期刊
TOXICOLOGY LETTERS
卷 316, 期 -, 页码 85-93出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.toxlet.2019.09.006
关键词
Apoptosis-stimulating protein 2 of p53; Autophagy; Acute hepatic injury; Apoptosis; Inflammation
类别
资金
- Natural Science Foundation of Beijing Municipality [7172102]
- Chinese Foundation for Hepatitis Prevention and Control [TQGB20190050]
- National Natural Science Foundation of China [81672026]
- National Key R&D Program of China [2017YFA0103000]
- National Science and Technology Key Project on Major Infectious Diseases such as HIV/AIDS, Viral Hepatitis Prevention and Treatment [2017ZX10203201-005]
- Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support [ZYLX201806]
Background: Apoptosis-stimulating protein 2 of p53 (ASPP2) has a variety of biological functions, and is involved in cellular apoptosis, autophagy and inflammatory reaction. However, the role of ASPP2 in acute hepatic injury remains unclear. Methods: We established an animal model of acute hepatic injury by intraperitoneal injection of CCl4. The expression profile of ASPP2 was measured in wild type (ASPP2(+/+)) mice with acute hepatic injury induced by CCl4. Hepatic pathological changes and liver function, apoptosis, inflammation and autophagic levels were measured in ASPP2(+/+)and ASPP2 haploid deletion (ASPP(2+/-)) mice with acute hepatic injury, respectively. After 3-methyladenine (3-MA) treatment, indicators of hepatic injury were observed in ASPP2(+/+) and ASPP2(+/-) mice with CCl4 injection. Results: During the development of acute hepatic injury, ASPP2 expression significantly upregulated at 24 h and 48 h after CCl4 injection. ASPP2 haplotype deletion protected against acute hepatic injury, and this was mainly reflected in decreased ALT and AST levels, less hepatic tissue hemorrhage and necrosis, and reduced cellular inflammation and apoptosis in ASPP2(+/-) mice compared with ASPP2(+/+) mice with acute hepatic injury. ASPP2 haploid deletion activates autophagy in mice with acute hepatic injury, and protects mice from acute hepatic injury via the autophagic signal pathway. Conclusion: ASPP2 haplotype deletion protected mice against acute hepatic injury through autophagy activation, which inhibited inflammation and apoptosis in acute hepatic injury.
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