PMID- 36705408
OWN - NLM
STAT- MEDLINE
DCOM- 20230130
LR  - 20230215
IS  - 2050-4527 (Electronic)
IS  - 2050-4527 (Linking)
VI  - 11
IP  - 1
DP  - 2023 Jan
TI  - Sevoflurane participates in the protection of rat renal ischemia-reperfusion 
      injury by down-regulating the expression of TRPM7.
PG  - e753
LID - 10.1002/iid3.753 [doi]
LID - e753
AB  - INTRODUCTION: To investigate the protective effect of sevoflurane preconditioning 
      on renal ischemia-reperfusion injury (renalischemiareperfusionmodel, RIRI) and 
      its related mechanism. METHODS: Eighty healthy adult male SD rats were randomly 
      divided into control group (Sham group), model group (RIRI group), sevoflurane 
      pretreatment group (Sev group) and TRPM7 inhibitor combined with sevoflurane 
      pretreatment group (T + Sev group), 20 animals in each group. Hematoxylin-eosin 
      (HE) staining was used to observe the pathological changes of renal tissue, and 
      the levels of creatinine and urea nitrogen in each group were detected. 
      Deoxyribonucleic acid terminal transferase-mediated dUTP nick end labeling 
      (TUNEL) assay was used to detect renal cell apoptosis, and Western blottingwas 
      used to detect the expression of apoptotic proteins cleaved-caspase-3, bax, 
      Bcl-2, and TRPM7 in renal tissue; Detection of oxidative stress-related index 
      levels in renal tissue and levels of inflammatory factors in renal tissue and 
      serum. RESULTS: Compared with the Sham group, the renal tissue pathological 
      damage was aggravated, the levels of creatinine and blood urea nitrogen were 
      increased, and the apoptosis was increased in the RIR group and the Sev group. 
      Death, malondialdehyde (MDA) levels and inflammatory factors were increased, and 
      superoxide dismutase (SOD) levels were decreased (all p < .05); The scores, 
      apoptosis rate, MDA level, and relative expression of inflammatory factor levels 
      were decreased, and SOD levels were increased (all p < .05). Compared with the 
      Sev group, the renal tissue pathological damage in the T + Sev group was 
      aggravated, creatinine, blood urea nitrogen levels increased, apoptosis 
      increased, apoptosis-related proteins cleaved-caspase-3, bax, Bcl-2 showed 
      increased apoptosis, malondialdehyde (MDA) levels, inflammatory factor levels 
      increased, ultrahigh The levels of oxide dismutase (SOD) were decreased (all 
      p < .05). CONCLUSIONS: Therefore, we believe that sevoflurane is involved in the 
      protection of rat renal ischemia-reperfusion injury by downregulating the 
      expression of TRPM7.
CI  - (c) 2022 The Authors. Immunity, Inflammation and Disease published by John Wiley & 
      Sons Ltd.
FAU - Xu, Xudong
AU  - Xu X
AUID- ORCID: 0000-0002-7674-7771
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Deng, Rongrong
AU  - Deng R
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Zou, Lu
AU  - Zou L
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Pan, Xiaoyan
AU  - Pan X
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Sheng, Zhifeng
AU  - Sheng Z
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Xu, Da
AU  - Xu D
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
FAU - Gan, Tingting
AU  - Gan T
AD  - Department of Anesthesiology, Changzhou Hospital of Traditional Chinese Medicine, 
      Changzhou, Jiangsu, China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immun Inflamm Dis
JT  - Immunity, inflammation and disease
JID - 101635460
RN  - 38LVP0K73A (Sevoflurane)
RN  - EC 3.4.22.- (Caspase 3)
RN  - 0 (bcl-2-Associated X Protein)
RN  - AYI8EX34EU (Creatinine)
RN  - 0 (TRPM Cation Channels)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - EC 1.15.1.1 (Superoxide Dismutase)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 2.7.11.1 (Trpm7 protein, rat)
SB  - IM
MH  - Rats
MH  - Male
MH  - Animals
MH  - Sevoflurane/pharmacology
MH  - Caspase 3/metabolism
MH  - Rats, Sprague-Dawley
MH  - bcl-2-Associated X Protein/metabolism
MH  - Creatinine
MH  - *TRPM Cation Channels
MH  - *Reperfusion Injury/prevention & control/metabolism/pathology
MH  - Proto-Oncogene Proteins c-bcl-2/metabolism
MH  - Superoxide Dismutase/metabolism
MH  - Malondialdehyde/metabolism
PMC - PMC9803933
OTO - NOTNLM
OT  - TRPM7
OT  - inflammatory factor
OT  - oxidative stress
OT  - renal ischemia-reperfusion injury
OT  - sevoflurane
COIS- The authors declare no conflict of interest.
EDAT- 2023/01/28 06:00
MHDA- 2023/01/31 06:00
PMCR- 2022/12/31
CRDT- 2023/01/27 08:22
PHST- 2022/12/02 00:00 [revised]
PHST- 2022/08/12 00:00 [received]
PHST- 2022/12/05 00:00 [accepted]
PHST- 2023/01/27 08:22 [entrez]
PHST- 2023/01/28 06:00 [pubmed]
PHST- 2023/01/31 06:00 [medline]
PHST- 2022/12/31 00:00 [pmc-release]
AID - IID3753 [pii]
AID - 10.1002/iid3.753 [doi]
PST - ppublish
SO  - Immun Inflamm Dis. 2023 Jan;11(1):e753. doi: 10.1002/iid3.753.