PMID- 35496304
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220716
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 13
DP  - 2022
TI  - Maslinic Acid Attenuates Ischemia/Reperfusion-Induced Acute Kidney Injury by 
      Suppressing Inflammation and Apoptosis Through Inhibiting NF-kappaB and MAPK 
      Signaling Pathway.
PG  - 807452
LID - 10.3389/fphar.2022.807452 [doi]
LID - 807452
AB  - 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-1beta), tumor 
      necrosis factor-alpha (TGF-alpha), 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 IkappaBalpha 
      degradation, blocked NF-kappaB/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-1beta, 
      MCP-1, and ICAM-1 were upregulated in H(2)O(2)-stimulated NRK52E cells, which was 
      attenuated by NF-kappaB 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-kappaB and MAPK signaling pathways and that MA is a promising agent in the 
      treatment of kidney diseases.
CI  - Copyright (c) 2022 Sun, Choi, Kim, Bae, Ma and Kim.
FAU - Sun, Wenjuan
AU  - Sun W
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
FAU - Choi, Hong Sang
AU  - Choi HS
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
FAU - Kim, Chang Seong
AU  - Kim CS
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
FAU - Bae, Eun Hui
AU  - Bae EH
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
FAU - Ma, Seong Kwon
AU  - Ma SK
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
FAU - Kim, Soo Wan
AU  - Kim SW
AD  - Department of Internal Medicine, Chonnam National University Medical School, 
      Gwangju, South Korea.
LA  - eng
PT  - Journal Article
DEP - 20220412
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC9039024
OTO - NOTNLM
OT  - MAPK
OT  - NF-kappaB
OT  - ischemia-reperfusion injury
OT  - kidney diseases
OT  - maslinic acid
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/05/03 06:00
MHDA- 2022/05/03 06:01
PMCR- 2022/04/12
CRDT- 2022/05/02 06:48
PHST- 2021/11/02 00:00 [received]
PHST- 2022/03/03 00:00 [accepted]
PHST- 2022/05/02 06:48 [entrez]
PHST- 2022/05/03 06:00 [pubmed]
PHST- 2022/05/03 06:01 [medline]
PHST- 2022/04/12 00:00 [pmc-release]
AID - 807452 [pii]
AID - 10.3389/fphar.2022.807452 [doi]
PST - epublish
SO  - Front Pharmacol. 2022 Apr 12;13:807452. doi: 10.3389/fphar.2022.807452. 
      eCollection 2022.