Crocin Suppresses Inflammatory Response in LPS-Induced Acute Lung Injury (ALI) Via Regulation of HMGB1/TLR4 Inflammation Pathway

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dc.authorid0000-0002-0917-0378
dc.contributor.authorAkin, Ali Tuğrul
dc.contributor.authorCeylan, Tayfun
dc.contributor.authorKaymak, Emin
dc.date.accessioned2022-11-03T13:39:19Z
dc.date.available2022-11-03T13:39:19Z
dc.date.issued2022en_US
dc.departmentKapadokya Üniversitesi, Diş Hekimliği Fakültesi, Diş Hekimliği Bölümü
dc.description.abstractAcute lung injury (ALI) is a frequent consequence which has high morbidity and mortality in sepsis. The most significant pathogen hypothesized to be causing the formation of ALI in sepsis is thought to be lipopolysaccharide (LPS), a key endotoxin component of gram-negative bacteria. Although endotoxin-induced inflammation is a complex process, it can be artificially produced via administration of lipopolysaccharide (LPS) in Experimental sepsis models. The main objective of thisstudy isto determine possible anti-inflammatory effects of crocin (CRO) which has many biological properties such as anti-inflammatory, antioxidant, and anti-apoptotic in LPS-induced ALI. For this purpose, total 40 Wistar albino rats randomly divided into four groups, ten rats in per group: Control (no treatment), CRO (given 50 mg/kg crocin for 9 days), LPS (given 30 mg/kg LPS at 9th day), LPS+CRO (given 50 mg/kg crocin for 9 days and 30 mg/kg LPS at 9th day). After experimental protocol, rats were sacrificed and lung tissues were extracted for further analysis. Histological examinations were performed for detecting histopathological changes in the lung tissue and the changes in the HMGB1 and TLR4 expressions were determined via immunohistochemical staining. Hemorrhage, mononuclear cell infiltration and HMGB1 and TLR4 expressions significantly increased in the LPS group (p<0.05). However, CRO administrations exerted a strong protective effect on the lung tissues in terms of these parameters in LPS+CRO group (p<0.05). According to our results, we suggest that CRO can be considered as a protective agent against bacterial endotoxin induced ALI via inhibition of HMGB1/TLR4 pathway-mediated inflammatory response.
dc.identifier.citationAKİN, A. T., CEYLAN, T., & KAYMAK, E. (2022). Crocin Suppresses Inflammatory Response in LPS-Induced Acute Lung Injury ALI Via Regulation of HMGB1 TLR4 Inflammation Pathway. Presented at the INTERNATIONAL CAPPADOCIA HEALTH AND LIFE CONFERENCE, NEVŞEHİR.
dc.identifier.endpage79en_US
dc.identifier.startpage78en_US
dc.identifier.urihttps://doi.org/10.35250/kun/9786054448357
dc.identifier.urihttps://hdl.handle.net/20.500.12695/1867
dc.institutionauthorCeylan, Tayfun
dc.language.isoen
dc.relation.ispartofINTERNATIONAL CAPPADOCIA HEALTH AND LIFE CONFERENCE
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectAcute lung injury
dc.subjectCrocin
dc.subjectInflammation
dc.subjectLipopolysaccharide
dc.titleCrocin Suppresses Inflammatory Response in LPS-Induced Acute Lung Injury (ALI) Via Regulation of HMGB1/TLR4 Inflammation Pathway
dc.title.alternativeKrosin, LPS Kaynaklı Akut Akciğer Hasarında (ALI) HMGB1/TLR4 İnflamasyon Yolağının Düzenlenmesi Yoluyla İnflamatuar Yanıtı Baskılar
dc.typeConference Object

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