Objective: To explore the effect and mechanism of Shanjing capsule on energy metabolism

oxyradical and apoptosis-related genes in myocardial ischemia rats. Method: The chronic myocardial ischemia models were established with ligating coronary artery. Then the modeled rats were randomly divided into Shanjing capsule low dose

middle dose and high dose groups (283.5

850.5

1 701.0 mg·kg-1)

positive drug group (324.0 mg·kg-1). The rats in sham operation group and model group received equivalent amount of 0.9% Sodium Chloride Injection for 10 days. Then ultraviolet visible spectrophotometer was used to detect the content and activity of lactic acid (LD)

free fatty acids (NEFA)

malondialdehyde (MDA)

total superoxide dismutase (SOD)

glutathione peroxidase (GSH-Px)

NO and ATP in serum and tissues. The expression levels of nuclear transcription factor-κB (NF-κB)

Caspase-3

B-cell lymphoma/leukemia-2(Bcl-2) and Bcl-2 associated X protein(Bax) in myocardial tissues were detected by Western blot and RT-PCR. Result: As compared with the sham operation group

contents of LD

NEFA

MDA were increased (P<0.05); levels of NO

Na+-K+-ATP

Ca2+-ATP enzyme

SOD and GSH-Px were decreased (P<0.05); the mRNA and protein expression of NF-κB

Caspase-3 and Bax in cardiomyocytes were up-regulated significantly (P<0.05)

while the mRNA and protein expression of Bcl-2 was decreased (P<0.05) in model group. As compared with the model group

Shanjing capsules could decrease the contents of LD

NEFA

MDA (P<0.05)

increase the levels of NO

Na+-K+-ATP

Ca2+-ATP enzyme

SOD and GSH-Px (P<0.05)

significantly down-regulate the mRNA and protein expression levels of NF-κB

Caspase-3

Bax in cardiomyocytes (P<0.05)

and up-regulate the mRNA and protein expression of Bcl-2 (P<0.05). Conclusion: Shanjing capsule could increase the ability of antioxidant and oxygen free radical scavenging in myocardial ischemia rats

improve energy metabolism of cardiomyocyte

regulate the expression of apoptosis related protein and genes by regulating the NF-κB signal pathway

which plays a role in myocardial preservation by inhibiting cardiomyocyte apoptosis and decreasing pathological lesion under cardiomyocyte ischemia and anoxia.