ReferenceID 5681
Maslinic Acid Attenuates Ischemia/Reperfusion-Induced Acute Kidney Injury by Suppressing Inflammation and Apoptosis Through Inhibiting NF-κB and MAPK Signaling Pathway
Front Pharmacol
Inflammation and apoptosis are the major contributors to the mechanisms of acute kidney injury (AKI) due to renal ischemia-reperfusion injury (IRI). Maslinic acid (MA), a pentacyclic triterpene acid mostly found in dieta
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Record Fields
Scalar fields from the final reference record.
- Reference Id
- 5681
- Evidence Id
- 22271
- Core Evidence Id
- 22271
- Source Reference Id
- 4606
- Herb2 Reference Id
- HBREF005403
- Subject Paper Key
- HBIN034527_35496304
- Pubmed Id
- 35496304
- Doi
- 10.3389/fphar.2022.807452
- Paper Title
- Maslinic Acid Attenuates Ischemia/Reperfusion-Induced Acute Kidney Injury by Suppressing Inflammation and Apoptosis Through Inhibiting NF-κB and MAPK Signaling Pathway
- Paper Abstract
- Inflammation and apoptosis are the major contributors to the mechanisms of acute kidney injury (AKI) due to renal ischemia-reperfusion injury (IRI). Maslinic acid (MA), a pentacyclic triterpene acid mostly found in dietary plants, the current study was to demonstrate the renoprotective effect of MA on IRI-induced AKI, and to investigate the role of inflammation and apoptosis-related signaling pathways as a molecular mechanism. C57BL/6J mice were subjected to IRI for 72 h, and MA was daily administered by intraperitoneal injection during this period. In parallel, rat renal proximal tubule cells (NRK52E) were prophylactically treated with MA and then exposed to hydrogen peroxide (H 2 O 2 ). MA treatment significantly inhibited the mRNA expression of interleukin (IL-1β), tumor necrosis factor-α (TGF-α), monocyte chemoattractant protein-1 (MCP-1), and intercellular adhesion molecule-1(ICAM-1). Also, MA reduced the expression of Bax/Bcl2 ratio and cleaved caspase-3. In NRK52 cells, MA inhibited the IκBα degradation, blocked NF-κB/p65 phosphorylation, and nuclear translocation. The phosphorylation of ERK, JNK, and p38 was attenuated by MA in IRI-induced kidney injury and H 2 O 2 -stimulated NRK52 cells. The expression levels of IL-1β, MCP-1, and ICAM-1 were upregulated in H 2 O 2 -stimulated NRK52E cells, which was attenuated by NF-κB inhibitor. H 2 O 2 treatment increased the Bax/Bcl2 ratio and cleaved caspase-3 in NRK52E cells, which was counteracted by MAPK inhibitors. Together, our data demonstrate that MA suppresses IR-induced AKI injury through NF-κB and MAPK signaling pathways and that MA is a promising agent in the treatment of kidney diseases.
- Journal
- Front Pharmacol
- Publish Year
- 2022
- Experiment Subject
- mouse; rat; nrk52 cells; nrk52e cells; rat renal proximal tubule cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Renal Ischemia-reperfusion Injury; Kidney Diseases; Acute Kidney Injury
- Paper Title Cn
- Paper Title En
- Maslinic Acid Attenuates Ischemia/Reperfusion-Induced Acute Kidney Injury by Suppressing Inflammation and Apoptosis Through Inhibiting NF-κB and MAPK Signaling Pathway
- Bilingual Status
- semi_complete