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Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway.
dc.creator | Jovanović Stojanov, Sofija | |
dc.creator | Martinović, Vesna | |
dc.creator | Bogojević, Desanka | |
dc.creator | Poznanović, Goran | |
dc.creator | Petrović, Anja | |
dc.creator | Ivanović Matić, Svetlana | |
dc.creator | Grigorov, Ilijana | |
dc.date.accessioned | 2018-05-29T09:34:05Z | |
dc.date.available | 2900-01-01 | |
dc.date.issued | 2018 | |
dc.identifier.issn | 1138-7548 | |
dc.identifier.uri | http://link.springer.com/10.1007/s13105-018-0626-0 | |
dc.identifier.uri | http://www.ncbi.nlm.nih.gov/pubmed/29611132 | |
dc.identifier.uri | https://radar.ibiss.bg.ac.rs/handle/123456789/3068 | |
dc.description.abstract | Chronic inflammation plays an essential role in the development of diabetic complications. Understanding the molecular mechanisms that support inflammation is a prerequisite for the design of novel anti-inflammatory therapies. These would take into consideration circulating levels of cytokines and damage-associated molecular patterns (DAMPs) that include the high mobility group box 1 (HMGB1) protein which, in part, promotes the inflammatory response through TLR4 signaling. The liver, as the source of circulating cytokines and acute-phase proteins, contributes to the control of systemic inflammation. We previously found that liver injury in streptozotocin-induced diabetic rats correlated with the level of oxidative stress, increased expression of HMGB1, and with the activation of TLR4-mediated cell death pathways. In the present work, we examined the effects of ethyl pyruvate (EP), an inhibitor of HMGB1 release/expression, on the modulation of activation of the HMGB1/TLR4 inflammatory cascade in diabetic liver. We observed that increased expression of inflammatory markers, TNF-α, IL-6, and haptoglobin in diabetic liver was associated with increased HMGB1/TLR4 interaction, activation of MAPK (p38, ERK, JNK)/NF-κB p65 and JAK1/STAT3 signaling pathways, and with decreased expression of Nrf2-regulated antioxidative enzymes. The reduction in HMGB1 expression as the result of EP administration reduced the pro-inflammatory activity of HMGB1 and exerted a protective effect on diabetic liver, which was observed as improved liver histology and antioxidant and inflammatory statuses. Our results suggest that prevention of HMGB1 release and blockage of the HMGB/TLR4 axis represents a potentially effective therapeutic strategy aimed at ameliorating diabetes-induced inflammation and ensuing liver injury. | en |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173020/RS// | |
dc.rights | restrictedAccess | |
dc.source | Journal of Physiology and Biochemistry | |
dc.subject | Diabetes | |
dc.subject | Ethyl pyruvate | |
dc.subject | HMGB1/TLR4 signaling | |
dc.subject | Inflammatory response | |
dc.subject | Liver | |
dc.title | Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway. | en |
dc.type | article | en |
dc.rights.license | ARR | |
dcterms.abstract | Григоров, Илијана; Ивановић Матић, Светлана; Јовановић Стојанов, Софија; Мартиновић, Весна; Богојевић, Десанка; Познановић, Горан; Петровић, Aња; | |
dc.rights.holder | © University of Navarra 2018 | |
dc.citation.issue | 2 | |
dc.citation.volume | 74 | |
dc.identifier.doi | 10.1007/s13105-018-0626-0 | |
dc.identifier.pmid | 29611132 | |
dc.identifier.scopus | 2-s2.0-85044728801 | |
dc.identifier.wos | 000433223400014 | |
dc.citation.apa | Jovanović Stojanov, S., Martinović, V., Bogojević, D., Poznanović, G., Petrović, A., Ivanović-Matić, S., & Grigorov, I. (2018). Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway. Journal of Physiology and Biochemistry, 74(2), 345–358. | |
dc.citation.vancouver | Jovanović Stojanov S, Martinović V, Bogojević D, Poznanović G, Petrović A, Ivanović-Matić S, Grigorov I. Modulation of diabetes-related liver injury by the HMGB1/TLR4 inflammatory pathway. J Physiol Biochem. 2018;74(2):345–58. | |
dc.citation.spage | 345 | |
dc.citation.epage | 358 | |
dc.type.version | publishedVersion | en |
dc.citation.rank | M22 |