PMID- 38505077
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240321
IS  - 2072-1439 (Print)
IS  - 2077-6624 (Electronic)
IS  - 2072-1439 (Linking)
VI  - 16
IP  - 2
DP  - 2024 Feb 29
TI  - Improvement of idiopathic pulmonary fibrosis through a combination of Astragalus 
      radix and Angelica sinensis radix via mammalian target of rapamycin signaling 
      pathway-induced autophagy in rat.
PG  - 1397-1411
LID - 10.21037/jtd-24-28 [doi]
AB  - BACKGROUND: There is a major need for effective, well-tolerated treatments for 
      idiopathic pulmonary fibrosis (IPF) in clinic. Astragalus radix (AR; Huangqi) and 
      Angelica sinensis radix (AS; Danggui) have been frequently used in the treatment 
      of IPF. This study aimed to reveal the pharmacological effects and the mechanisms 
      of the action of an AR-AS combination in treating IPF. METHODS: Sprague-Dawley 
      rats were randomly divided into six groups (n=5): control, bleomycin (BLM) model, 
      AR, AS, AR + AS, and prednisone (PDN) groups. A transforming growth factor-beta1 
      (TGF-beta1)-induced MRC-5 cell model were also used. Pulmonary fibrosis, 
      inflammation, oxidative stress, and autophagy were evaluated by performing 
      hematoxylin and eosin (H&E) staining, Masson staining, immunohistochemical 
      staining, quantitative real-time polymerase chain reaction (qRT-PCR), Western 
      blotting, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, and 
      hydroxyproline assay following the treatment of AR, AS, and the AR-AS herb pair. 
      RESULTS: Rats administered the AR-AS herb pair had lower alpha-smooth muscle actin 
      (alpha-SMA), collagen I, fibronectin, and vimentin levels in lung tissues, and lower 
      inflammatory cytokine levels in rat serum. In addition, the AR-AS herb pair 
      induced mammalian target of rapamycin (mTOR)-mediated autophagy and reduced 
      oxidative stress in BLM-induced rats. The effects of the AR and AS combination 
      were confirmed in MRC-5 cells treated with TGF-beta1. Specifically, the combination 
      of AR and AS attenuated MRC-5 cell fibrosis, inflammation, and oxidative stress 
      while inducing autophagy. CONCLUSIONS: The combination of AR and AS protects 
      against IPF by inducing autophagy via inhibiting the mTOR signaling pathway. The 
      synergistic action of AR and AS is superior to that of either AR or AS alone.
CI  - 2024 Journal of Thoracic Disease. All rights reserved.
FAU - Sun, Chao
AU  - Sun C
AD  - Department of Disease Prevention, The Second Affiliated Hospital of Shandong 
      University of Traditional Chinese Medicine, Jinan, China.
FAU - Liu, Huaman
AU  - Liu H
AD  - Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of 
      Shandong University of Traditional Chinese Medicine, Jinan, China.
FAU - Chi, Baihong
AU  - Chi B
AD  - Department of Pulmonary and Critical Medicine, People's Hospital Rizhao, Rizhao, 
      China.
FAU - Han, Jia
AU  - Han J
AD  - Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of 
      Shandong University of Traditional Chinese Medicine, Jinan, China.
FAU - Koga, Yasuhiko
AU  - Koga Y
AD  - Department of Allergy and Respiratory Medicine, Gunma University Graduate School 
      of Medicine, Gunma, Japan.
FAU - Afshar, Kamyar
AU  - Afshar K
AD  - Division of Pulmonary, Critical Care, and Sleep Medicine, University of 
      California San Diego, La Jolla, CA, USA.
FAU - Liu, Xue
AU  - Liu X
AD  - Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of 
      Shandong University of Traditional Chinese Medicine, Jinan, China.
LA  - eng
PT  - Journal Article
DEP - 20240227
PL  - China
TA  - J Thorac Dis
JT  - Journal of thoracic disease
JID - 101533916
PMC - PMC10944740
OTO - NOTNLM
OT  - Angelica sinensis radix (AS)
OT  - Astragalus radix (AR)
OT  - autophagy
OT  - pulmonary fibrosis
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at 
      https://jtd.amegroups.com/article/view/10.21037/jtd-24-28/coif). Y.K. receives a 
      research grant from the Nippon Boehringer Ingelheim Co., Ltd. C.S., H.L., J.H., 
      B.C., and X.L. report funding support from the National Natural Science 
      Foundation of China (No. 82004285). The other author has no conflicts of interest 
      to declare.
EDAT- 2024/03/20 06:45
MHDA- 2024/03/20 06:46
PMCR- 2024/02/29
CRDT- 2024/03/20 04:02
PHST- 2024/01/05 00:00 [received]
PHST- 2024/02/18 00:00 [accepted]
PHST- 2024/03/20 06:46 [medline]
PHST- 2024/03/20 06:45 [pubmed]
PHST- 2024/03/20 04:02 [entrez]
PHST- 2024/02/29 00:00 [pmc-release]
AID - jtd-16-02-1397 [pii]
AID - 10.21037/jtd-24-28 [doi]
PST - ppublish
SO  - J Thorac Dis. 2024 Feb 29;16(2):1397-1411. doi: 10.21037/jtd-24-28. Epub 2024 Feb 
      27.