PMID- 28526985
OWN - NLM
STAT- MEDLINE
DCOM- 20180815
LR  - 20181113
IS  - 1573-2576 (Electronic)
IS  - 0360-3997 (Linking)
VI  - 40
IP  - 5
DP  - 2017 Oct
TI  - Salidroside Attenuates LPS-Induced Acute Lung Injury in Rats.
PG  - 1520-1531
LID - 10.1007/s10753-017-0593-6 [doi]
AB  - The purpose of the present study was to investigate the effects of salidroside 
      (Sal) on lung injury in lipopolysaccharide (LPS)-induced endotoxemic in vitro and 
      in vivo. SD rats were randomly divided into five groups: control group, LPS group 
      (15 mg kg(-1)), LPS plus dexamethasone (2 mg kg(-1)), and LPS plus Sal groups 
      with different Sal doses (20 mg kg(-1), 40 mg kg(-1)). Wet-to-dry weight (W/D) 
      ratio was performed. Hematoxylin-eosin (HE) staining of lung was performed. Lung 
      level of myeloperoxidase (MPO) was measured. Serum levels of the activities of 
      the anti-oxidant superoxide dismutase (SOD), glutathione peroxidase (GSH-px), 
      glutathione (GSH), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and 
      interleukin-1beta (IL-1beta) were measured. Caveolin-1 and TLR/NF-kappaB pathway proteins 
      were detected by Western blot. In vitro, we evaluated the protective effect of 
      Sal on A549 cell line induced by LPS. The activities of the antioxidant SOD, CAT, 
      GSH and GPX, TNF-alpha, IL-6, and IL-1beta in cellular supernatant were measured. 
      Caveolin-1 and TLR/NF-kappaB pathway was examined by Western blot. As a result, Sal 
      significantly attenuated the above indices. In addition, Sal exerts pronounced 
      protective effects in rats subjected to LPS possibly through inhibiting the 
      caveolin-1 and TLR/NF-kappaB pathway in vivo. Our results indicated that Sal could be 
      a potential therapeutic agent for the treatment of lung injury disease.
FAU - Jingyan, Liu
AU  - Jingyan L
AD  - Department of Physiology and Pharmacology, China Pharmaceutical University, 
      Nanjing, China.
FAU - Yujuan, Guo
AU  - Yujuan G
AD  - Department of Physiology and Pharmacology, China Pharmaceutical University, 
      Nanjing, China.
FAU - Yiming, Yang
AU  - Yiming Y
AD  - Department of Physiology and Pharmacology, China Pharmaceutical University, 
      Nanjing, China.
FAU - Lingpeng, Zhu
AU  - Lingpeng Z
AD  - Department of Physiology and Pharmacology, China Pharmaceutical University, 
      Nanjing, China.
FAU - Tianhua, Yan
AU  - Tianhua Y
AD  - Department of Physiology and Pharmacology, China Pharmaceutical University, 
      Nanjing, China. yantianhuabest@126.com.
FAU - Mingxing, Miao
AU  - Mingxing M
AD  - National Experimental Teaching Demonstration Center of Pharmacy, China 
      Pharmaceutical University, Nanjing, China. mmx0224@cpu.edu.cn.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Antioxidants)
RN  - 0 (Caveolin 1)
RN  - 0 (Glucosides)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Phenols)
RN  - M983H6N1S9 (rhodioloside)
SB  - IM
MH  - A549 Cells
MH  - Animals
MH  - Antioxidants
MH  - Caveolin 1/antagonists & inhibitors
MH  - Endotoxemia/chemically induced
MH  - Glucosides/*pharmacology
MH  - Humans
MH  - Lipopolysaccharides
MH  - Lung/pathology
MH  - Lung Injury/*drug therapy
MH  - NF-kappa B/antagonists & inhibitors
MH  - Phenols/*pharmacology
MH  - Rats
OTO - NOTNLM
OT  - LPS
OT  - TLR/NF-kappaB
OT  - caveolin-1
OT  - lung injury
OT  - salidroside
EDAT- 2017/05/21 06:00
MHDA- 2018/08/16 06:00
CRDT- 2017/05/21 06:00
PHST- 2017/05/21 06:00 [pubmed]
PHST- 2018/08/16 06:00 [medline]
PHST- 2017/05/21 06:00 [entrez]
AID - 10.1007/s10753-017-0593-6 [pii]
AID - 10.1007/s10753-017-0593-6 [doi]
PST - ppublish
SO  - Inflammation. 2017 Oct;40(5):1520-1531. doi: 10.1007/s10753-017-0593-6.