Details

Autor(en) / Beteiligte

• Ren-an, Qin
• Juan, Lin
• Chuyuan, Li
• Wenjuan, Fu
• Chunyan, Huang
• Xuemei, Yu
• Lin, Huang
• Hong, Nie

Titel

Study of the protective mechanisms of Compound Danshen Tablet (Fufang Danshen Pian) against myocardial ischemia/reperfusion injury via the Akt-eNOS signaling pathway in rats

Ist Teil von

• Journal of ethnopharmacology, 2014-10, Vol.156, p.190-198

Ort / Verlag

Ireland: Elsevier Ireland Ltd

Erscheinungsjahr

2014

Quelle

MEDLINE

Beschreibungen/Notizen

• Compound Danshen Tablet (CDT), an herbal preparation consisting of Salvia miltiorrhiza (Radix and rhizome of Salvia miltiorrhiza Bge.), Notoginseng (Radix and rhizome of Panax notoginseng (Burk.) F. H. Chen) and Borneolum Syntheticum, is widely used to improve coronary heart disease, cardiac angina and atherosclerosis in clinic in Asia and Pacific Ocean area, especially in China. The study is to research the protective mechanisms of Compound Danshen Tablet (CDT) against myocardial ischemia/reperfusion (MI/R) injury via the Akt-eNOS signaling Pathway in rats. Rats were randomized into 7 groups: Sham group; Model group; Low-Dose CDT group (0.315g/kg/d, i.g); Middle-Dose CDT group (0.63g/kg/d, i.g); High-Dose CDT group (1.26g/kg/d, i.g); Compound Danshen Dripping Pills (CDDP) group (0.0945g/kg/d, i.g); Sulfotanshinone Sodium Injection (Tan II A) group (5mg/kg/d, i.m). After the administration, the hearts of the rats were subjected to 30min of coronary artery occlusion and 2h of reperfusion except the Sham group rats. CDT significantly decreased infarct size, apoptosis, caspase-3 protein expression, MDA level in myocardial tissues, the activities of serum CK, LDH and cTnI; on the contrary, it increased p-Akt, p-eNOS, bcl-2 protein expression, the activities of SOD and tissue LDH, and the level of NO. CDT can protect cardiomyocytes against MI/R injury and inhibits apoptosis in rats by activating Akt-eNOS signaling pathway. Compound Danshen Tablet can up-regulate the eNOS phosphorylation level, activate the Akt-eNOS signal pathway of RISK pathway, increase the release of NO, inhibit apoptosis pathway, up-regulate Bcl-2, and down-regulate Bax, Caspsase-3 to protect cardiomyocyte against MI/R injury. [Display omitted]