PMID- 27499938
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160808
LR  - 20201001
IS  - 2072-1439 (Print)
IS  - 2077-6624 (Electronic)
IS  - 2072-1439 (Linking)
VI  - 8
IP  - 7
DP  - 2016 Jul
TI  - Ginsenoside Rg1 attenuates hypoxia and hypercapnia-induced vasoconstriction in 
      isolated rat pulmonary arterial rings by reducing the expression of p38.
PG  - 1513-23
LID - 10.21037/jtd.2016.05.71 [doi]
AB  - BACKGROUND: Pulmonary arterial hypertension (PAH) is a fatal disease 
      characterized by increased pulmonary arteriolar resistance. Pulmonary 
      vasoconstriction has been proved to play a significant role in PAH. We previously 
      reported that Panax notoginseng saponins (PNS) might attenuate hypoxia and 
      hypercapnia-induced pulmonary vasoconstriction (HHPV). METHODS: In the present 
      study, our specific objective was to investigate the role of ginsenoside Rg1, a 
      major component of PNS, in this process and the possible underlying mechanism. 
      The second order pulmonary rings isolated from the Sprague-Dawley rats were 
      treated with different dosage of ginsenoside Rg1 at 8, 40, or 100 mg/L 
      respectively, both before and during the conditions of hypoxia and hypercapnia. 
      Contractile force changes of the rings were detected. Furthermore, SB203580, the 
      selective inhibitor for p38 activation was applied to the rings. Pulmonary 
      arterial smooth muscle cells (PASMCs) were cultured under hypoxic and hypercapnic 
      conditions, and ginsenoside Rg1 was administered to detect the changes induced by 
      p38. RESULTS: Under the hypoxic and hypercapnic conditions, we observed a 
      biphasic pulmonary artery contractile response to the second pulmonary artery 
      rings. It is hypothesized that the observed attenuation of vasoconstriction and 
      the production of vasodilation could have been induced by ginsenoside Rg1. This 
      effect was significantly reinforced by SB203580 (P<0.05 or P<0.01). The 
      expression of p38 in the PASMCs under hypoxic and hypercapnic conditions was 
      significantly activated (P<0.05 or P<0.01) and the observed activation was 
      attenuated by ginsenoside Rg1 (P<0.05 or P<0.01). CONCLUSIONS: Our findings 
      strongly support the significant role of ginsenoside Rg1 in the inhibition of 
      hypoxia and hypercapnia-induced vasoconstriction by the p38 pathway.
FAU - Zheng, Mengxiao
AU  - Zheng M
AD  - Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China 
      ;
FAU - Zhao, Meiping
AU  - Zhao M
AD  - Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China 
      ;
FAU - Tang, Lanlan
AU  - Tang L
AD  - Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China 
      ;
FAU - Zhang, Congcong
AU  - Zhang C
AD  - Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China 
      ;
FAU - Song, Longsheng
AU  - Song L
AD  - Division of Cardiovascular Medicine University of Iowa Carver College of 
      Medicine, Iowa City 52242, USA.
FAU - Wang, Wantie
AU  - Wang W
AD  - Department of Pathophysiology, Wenzhou Medical University, Wenzhou 325035, China 
      ;
LA  - eng
PT  - Journal Article
PL  - China
TA  - J Thorac Dis
JT  - Journal of thoracic disease
JID - 101533916
PMC - PMC4958841
OTO - NOTNLM
OT  - Ginsenoside Rg1
OT  - hypercapnia
OT  - hypoxia
OT  - p38
OT  - pulmonary hypertension
COIS- Conflicts of Interest: The authors have no conflicts of interest to declare.
EDAT- 2016/08/09 06:00
MHDA- 2016/08/09 06:01
PMCR- 2016/07/01
CRDT- 2016/08/09 06:00
PHST- 2016/08/09 06:00 [entrez]
PHST- 2016/08/09 06:00 [pubmed]
PHST- 2016/08/09 06:01 [medline]
PHST- 2016/07/01 00:00 [pmc-release]
AID - jtd-08-07-1513 [pii]
AID - 10.21037/jtd.2016.05.71 [doi]
PST - ppublish
SO  - J Thorac Dis. 2016 Jul;8(7):1513-23. doi: 10.21037/jtd.2016.05.71.