期刊
ACS BIOMATERIALS SCIENCE & ENGINEERING
卷 7, 期 4, 页码 1552-1563出版社
AMER CHEMICAL SOC
DOI: 10.1021/acsbiomaterials.0c01610
关键词
hepatic acellular matrix; hydrogel; ischemia/reperfusion injury; macrophage polarization; TLR4/NF-kappa B signaling
资金
- National Natural Science Foundation of China [31400818]
- China Postdoctoral Science Foundation [2017T100821, 2016M603056]
- National Key Clinical Specialist Construction Program of China
The study demonstrates that HAM hydrogels alleviate hepatic IRI by promoting M2 polarization, thereby exerting hepatoprotective effects. HAM hydrogels inhibit macrophage M1 (CD68/CCR7) differentiation while promoting M2 (CD68/CD206) differentiation.
Injectable acellular matrix hydrogels are proven to be potential translational materials to facilitate the repairment in various tissues. However, their potential to repair hepatic ischemia/reperfusion injury (IRI) has not been explored. In this work, we made hepatic acellular matrix (HAM) hydrogels based on the decellularized process and evaluated the biocompatibility and hepatoprotective effects in a rat IRI model. HAM hydrogels supported viability, proliferation, and attachment of hepatocytes in vitro. Treatment with HAM hydrogels significantly attenuated hepatic damage caused by IRI, as evidenced by hepatic biochemistry, histology, and inflammatory responses. Importantly, HAM hydrogels inhibited macrophage M1 (CD68/CCR7) differentiation but promoted M2 (CD68/CD206) differentiation. Additionally, TLR4/NF-kappa B signaling was found to be involved in the hepatoprotective effect of HAM hydrogels. Collectively, our study reveals that HAM hydrogels ameliorate hepatic IRI by facilitating M2 polarization via TLR4/NF-kappa B signaling.
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