Alleviation of Hepatic Ischemia Reperfusion Injury by Oleanolic Acid Pretreating via Reducing HMGB1 Release and Inhibiting Apoptosis and Autophagy

Hepatic ischemia reperfusion (IR) injury (IRI) occurs during liver transplantation, hepatectomy, and hemorrhagic shock. Oleanolic acid (OA) is a natural compound with antioxidant and anti-inflammatory activity that has been used to treat liver disorders in clinical practice for several years. Here,...

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Main Authors: Wenwen Wang (Author), Liwei Wu (Author), Jingjing Li (Author), Jie Ji (Author), Kan Chen (Author), Qiang Yu (Author), Sainan Li (Author), Jiao Feng (Author), Tong Liu (Author), Jie Zhang (Author), Jiaojiao Chen (Author), Yuting Zhou (Author), Yuqing Mao (Author), Fan Wang (Author), Weiqi Dai (Author), Xiaoming Fan (Author), Chuanyong Guo (Author), Jianye Wu (Author)
Format: Book
Published: Hindawi Limited, 2019-01-01T00:00:00Z.
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042 |a dc 
100 1 0 |a Wenwen Wang  |e author 
700 1 0 |a Liwei Wu  |e author 
700 1 0 |a Jingjing Li  |e author 
700 1 0 |a Jie Ji  |e author 
700 1 0 |a Kan Chen  |e author 
700 1 0 |a Qiang Yu  |e author 
700 1 0 |a Sainan Li  |e author 
700 1 0 |a Jiao Feng  |e author 
700 1 0 |a Tong Liu  |e author 
700 1 0 |a Jie Zhang  |e author 
700 1 0 |a Jiaojiao Chen  |e author 
700 1 0 |a Yuting Zhou  |e author 
700 1 0 |a Yuqing Mao  |e author 
700 1 0 |a Fan Wang  |e author 
700 1 0 |a Weiqi Dai  |e author 
700 1 0 |a Xiaoming Fan  |e author 
700 1 0 |a Chuanyong Guo  |e author 
700 1 0 |a Jianye Wu  |e author 
245 0 0 |a Alleviation of Hepatic Ischemia Reperfusion Injury by Oleanolic Acid Pretreating via Reducing HMGB1 Release and Inhibiting Apoptosis and Autophagy 
260 |b Hindawi Limited,   |c 2019-01-01T00:00:00Z. 
500 |a 0962-9351 
500 |a 1466-1861 
500 |a 10.1155/2019/3240713 
520 |a Hepatic ischemia reperfusion (IR) injury (IRI) occurs during liver transplantation, hepatectomy, and hemorrhagic shock. Oleanolic acid (OA) is a natural compound with antioxidant and anti-inflammatory activity that has been used to treat liver disorders in clinical practice for several years. Here, we investigated the effects and underlying mechanisms of OA in hepatic IRI. A 60-minute partial (70%) hepatic, warm, ischemic reperfusion model was established in BALB/c mice, and two doses (30 and 60 mg/kg) of OA were administered intragastrically for 7 consecutive days prior to hepatic IR. Orbital blood and liver specimens were collected at 2, 8, and 24 h after IR. The results showed that OA preconditioning significantly alleviated hepatic injury, as evidenced by decreased alanine aminotransferase and aspartate aminotransferase levels; improved histology, inhibition of JNK phosphorylation, and high mobility group box 1 (HMGB1); and tumor necrosis factor-α downregulation in hepatic IR mice. OA upregulated Bcl-2 and downregulated caspase-3, caspase-9, Bax, Beclin 1, and LC3, which play crucial roles in the regulation of apoptosis and autophagy. These findings highlighted the protective effects of OA against hepatic IRI mediated by the inhibition of apoptosis and autophagy and the release of HMGB1, which acted as a late inflammatory mediator in hepatic IRI. 
546 |a EN 
690 |a Pathology 
690 |a RB1-214 
655 7 |a article  |2 local 
786 0 |n Mediators of Inflammation, Vol 2019 (2019) 
787 0 |n http://dx.doi.org/10.1155/2019/3240713 
787 0 |n https://doaj.org/toc/0962-9351 
787 0 |n https://doaj.org/toc/1466-1861 
856 4 1 |u https://doaj.org/article/54060b97fdbf4d99a66cfa0a4e39f83b  |z Connect to this object online.