatory mediators, apoptosis- and autophagy-related proteins, key proteins in P38 and c-Jun N-terminal kinase (JNK) cascades, and evaluation of liver histopathology. Results: BPS preconditioning effectively reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, improved pathological damage, ameliorated production of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and affected expressions of Bax, Bcl-2, Caspase-3, Caspase-8, and Caspase-9, microtubule-associated protein 1 light chain 3 (LC3), Beclin-1, and P62. The protective effects of BPS preconditioning were associated with reduced P38 and JNK phosphorylation. Conclusion: BPS preconditioning ameliorated hepatic IR injury by suppressing inflammation, apoptosis, and autophagy, partially via inhibiting activation of the P38 and JNK cascades. Keywords: liver injury, beraprost sodium, inflammation, apoptosis, autophagy, MAPK pathwayhttps://www.dovepress.com/beraprost-sodium-preconditioning-prevents-inflammation-apoptosis-and-a-peer-reviewed-article-DDDTliver ischemia-reperfusion injuryBeraprost sodiuminflammationapoptosisautophagyMAPK pathway. |
| spellingShingle | Deng J Feng J Liu T Lu X Wang W Liu N Lv Y Liu Q Guo C Zhou Y Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways Drug Design, Development and Therapy liver ischemia-reperfusion injury Beraprost sodium inflammation apoptosis autophagy MAPK pathway. |
| title | Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways |
| title_full | Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways |
| title_fullStr | Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways |
| title_full_unstemmed | Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways |
| title_short | Beraprost sodium preconditioning prevents inflammation, apoptosis, and autophagy during hepatic ischemia-reperfusion injury in mice via the P38 and JNK pathways |
| title_sort | beraprost sodium preconditioning prevents inflammation apoptosis and autophagy during hepatic ischemia reperfusion injury in mice via the p38 and jnk pathways |
| topic | liver ischemia-reperfusion injury Beraprost sodium inflammation apoptosis autophagy MAPK pathway. |
| url | https://www.dovepress.com/beraprost-sodium-preconditioning-prevents-inflammation-apoptosis-and-a-peer-reviewed-article-DDDT |
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