Prevention of LPS-Induced Acute Kidney Injury in Mice by Bavachin and Its Potential Mechanisms
DC Field | Value | Language |
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dc.contributor.author | Ban, Ka-Yun | - |
dc.contributor.author | Nam, Ga-Young | - |
dc.contributor.author | Kim, Donghee | - |
dc.contributor.author | Oh, Yoon Sin | - |
dc.contributor.author | Jun, Hee-Sook | - |
dc.date.accessioned | 2022-12-30T01:40:13Z | - |
dc.date.available | 2022-12-30T01:40:13Z | - |
dc.date.created | 2022-12-16 | - |
dc.date.issued | 2022-11 | - |
dc.identifier.issn | 2076-3921 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/86347 | - |
dc.description.abstract | Acute kidney injury (AKI) is a serious complication of sepsis with a rapid onset and high mortality rate. Bavachin, an active component of Psoralea corylifolia L., reportedly has antioxidant, anti-apoptotic, and anti-inflammatory effects; however, its beneficial effects on AKI remain undetermined. We investigated the protective effect of bavachin on lipopolysaccharide (LPS)-induced AKI in mice and elucidated the underlying mechanism in human renal tubular epithelial HK-2 cells. Increased serum creatinine and blood urea nitrogen levels were observed in LPS-injected mice; however, bavachin pretreatment significantly inhibited this increase. Bavachin improved the kidney injury score and decreased the expression level of tubular injury markers, such as neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), in both LPS-injected mice and LPS-treated HK-2 cells. LPS-induced oxidative stress via phosphorylated protein kinase C (PKC) beta and upregulation of the NADPH oxidase (NOX) 4 pathway was also significantly decreased by treatment with bavachin. Moreover, bavachin treatment inhibited the phosphorylation of MAPKs (P38, ERK, and JNK) and nuclear factor (NF)-kappa B, as well as the increase in inflammatory cytokine levels in LPS-injected mice. Kruppel-like factor 5 (KLF5) expression was upregulated in the LPS-treated HK-2 cells and kidneys of LPS-injected mice. However, RNAi-mediated silencing of KLF5 inhibited the phosphorylation of NF-kB, consequently reversing LPS-induced KIM-1 and NGAL expression in HK-2 cells. Therefore, bavachin may ameliorate LPS-induced AKI by inhibiting oxidative stress and inflammation via the downregulation of the PKC beta/MAPK/KLF5 axis. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | MDPI | - |
dc.relation.isPartOf | ANTIOXIDANTS | - |
dc.title | Prevention of LPS-Induced Acute Kidney Injury in Mice by Bavachin and Its Potential Mechanisms | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000880700200001 | - |
dc.identifier.doi | 10.3390/antiox11112096 | - |
dc.identifier.bibliographicCitation | ANTIOXIDANTS, v.11, no.11 | - |
dc.description.isOpenAccess | Y | - |
dc.identifier.scopusid | 2-s2.0-85141732122 | - |
dc.citation.title | ANTIOXIDANTS | - |
dc.citation.volume | 11 | - |
dc.citation.number | 11 | - |
dc.contributor.affiliatedAuthor | Ban, Ka-Yun | - |
dc.contributor.affiliatedAuthor | Nam, Ga-Young | - |
dc.contributor.affiliatedAuthor | Kim, Donghee | - |
dc.contributor.affiliatedAuthor | Jun, Hee-Sook | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | acute kidney injury | - |
dc.subject.keywordAuthor | lipopolysaccharide | - |
dc.subject.keywordAuthor | bavachin | - |
dc.subject.keywordAuthor | oxidative stress | - |
dc.subject.keywordAuthor | inflammatory response | - |
dc.subject.keywordPlus | ACUTE-RENAL-FAILURE | - |
dc.subject.keywordPlus | NADPH OXIDASE | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | SEPSIS | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | AKI | - |
dc.subject.keywordPlus | DEFINITIONS | - |
dc.subject.keywordPlus | APOPTOSIS | - |
dc.subject.keywordPlus | STRESS | - |
dc.subject.keywordPlus | FAMILY | - |
dc.relation.journalResearchArea | Biochemistry & Molecular Biology | - |
dc.relation.journalResearchArea | Pharmacology & Pharmacy | - |
dc.relation.journalResearchArea | Food Science & Technology | - |
dc.relation.journalWebOfScienceCategory | Biochemistry & Molecular Biology | - |
dc.relation.journalWebOfScienceCategory | Chemistry, Medicinal | - |
dc.relation.journalWebOfScienceCategory | Food Science & Technology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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