RESUMO
Objective: To investigate the effects of Linggui Zhugan Decoction on mitochondrial and oxidative damage in rats with chronic heart failure after myocardial infarction and the related mechanisms. Methods: Chronic heart failure after myocardial infarction was established by coronary artery ligation. Heart failure rats were randomly divided into three groups: Model group (n = 11), Linggui Zhugan Decoction group (n = 12), and captopril group (n = 11). Rats whose coronary arteries were only threaded and not ligated were sham group (n = 11). Cardiac function, superoxide dismutase (SOD), malondialdehyde (MDA) contents, soluble growth-stimulating expression factor (ST2), and N-terminal B-type brain natriuretic peptide precursor (NTproBNP) levels were analyzed after treatment. Moreover, the level of mitochondrial membrane potential was detected by JC-1 staining, the ultrastructural of myocardial mitochondria were observed by transmission electron microscopy. The related signal pathway of silent information regulator factor 2-related enzyme 1 (SIRT1), adenylate activated protein kinase (AMPK), phosphorylated adenylate activated protein kinase (p-AMPK), and peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is an important pathway to regulate mitochondrial energy metabolism, and to initiate mitochondrial biogenesis. The expression level was detected by Western blot and reverse transcription to explore the mechanism of the decoction. Results: Compared with the model rats, Linggui Zhugan Decoction significantly improved cardiac function (p < 0.05), reduced MDA production (p < 0.01), increased SOD activity (p < 0.05), reduced ST-2(p < 0.01), and NT-proBNP(p < 0.05) levels, increased mitochondrial membrane potential, and improved mitochondria function. In addition, Linggui Zhugan Decoction upregulated the expression of SIRT1, p-AMPK, PGC-1α protein, and mRNA in cardiac myocytes. Conclusion: Linggui Zhugan Decoction can improve the cardiac function of heart failure rats by enhancing myocardial antioxidant capacity and protecting the mitochondrial function, the mechanism is related to activating SIRT1/AMPK/PGC-1α signaling pathway.
RESUMO
OBJECTIVE: To observe the effects of Dachengqi decoction on serum levels of mast cell tryptase, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) in rabbits with post-cardiac arrest syndrome (PCAS). METHODS: Thirty healthy male Japanese rabbits were randomly divided into three groups: sham-operation group, PCAS model group and Dachengqi decoction treatment group. The model of PCAS was established by asphyxia-induced cardiac arrest. Fifteen minutes after return of spontaneous circulation, Dachengqi decoction [15 g/(kg.d), bid] was given by intra-gastric administration in Dachengqi decoction treatment group. The indicators of organ function were evaluated 24, 48 and 72 hours after cardiac arrest. The serum levels of mast cell tryptase, MCP-1 and IL-8 were determined by ELISA. RESULTS: Dachengqi decoction alleviated the dysfunction significantly in heart, brain, liver and kidney. Compared with the sham group, the serum levels of mast cell tryptase, MCP-1 and IL-8 increased significantly in PCAS group (P<0.01). Compared with the PCAS group, the serum levels of mast cell tryptase (at 6 hours), MCP-1 (at 6, 24 and 48 hours) and IL-8 (at 6 and 24 hours) decreased significantly in Dachengqi decoction treatment group (P<0.05 or P<0.01). CONCLUSION: Dachengqi decoction can reduce the serum levels of mast cell tryptase, MCP-1 and IL-8 in rabbits with post-cardiac arrest syndrome.