PMID- 37802812
OWN - NLM
STAT- MEDLINE
DCOM- 20231101
LR  - 20231101
IS  - 1001-5302 (Print)
IS  - 1001-5302 (Linking)
VI  - 48
IP  - 17
DP  - 2023 Sep
TI  - [Matrine inhibits inflammatory response induced by TNF-alpha in human umbilical vein 
      endothelial cells through miR-25-3p-mediated Klf4 pathway].
PG  - 4731-4737
LID - 10.19540/j.cnki.cjcmm.20230510.709 [doi]
AB  - This study aimed to analyze the effect of matrine on tumor necrosis 
      factor-alpha(TNF-alpha)-induced inflammatory response in human umbilical vein endothelial 
      cells(HUVECs) and explore whether the underlying mechanism was related to the 
      miR-25-3p-mediated Kruppel-like factor 4(Klf4) pathway. The HUVEC cell 
      inflammation model was induced by TNF-alpha stimulation. After 24 or 48 hours of 
      incubation with different concentrations of matrine(0.625, 1.25, and 2.5 
      mmol.L~(-1)), CCK-8 assay was used to detect cell proliferation. After treatment 
      with 2.5 mmol.L~(-1) matrine for 48 h, the expression of TNF-alpha, 
      interleukin-6(IL-6), interleukin-1beta(IL-1beta), and Klf4 mRNA and miR-25-3p was 
      detected by real-time fluorescence-based quantitative PCR, and the protein 
      expression of TNF-alpha, IL-6, IL-1beta, and Klf4 was detected by Western blot. The 
      anti-miR-25-3p was transfected into HUVECs, and the effect of anti-miR-25-3p on 
      TNF-alpha-induced cell proliferation and inflammatory factors was detected by the 
      above method. The cells were further transfected with miR-25-3p and incubated 
      with matrine to detect the changes in proliferation and expression of related 
      inflammatory factors, miR-25-3p, and Klf4. The targeting relationship between 
      miR-25-3p and Klf4 was verified by bioinformatics analysis and dual luciferase 
      reporter gene assay. The results displayed that matrine could inhibit 
      TNF-alpha-induced HUVEC proliferation, decrease the mRNA and protein expression of 
      TNF-alpha, IL-6, and IL-1beta, increase the mRNA and protein expression of Klf4, and 
      reduce the expression of miR-25-3p. Bioinformatics analysis showed that there 
      were specific complementary binding sites between miR-25-3p and Klf4 sequences. 
      Dual luciferase reporter gene assay confirmed that miR-25-3p negatively regulated 
      Klf4 expression in HUVECs by targeting. The inhibition of miR-25-3p expression 
      can reduce TNF-alpha-induced cell proliferation and mRNA and protein expression of 
      TNF-alpha, IL-6, and IL-1beta. MiR-25-3p overexpression could reverse the effect of 
      matrine on TNF-alpha-induced cell proliferation and the mRNA and protein expression 
      of TNF-alpha, IL-6, IL-1beta, and Klf4. This study shows that matrine inhibits the 
      inflammatory response induced by TNF-alpha in HUVECs through miR-25-3p-mediated Klf4 
      pathway.
FAU - Xiang, Zi-Ping
AU  - Xiang ZP
AD  - Graduate School, North China University of Science and Technology Tangshan 
      063210, China Key Laboratory of Metabolic Disease, Hebei General Hospital 
      Shijiazhuang 050051, China.
FAU - Li, Yan-Jie
AU  - Li YJ
AD  - Graduate School, North China University of Science and Technology Tangshan 
      063210, China Key Laboratory of Metabolic Disease, Hebei General Hospital 
      Shijiazhuang 050051, China.
FAU - Ma, Huan
AU  - Ma H
AD  - Key Laboratory of Metabolic Disease, Hebei General Hospital Shijiazhuang 050051, 
      China.
FAU - Wang, Xing
AU  - Wang X
AD  - Key Laboratory of Metabolic Disease, Hebei General Hospital Shijiazhuang 050051, 
      China.
FAU - Zhang, Hui-Xin
AU  - Zhang HX
AD  - Chemical Engineering Institute, Shijiazhuang University Shijiazhuang 050035, 
      China.
FAU - Wang, Chao
AU  - Wang C
AD  - Key Laboratory of Metabolic Disease, Hebei General Hospital Shijiazhuang 050051, 
      China.
LA  - chi
PT  - English Abstract
PT  - Journal Article
PL  - China
TA  - Zhongguo Zhong Yao Za Zhi
JT  - Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese 
      materia medica
JID - 8913656
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (MicroRNAs)
RN  - 0 (Matrines)
RN  - 0 (Interleukin-6)
RN  - 0 (Antagomirs)
RN  - EC 1.13.12.- (Luciferases)
RN  - 0 (RNA, Messenger)
RN  - 0 (MIRN25 microRNA, human)
SB  - IM
MH  - Humans
MH  - *Tumor Necrosis Factor-alpha/genetics/pharmacology/metabolism
MH  - *MicroRNAs/genetics/metabolism
MH  - Human Umbilical Vein Endothelial Cells
MH  - Matrines
MH  - Interleukin-6/genetics
MH  - Signal Transduction
MH  - Antagomirs
MH  - Inflammation/drug therapy/genetics/metabolism
MH  - Luciferases/metabolism/pharmacology
MH  - RNA, Messenger
MH  - Apoptosis
OTO - NOTNLM
OT  - Kruppel like transcription factor 4
OT  - human umbilical vein endothelial cells
OT  - inflammatory response
OT  - matrine
OT  - miR-25-3p
EDAT- 2023/10/07 00:42
MHDA- 2023/11/01 12:45
CRDT- 2023/10/06 22:03
PHST- 2023/11/01 12:45 [medline]
PHST- 2023/10/07 00:42 [pubmed]
PHST- 2023/10/06 22:03 [entrez]
AID - 10.19540/j.cnki.cjcmm.20230510.709 [doi]
PST - ppublish
SO  - Zhongguo Zhong Yao Za Zhi. 2023 Sep;48(17):4731-4737. doi: 
      10.19540/j.cnki.cjcmm.20230510.709.