The effect of 5-HD on expression of PKC-alpha in rats of chronic hypoxic pulmonary hypertension.
- Author:
Ying SHU
1
;
Qiu LI
;
Yun-lei LI
;
Li-ping ZHANG
;
Cheng-shui CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Decanoic Acids; pharmacology; Hydroxy Acids; pharmacology; Hypertension, Pulmonary; etiology; metabolism; physiopathology; Hypoxia; complications; physiopathology; Male; Muscle, Smooth, Vascular; metabolism; Potassium Channel Blockers; pharmacology; Potassium Channels; drug effects; Protein Kinase C-alpha; genetics; metabolism; Pulmonary Artery; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2011;27(3):311-314
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of mito chondrial K(ATP) channels (mitoK(ATP)) inhibitor 5-hydroxydecanoate(5-HD) on chronic hypoxic pulmonary artery hypertension (CHPAH) rats and its underlying mechanisms.
METHODSForty-eight male SD rats were equally divided into 4 groups randomly (n=12): normal group, hypoxia group, hypoxia + 5-HD group, hypoxia + Diazoxide group. Except the first group, the other three groups were put into hypoxic [O2 (10.0% +/- 0.3%] and nonrmobaric chamber for four weeks to establish chronic hypoxic model and received different interference. When the interference completed, right heart catheter was used to detect the mean pulmonary arterial pressure (mPAP) of each rat and PKC-alpha mRNA expression in pulmonary arteries was detected by reverse transcription-polymerase chain reaction (RT-PCR) and protein expression by Western blot.
RESULTS(mPAP was much higher in hypoxia group than that in normal group (P < 0.01) while in hypoxia + 5-HD group and hypoxia + diazoxide were decreased significantly compared to hypoxia group (P < 0.01). (2) The protein and mRNA levels of PKC-alpha in the hypoxic group were higher than those in normal group (P < 0.05).
CONCLUSION5-HD plays a protective role on CHPAH. The mechanism of its effect may be attributed to inhibiting MitoK(ATP).
