{'fraction_non_alphanumeric': 0.038202247191011236, 'fraction_numerical': 0.012734082397003745, 'mean_word_length': 4.733905579399142, 'pattern_counts': {'":': 0, '<': 3, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Mechanism of sini decoction in regulating beta-adrenergic receptor signal transduction in rats with myocardial ischemia].

OBJECTIVE
To investigate the effect of Sini Decoction (SND) on beta-adrenergic receptor (beta-AR) signal transduction in rats with myocardial ischemia.


METHODS
After beta-AR had been blocked by propranolol, the myocardial ischemia rats were established by pituitrin injection. The density of beta-AR in myocardial cell membrane was determined by radioligand binding assay, cAMP level in plasma and myocardial tissue was detected by radioimmunoassay (RIA), and the mRNA expression of beta 1-AR and beta 1-AR kinase (beta ARK-1) was measured by quantitative reverse transcriptase polymerase chain reaction (RT-PCR) amplifying assay.


RESULTS
In myocardial ischemia group, the density of beta 1-AR was up-regulated and the mRNA expression of beta ARK-1 increased (P < 0.01), but the cAMP level in plasma and myocardium was lower than that in the normal group (P < 0.01 and P < 0.05). SND could promote beta 1-AR mRNA expression and inhibit beta ARK-1 mRNA expression so as to increase the density of beta-AR and cause significant raising of cAMP level in plasma and myocardium.


CONCLUSION
SND could reduce the desensitization of beta 1-AR during myocardial ischemia and improve signal transduction of beta-AR.