A Review Many studies indicate that apoptosis is involved in the progression of congestive heart failure. At present, mechanisms that mitochondria regulates cell apoptosis is widely accepted.Cardiac myocytes have abun...A Review Many studies indicate that apoptosis is involved in the progression of congestive heart failure. At present, mechanisms that mitochondria regulates cell apoptosis is widely accepted.Cardiac myocytes have abundant mitochondria,which plays an important role in maintenance of cell physiological function. Recent studies find that cardiac energy metabolic shifts occur as a normal response to diverse physiologic and dietary conditions and as a component of the pathophysiologic processes which accompany cardiac hypertrophy, heart failure, and myocardial ischemia.Both clinical and experimental studies show that cardiac function can be improved and apoptosis is inhibited by intervention in energetic metabolism of myocytes. [展开更多
Objective To examine the effect of neuropeptide Y （NPY） on TGF-β1 production in RAW264.7 macrophages. Methods Enzyme linked immunosorbent assay （ELISA） was used to detect TGF-β1 production. Cell counting kit 8 ...Objective To examine the effect of neuropeptide Y （NPY） on TGF-β1 production in RAW264.7 macrophages. Methods Enzyme linked immunosorbent assay （ELISA） was used to detect TGF-β1 production. Cell counting kit 8 （CCK-8） was used to assay the viability of RAW264.7 cells. Western blot was used to detect the phosphorylation of PI3K p85. Results NPY treatment could promote TGF-β1 production and rapid phosphorylation of PI3K p85 in RAW264.7 cells via Y1 receptor. The elevated TGF-β 1 production induced by NPY could be abolished by wortrnannin pretreatment. Conclusion NPY may elicit TGF-β production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.展开更多
文摘A Review Many studies indicate that apoptosis is involved in the progression of congestive heart failure. At present, mechanisms that mitochondria regulates cell apoptosis is widely accepted.Cardiac myocytes have abundant mitochondria,which plays an important role in maintenance of cell physiological function. Recent studies find that cardiac energy metabolic shifts occur as a normal response to diverse physiologic and dietary conditions and as a component of the pathophysiologic processes which accompany cardiac hypertrophy, heart failure, and myocardial ischemia.Both clinical and experimental studies show that cardiac function can be improved and apoptosis is inhibited by intervention in energetic metabolism of myocytes. [
文摘Objective To examine the effect of neuropeptide Y （NPY） on TGF-β1 production in RAW264.7 macrophages. Methods Enzyme linked immunosorbent assay （ELISA） was used to detect TGF-β1 production. Cell counting kit 8 （CCK-8） was used to assay the viability of RAW264.7 cells. Western blot was used to detect the phosphorylation of PI3K p85. Results NPY treatment could promote TGF-β1 production and rapid phosphorylation of PI3K p85 in RAW264.7 cells via Y1 receptor. The elevated TGF-β 1 production induced by NPY could be abolished by wortrnannin pretreatment. Conclusion NPY may elicit TGF-β production in RAW264.7 cells via Y1 receptor, and the activated PI3K pathway may account for this effect.
