PMID- 31773715
OWN - NLM
STAT- MEDLINE
DCOM- 20201214
LR  - 20201214
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 21
DP  - 2019 Nov
TI  - Effects of butylphthalide on oxidative stress and inflammatory response in rats 
      with myocardial infarction through Akt/Nrf2 signaling pathway.
PG  - 9642-9650
LID - 19458 [pii]
LID - 10.26355/eurrev_201911_19458 [doi]
AB  - OBJECTIVE: The aim of this study was to investigate the effects of butylphthalide 
      on oxidative stress and inflammatory response in rats with myocardial infarction 
      through the protein kinase B/nuclear factor E2-related factor 2 (Akt/Nrf2) 
      signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were 
      randomly divided into three groups, including sham group (n=12), model group 
      (n=12) and butylphthalide group (n=12). In the sham group, the heart was exposed, 
      and normal saline was intraperitoneally injected after the operation. In the 
      model group, acute myocardial infarction (AMI) model was established, and normal 
      saline was intraperitoneally injected after the operation. In the butylphthalide 
      group, AMI model was established, and butylphthalide was intraperitoneally 
      injected after the operation. After intervention for 4 weeks, the rats were 
      killed, and the samples were collected. The morphology of heart tissues was 
      observed via hematoxylin-eosin (HE) staining. The expression of nicotinamide 
      adenine dinucleotide phosphate oxidase-1 (NOX-1) was detected via 
      immunohistochemistry. The protein expressions of phosphorylated Akt (p-Akt) and 
      p-Nrf2 were detected via Western blotting. Moreover, the content of 
      interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) was detected via 
      enzyme-linked immunosorbent assay (ELISA). The messenger ribonucleic acid (mRNA) 
      expression levels of IL-1beta, TNF-alpha and NOX-1 were detected via quantitative 
      Polymerase Chain reaction (qPCR). Furthermore, the apoptosis rate of the cells 
      was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end 
      labeling (TUNEL) assay. RESULTS: The morphology of heart tissues was 
      significantly damaged in the model group and butylphthalide group compared with 
      the sham group. However, it was significantly improved in the butylphthalide 
      group when compared with the model group. The expression level of NOX-1 increased 
      markedly in the model group and butylphthalide group compared with the sham group 
      (p<0.05). However, it was remarkably reduced in the butylphthalide group compared 
      with the model group (p<0.05). Meanwhile, the protein expression levels of p-Akt 
      and p-Nrf2 were significantly higher in the model group and butylphthalide group 
      than those of the sham group (p<0.05). However, the protein expression levels of 
      p-Akt and p-Nrf2 in the butylphthalide group were remarkably lower than the model 
      group (p<0.05). The mRNA expression levels of IL-1beta, TNF-alpha and NOX-1 were 
      markedly higher in the model group and butylphthalide group than those of the 
      sham group (p<0.05). However, they remarkably declined in the butylphthalide 
      group compared with the model group (p<0.05). In addition, the content of IL-1beta 
      and TNF-alpha increased in the model group and butylphthalide group when compared 
      with the sham group (p<0.05). The content of IL-1beta and TNF-alpha in the 
      butylphthalide group was significantly lower than the model group (p<0.05). 
      Furthermore, the apoptosis rate was significantly higher in the model group and 
      butylphthalide group than the sham group (p<0.05), which was significantly lower 
      in the butylphthalide group than the model group (p<0.05). CONCLUSIONS: 
      Butylphthalide inhibits inflammatory and oxidative stress responses after AMI by 
      regulating the Akt/Nrf2 signaling pathway, thereby inhibiting myocardial 
      apoptosis and benefiting the morphological repair of myocardial tissues.
FAU - Bai, M
AU  - Bai M
AD  - Department of Cardiology, The First Hospital of Lanzhou University, Lanzhou, 
      China. 2219896654@qq.com.
FAU - Pan, C-L
AU  - Pan CL
FAU - Jiang, G-X
AU  - Jiang GX
FAU - Zhang, Y-M
AU  - Zhang YM
FAU - Zhang, Z
AU  - Zhang Z
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Benzofurans)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Nfe2l2 protein, rat)
RN  - 822Q956KGM (3-n-butylphthalide)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
SB  - IM
MH  - Animals
MH  - Benzofurans/*pharmacology
MH  - Disease Models, Animal
MH  - Inflammation/*drug therapy/metabolism/pathology
MH  - Male
MH  - Myocardial Infarction/*drug therapy/metabolism/pathology
MH  - NF-E2-Related Factor 2/genetics/*metabolism
MH  - Neuroprotective Agents/*pharmacology
MH  - Oxidative Stress/drug effects
MH  - Proto-Oncogene Proteins c-akt/genetics/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Signal Transduction/drug effects
EDAT- 2019/11/28 06:00
MHDA- 2020/12/15 06:00
CRDT- 2019/11/28 06:00
PHST- 2019/11/28 06:00 [entrez]
PHST- 2019/11/28 06:00 [pubmed]
PHST- 2020/12/15 06:00 [medline]
AID - 19458 [pii]
AID - 10.26355/eurrev_201911_19458 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Nov;23(21):9642-9650. doi: 
      10.26355/eurrev_201911_19458.