PMID- 19567157
OWN - NLM
STAT- MEDLINE
DCOM- 20091015
LR  - 20161125
IS  - 2542-5641 (Electronic)
IS  - 0366-6999 (Linking)
VI  - 122
IP  - 12
DP  - 2009 Jun 20
TI  - Effects and mechanism of oridonin on pulmonary hypertension induced by chronic 
      hypoxia-hypercapnia in rats.
PG  - 1380-7
AB  - BACKGROUND: Pulmonary arterial hypertension (PAH) is characterized by suppressing 
      apoptosis and enhancing cell proliferation in the vascular wall. Inducing 
      pulmonary artery smooth muscle cells (PASMC) apoptosis had been regarded as a 
      therapeutic approach for PAH. Oridonin can cause apoptosis in many cell lines, 
      while little has been done to evaluate its effect on PASMC. METHODS: Thirty male 
      Sprague-Dawley rats were randomly assigned to three groups: normal control (NC); 
      hypoxia-hypercapnia (HH); Hypoxia-hypercapnia + oridonin (HHO). Rats were exposed 
      to hypoxia-hypercapnia for four weeks. Cultured human PASMC (HPASMC) were 
      assigned to three groups: normoxia (NO); hypoxia (HY); hypoxia + oridonin (HO). 
      The mean pulmonary artery pressure, mass ratio of right ventricle over left 
      ventricle plus septum (RV/(LV + S)), the ratio of thickness of the pulmonary 
      arteriole wall to vascular external diameter (WT%) and the ratio of the vessel 
      wall area to the total area (WA%) were measured. Morphologic changes of pulmonary 
      arteries were observed under light and electron microscopes. The apoptotic 
      characteristics in vitro and in vivo were detected. RESULTS: The mPAP, RV/(LV + 
      S), WT%, and WA% in the HH group were significantly greater than those in the NC 
      (P < 0.01) and HHO groups (P < 0.01); the activities of caspase-3 and caspase-9, 
      and the expressions of Bax, cyt-C and apoptotic index (AI) in the group HH were 
      less than those in the NC and HHO groups; and the expression of Bcl-2 in group HH 
      was greater than that in the NC and HHO groups. HPASMC mitochondrial membrane 
      potentials in group HO was lower than in group HY (P < 0.01), and cyt-C in the 
      cytoplasm, AI, and caspase-9 in the HO group were greater than that in the HY 
      group (P < 0.01), but the expression of Bcl-2 in the HO group was less than that 
      in the HY group (P < 0.05). CONCLUSIONS: The results suggest that oridonin can 
      lower pulmonary artery pressure effectively, and inhibit pulmonary artery 
      structural remodeling by inducing smooth cell apoptosis via a 
      mitochondria-dependent pathway.
FAU - Wang, Liang-Xing
AU  - Wang LX
AD  - Department of Respiratory Medicine, First Affiliated Hospital of Wenzhou Medical 
      College, Wenzhou, Zhejiang 325003, China. 38805@163.com
FAU - Sun, Yu
AU  - Sun Y
FAU - Chen, Chan
AU  - Chen C
FAU - Huang, Xiao-Ying
AU  - Huang XY
FAU - Lin, Quan
AU  - Lin Q
FAU - Qian, Guo-Qing
AU  - Qian GQ
FAU - Dong, Wei
AU  - Dong W
FAU - Chen, Yan-Fan
AU  - Chen YF
LA  - eng
PT  - Journal Article
PL  - China
TA  - Chin Med J (Engl)
JT  - Chinese medical journal
JID - 7513795
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Diterpenes, Kaurane)
RN  - 0APJ98UCLQ (oridonin)
SB  - IM
MH  - Animals
MH  - Antihypertensive Agents/*pharmacology
MH  - Apoptosis
MH  - Blotting, Western
MH  - Diterpenes, Kaurane/*pharmacology
MH  - Hypercapnia/*physiopathology
MH  - *Hypertension, Pulmonary/drug therapy
MH  - Hypoxia/*physiopathology
MH  - Immunohistochemistry
MH  - Male
MH  - Membrane Potential, Mitochondrial
MH  - Microscopy
MH  - Microscopy, Electron, Transmission
MH  - Pulmonary Artery/*drug effects
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2009/07/02 09:00
MHDA- 2009/10/16 06:00
CRDT- 2009/07/02 09:00
PHST- 2009/07/02 09:00 [entrez]
PHST- 2009/07/02 09:00 [pubmed]
PHST- 2009/10/16 06:00 [medline]
PST - ppublish
SO  - Chin Med J (Engl). 2009 Jun 20;122(12):1380-7.