In:
Journal of Cellular Biochemistry, Wiley, Vol. 120, No. 9 ( 2019-09), p. 14960-14970
Abstract:
This study aimed to investigate the protective effect of ulinastatin in hepatic ischemia‐reperfusion progress, involving its association with the role of autophagy during hypoxia‐induced hypoxia‐reoxygenation injury in vitro. The model of hepatic hypoxia/reoxygenation (H/R) injury in Chang liver cells was established. After treatment with ulinastatin at the doses of 10, 100, and 1000 U/mL in H/R liver cells, the cell proliferation was significantly increased, morphological damage was reduced, and the cell apoptosis rate was decreased. The protein levels of antiapoptotic myeloid cell leukemia‐1 (Mcl‐1) and caspase‐3 were upregulated, and C‐PARP protein was downregulated. Meanwhile, ulinastatin led to an increase in the messenger RNA and protein levels of autophagy maker Unc‐like kinase 1 (ULK1), Beclin‐1, and microtubule‐associated protein 1 light chain 3 (LC‐3) and a decrease in p62. Then, 3‐methyladenine (3‐MA), an inhibitor of autophagy, made morphological damage and cell apoptosis worsen in ulinastatin‐treated H/R liver cells. And the expression levels of caspase‐3, C‐PARP, p62, Beclin‐1, and LC‐3, proteins were also reversed by 3‐MA. Taken together, our results demonstrate that ulinastatin inhibited the hepatic H/R injury in Chang liver cells, which was, to some extent, related to the autophagy activation.
Type of Medium:
Online Resource
ISSN:
0730-2312
,
1097-4644
Language:
English
Publisher:
Wiley
Publication Date:
2019
detail.hit.zdb_id:
1479976-5
SSG:
12
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