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Monophosphoryl lipid A pretreatment on the heart of aged rats and its mechanism of delayed protection


. However, limited clinical application of its methods; and pharmacological preconditioning is a good prospect for clinical application. Asia has proved to cause loss of one dose of interleukin l,[link widoczny dla zalogowanych], tumor necrosis factor, endothelin, endotoxin, and IVlLA pre-treatment can induce cardioprotection, including the effect of MLA obvious advantages of less side effects. Has a good prospect for clinical application. :. In this experiment, isolated perfused rat heart I,[link widoczny dla zalogowanych], / R model on the show, MLA pretreatment significantly improved I / R caused by the coronary circulation disorders (CPF reduced). Increased membrane stability (LDH and Mb leakage reduction), increased phosphorylation of Taiwan high-energy materials (ATP) levels, reduce edema (wet, the weight ratio), and calcium overload (total calcium content), indicating that the pretreatment can reduce the elderly blLA Myocardial I, / R injury. The same drugs in adult rats pretreated with the mechanism is very complex, and 24 hours after ischemic preconditioning showed similar protective effect of the delay may be related to induction of myocardial endogenous myocardial protective substances (such as antioxidant enzymes,[link widoczny dla zalogowanych], heat shock protein) units into more relevant. . Older tissues of certain proteins (such as heat shock proteins, oxygen free radical scavenging enzymes) reduce the synthesis,[link widoczny dla zalogowanych], resulting in decreased body reaction. Protective effect of preconditioning is unclear. Metallothionein (MT) is a stress protein, has a clear radical, stable cell, regulating intracellular calcium homeostasis and other heart protective effect of the experimental results show that, MLA l2 hours after preconditioning was significantly increased myocardial IVIT 24 hours more with, at which point I / R injury also caused significantly reduced, suggesting that MT participated in the cardioprotective effect of preconditioning MIA MIA as an extracellular signal to intracellular MT content increased. It is not clear. MAPK extracellular signal system is the reaction of poly Eucalyptus caused by cell pathway. MAPK activation induced translocation into the nuclear transcription factor phosphorylation (activation). Thus promoting and stress-related protein gene expression, synthesis. Experimental results show that the protective mechanism of ischemic preconditioning involves the activation of MAPK in this experiment show, MLA pretreatment significantly increased MAPK and continue to live Majesty l2 hours, while the MT synthesis also began to increase in the I2-hour,[link widoczny dla zalogowanych], 24-hour level higher. Tip IVIT synthesis may be due to increased activation of MAPK-mediated, so as to explore the mechanism of pharmacological preconditioning provides a new way of thinking.