Autophagy is a common phenomenon which widely ex-ists in eukaryotic cells. Researches have shown that autophagy plays a critical role in maintaining cellular hemostasis, cell com-ponents update and keeping a normal physiological state. In re-cent years, the study has found that autophagy is closely related to the growth, the development of cardiovascular diseases and tumors. Further studies show that in different pathological condi-tions, autophagy could both promote angiogenesis and inhibit the formation of blood vessels. Therefore, it is particularly critical to elucidate the mechanisms of autophagy in the regulation of angio-genesis in different pathological conditions. The role of autophagy in cardiovascular diseases especially in the regulation of angio-genesis is discussed in this paper. Besides, the paper also in-cludes the discussion about the mechanisms of autophagy in the regulation angiogenesis, which may provide references for follow-up research and clinical treatment.

Cardiovascular disease is a serious threat to human health and quality of life ,and it has become the leading cause of death in human.Thus,looking for effective drugs to reduce the mortality and morbidity of such a disease has become a problem to be solved.Due to its good efficacy of activating blood circula-tion and dissipating blood stasis,salvia miltiorrhiza has been widely used in the treatment of cardiovascular disease and ob-tained a good curative effect.Salvianolic acid B is one of the main water-soluble components of salvia miltiorrhiza extract and studies have shown that salvianolic acid B possesses many biolog-ical activities,which not only has a good protective effect on my-ocardial infarction,but could significantly alleviate myocardial ischemia-reperfusion injury.This article reviews the research progress of salvianolic acid B in cardiovascular diseases,and al-so includes discussion about the mechanisms of salvianolic acid B in the regulation of cardiovascular diseases,which may provide references for follow-up research and clinical treatment.

Objective To explore the effect of NPY on activation of primary microglia and the production of in?terleukin-1β. Methods Rat primary cortical microglia was cultured and divided into control group, LPS group, NPY+LPS group, NPY group and BIBP3226+NPY+LPS group. Microglia in control group were incubated with serum-free me?dium for 6 h;microglia in LPS group were incubated with serum-free medium plus LPS for 6 h;microglia in NPY+LPS group were incubated with serum-free medium plus NPY and LPS for 6 h; microglia cells in NPY group were incubat?ed in serum-free medium plus NPY for 6 h; microglia cells in BIBP3226+NPY+LPS group were incubated in se?rum-free medium including BIBP3226 、NPY and LPS for 6 h. After 6 h , Primary cultured microglia were stained us?ing IBA-1 antibody and examined under the fluorescence microscope. The protein levels of IL-1βin the culture media and the mRNA expression levels of IL-1βin the microglia of different groups were detected using the methods of Elisa and RT-PCR. Results After 6 h, the contents of IL-1 βin the culture media and the mRNA expression levels of IL-1βin the cells of LPS group increased remarkably compared with control group (P<0.05) and the microglia were activat? ed. Compared with LPS group, the contents of IL-1 βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in LPS+NPY group were significantly decreased .Compared with LPS+NPY group, the contents of IL-1βin the culture media. the mRNA expression levels of IL-1β and the activity of microglia in BIBP3226+NPY+LPS group were increased (P<0.05). There were no significant differences in the contents of IL-1βin the culture media. the mRNA expression levels of IL-1βand the activity of microglia between BIBP3226+NPY+LPS group and LPS group or between NPY group and the control group. Conclusion NPY can inhibit the biological activity of microglia and IL-1βproduction through NPY Y1 receptorin the microglia.

Objective:To investigate the mechanism of crush syndrome (CS) induced by crush injury on myocardial cells in rats.Methods:Thirty two male Sprague Dawley (SD) rats were randomly divided into control group, CS-0 group, CS-12 group and CS-24 group with 8 rats in each group. CS model was made by self-made extruder and perfused with 4% paraformaldehyde for 0, 12 and 24 h. The morphological changes of myocardial tissue were observed by hematoxylin staining. The apoptosis of cardiomyocytes was detected by terminal dexynucleotide transferase-mediated nick end labeling (TUNEL). The levels and activities of malondialdehyde (MDA), superoxide dismutase (SOD), lactose dehydrogenase (LDH), interleukin-6 (IL-6), interleukin-1 β (IL-1 β), tumor necrosis factor-α (TNF- α) in myocardial homogenate were detected by enzyme-linked immunosorbent assay (ELISA). The expressions of Caspase-3, Bax, Bcl-2 and necrosis factor-κB (NF-κ B) were detected by Western blot.Results:Compared with the control group, the myocardial tissue of CS model group had different degrees of morphological damage; compared with the control group, the apoptosis rate, Caspase-3 and Bax protein expression levels of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and the expression level of Bcl-2 protein was significantly decreased ( P<0.05); compared with the control group, the levels of MDA, LDH, IL-6, IL-1β, TNF-α and p65 protein phosphorylation in the myocardial homogenate of CS-0 group, CS-12 group and CS-24 group were significantly increased ( P<0.05), and SOD activity was significantly decreased ( P<0.05). Conclusions:CS may inhibit oxidative stress and induce inflammatory reaction by activating NF-κ B pathway, thus damaging myocardial cells in rats.