PMID- 35481609
OWN - NLM
STAT- MEDLINE
DCOM- 20220816
LR  - 20220819
IS  - 1099-0461 (Electronic)
IS  - 1095-6670 (Linking)
VI  - 36
IP  - 8
DP  - 2022 Aug
TI  - Dioscin exhibits protective effects on in vivo and in vitro asthma models via 
      suppressing TGF-beta1/Smad2/3 and AKT pathways.
PG  - e23084
LID - 10.1002/jbt.23084 [doi]
AB  - Dioscin is a natural product that possesses protective effects on multiple 
      chronic injuries, but its effects on asthma are not fully understood. Herein, we 
      evaluated its effects on asthmatic mice established by ovalbumin (OVA) 
      sensitization and challenges and further explored the mechanism. Inflammatory 
      cells in bronchoalveolar lavage fluids (BALFs) were analyzed using Diff-Quik 
      staining. OVA-specific immunoglobulin E (IgE)/IgG1 in serum and inflammatory 
      cytokines (interleukin 4[IL-4], IL-5, IL-13, and tumor necrosis factor-alpha) in 
      BALFs and lung tissues were measured using Enzyme-Linked Immunosorbent Assay 
      Kits. Hematoxylin and eosin, periodic acid-Schiff, and immunohistochemistry 
      staining showed histopathological changes in lung tissues. Epithelial-mesenchymal 
      transition (EMT) in human bronchial epithelial (16HBE) cells was assessed by 
      immunofluorescence staining. Hydroxyproline content was used to evaluate collagen 
      deposition. Polymerase chain reaction and Western blot were performed to measure 
      messenger RNA and protein expression. We found that dioscin treatment 
      (particularly at the dose of 80 mg/kg) significantly inhibited pulmonary 
      inflammation in asthmatic mice, as evidenced by the decreased serum OVA-specific 
      IgE/IgG1 and the reduced inflammatory cells and cytokines in BALFs and lung 
      tissues. Moreover, dioscin effectively ameliorated the goblet cell hyperplasia, 
      mucus hypersecretion, collagen deposition, and smooth muscle hyperplasia in the 
      airways of asthmatic mice. Mechanistically, dioscin restrained the activated 
      TGF-beta1/Smad2/3 and protein kinase B (AKT) signal pathways in lung tissues and 
      potently reversed the TGF-beta1-induced EMT and phosphorylation of Smad2/3 and AKT 
      in 16HBE cells. Collectively, dioscin displayed protective effects on OVA-induced 
      asthmatic mice via adjusting TGF-beta1/Smad2/3 and AKT signal pathways, supporting 
      the fact that dioscin could be a candidate for chronic asthma prevention in the 
      future.
CI  - (c) 2022 Wiley Periodicals LLC.
FAU - Shang, Qian
AU  - Shang Q
AD  - Department of Respiratory and Critical Care Medicine, Henan Provincial People's 
      Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan 
      University, Zhengzhou, Henan, China.
FAU - Zhu, Li
AU  - Zhu L
AD  - Department of Pulmonary and Critical Care Medicine, People's Hospital of 
      Zhengzhou University, Henan Provincial People's Hospital, Zhengzhou, Henan, 
      China.
AD  - Academy of Medical Science, Zhengzhou University, Zhengzhou, Henan, China.
FAU - Shang, Weina
AU  - Shang W
AD  - Department of Respiratory and Critical Care Medicine, Henan Provincial People's 
      Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan 
      University, Zhengzhou, Henan, China.
FAU - Zeng, Jia
AU  - Zeng J
AD  - Department of Pulmonary and Critical Care Medicine, People's Hospital of 
      Zhengzhou University, Henan Provincial People's Hospital, Zhengzhou, Henan, 
      China.
FAU - Qi, Yong
AU  - Qi Y
AUID- ORCID: 0000-0002-2653-1307
AD  - Department of Respiratory and Critical Care Medicine, Henan Provincial People's 
      Hospital, People's Hospital of Zhengzhou University, People's Hospital of Henan 
      University, Zhengzhou, Henan, China.
LA  - eng
GR  - YXKC2020005/Henan Young and Middle-aged Health Innovation Leading Talent Training 
      Project/
GR  - SBGJ202102044/Provincial and Ministerial Co-construction Project of Henan 
      Province Medical Science and Technology Research Program/
PT  - Journal Article
DEP - 20220428
PL  - United States
TA  - J Biochem Mol Toxicol
JT  - Journal of biochemical and molecular toxicology
JID - 9717231
RN  - 0 (Immunoglobulin G)
RN  - 0 (Smad2 Protein)
RN  - 0 (Smad3 Protein)
RN  - 0 (Transforming Growth Factor beta1)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 3B95U4OLWV (dioscin)
RN  - 9006-59-1 (Ovalbumin)
RN  - 9007-34-5 (Collagen)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - K49P2K8WLX (Diosgenin)
SB  - IM
MH  - Airway Remodeling
MH  - Animals
MH  - *Asthma/chemically induced/drug therapy
MH  - Bronchoalveolar Lavage Fluid
MH  - Collagen/metabolism
MH  - *Diosgenin/analogs & derivatives/pharmacology
MH  - Disease Models, Animal
MH  - Humans
MH  - Hyperplasia/metabolism/pathology
MH  - Immunoglobulin E/metabolism
MH  - Immunoglobulin G/metabolism
MH  - Lung/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Ovalbumin/adverse effects
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Smad2 Protein/metabolism
MH  - Smad3 Protein/metabolism
MH  - Transforming Growth Factor beta1/metabolism
OTO - NOTNLM
OT  - TGF-beta1/Smad2/3/AKT pathway
OT  - airway inflammation
OT  - airway remodeling
OT  - asthma
OT  - dioscin
EDAT- 2022/04/29 06:00
MHDA- 2022/08/17 06:00
CRDT- 2022/04/28 08:45
PHST- 2022/03/02 00:00 [revised]
PHST- 2021/08/11 00:00 [received]
PHST- 2022/04/14 00:00 [accepted]
PHST- 2022/04/29 06:00 [pubmed]
PHST- 2022/08/17 06:00 [medline]
PHST- 2022/04/28 08:45 [entrez]
AID - 10.1002/jbt.23084 [doi]
PST - ppublish
SO  - J Biochem Mol Toxicol. 2022 Aug;36(8):e23084. doi: 10.1002/jbt.23084. Epub 2022 
      Apr 28.