PMID- 36545745
OWN - NLM
STAT- MEDLINE
DCOM- 20230522
LR  - 20230522
IS  - 2212-3873 (Electronic)
IS  - 1871-5303 (Linking)
VI  - 23
IP  - 7
DP  - 2023
TI  - Effects and Mechanisms of Ban-Xia Xie-Xin Decoction on Type 2 Diabetes Mellitus: 
      Network Pharmacology Analysis and Experimental Evidence.
PG  - 947-963
LID - 10.2174/1871530323666221220141716 [doi]
AB  - BACKGROUND: Studies have indicated that Ban-Xia Xie-Xin Decoction (BXXXD) has 
      therapeutic effects on type 2 diabetes mellitus (T2DM). However, due to the 
      complexity of components and diversity of targets, the mechanisms are still not 
      fully elucidated. OBJECTIVE: In this research, we systematically analysed the 
      targets of BXXXD through the method of network pharmacology and further validated 
      them through experiments. METHODS: The active components and therapeutic targets 
      were identified, and these targets were analysed by the methods of gene ontology 
      (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), and protein-protein 
      interaction (PPI) analysis. Then, based on these network pharmacology analyses, 
      we validated the main targets through animal experiments. RESULTS: A total of 169 
      active components and 159 targets were identified. KEGG analysis showed that the 
      mitogen-activated protein kinase (MAPK) signalling pathway, tumour necrosis 
      factor (TNF) signalling pathway, the phosphatidylinositol 3' -kinase (PI3K), Akt 
      signalling pathway, and other pathways were related to the treatment of T2DM by 
      BXXXD. PPI network analysis showed that the key genes included signal transducers 
      and activators of transcription 3 (STAT3), JUN, TNF, Recombinant V-Rel 
      Reticuloendotheliosis Viral Oncogene Homolog A (RELA), Akt/PKB- 1 (Protein kinase 
      B), TP53, mitogen-activated protein kinase-1 (MAPK-1), mitogen-activated protein 
      kinase-3 (MAPK-3), interleukin- 6 (IL6), and mitogen-activated protein kinase-14 
      (MAPK- 14), respectively. Animal experiments showed that BXXXD could reduce blood 
      glucose and improve insulin resistance, which may be related to the mechanisms of 
      inhibiting TNF, interleukin-1 (IL-1), IL-6, and interleukin-17 (IL-17) and 
      promoting Akt phosphorylation. CONCLUSION: Our research revealed the mechanisms 
      of BXXXD in the treatment of diabetes, which laid a solid foundation for further 
      studies on the molecular mechanisms of BXXXD in the treatment of T2DM.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Yang, Maoyi
AU  - Yang M
AD  - Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, 
      China.
FAU - Hu, Zhipeng
AU  - Hu Z
AD  - Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, 
      China.
FAU - Zhang, Lili
AU  - Zhang L
AD  - Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, 
      China.
FAU - Yue, Rensong
AU  - Yue R
AD  - Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, 
      China.
LA  - eng
GR  - NO.2018SZ0068/Sichuan Province Science and Technology Support Program/
GR  - No.81774279/National Natural Science Foundation of China (NSFC)/
PT  - Journal Article
PL  - United Arab Emirates
TA  - Endocr Metab Immune Disord Drug Targets
JT  - Endocrine, metabolic & immune disorders drug targets
JID - 101269157
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - 0 (Blood Glucose)
RN  - 0 (Interleukin-6)
SB  - IM
MH  - Animals
MH  - *Diabetes Mellitus, Type 2/drug therapy
MH  - Proto-Oncogene Proteins c-akt
MH  - Network Pharmacology
MH  - Signal Transduction
MH  - Blood Glucose
MH  - Interleukin-6
MH  - Molecular Docking Simulation
OTO - NOTNLM
OT  - Ban-Xia Xie-Xin decoction
OT  - gene ontology
OT  - network pharmacology
OT  - protein-protein interaction
OT  - traditional Chinese medicine
OT  - type 2 diabetes mellitus
EDAT- 2022/12/23 06:00
MHDA- 2023/05/22 06:42
CRDT- 2022/12/22 02:46
PHST- 2022/07/01 00:00 [received]
PHST- 2022/11/07 00:00 [revised]
PHST- 2022/11/09 00:00 [accepted]
PHST- 2023/05/22 06:42 [medline]
PHST- 2022/12/23 06:00 [pubmed]
PHST- 2022/12/22 02:46 [entrez]
AID - EMIDDT-EPUB-128336 [pii]
AID - 10.2174/1871530323666221220141716 [doi]
PST - ppublish
SO  - Endocr Metab Immune Disord Drug Targets. 2023;23(7):947-963. doi: 
      10.2174/1871530323666221220141716.