目的:观察甘氨酸(glycine,GLY)对缺氧/复氧离体心脏功能的影响,探讨甘氨酸对心肌缺血-再灌注(ischemia/reperfusion,I/R)损伤的防治作用及其机制。方法:利用Langendorff灌流装置复制心肌缺氧/复氧(hypoxia/reoxygenation,H/R)模型,观察不同浓度GLY处理后心脏左室收缩压(left ventricular systolic pressure,LVSP)、左室舒张末压(left ventricular end diastolic pressure,LVEDP)、左室发展压(left ventricular developed pres-sure,LVDP=LVSP-LVEDP)、左室收缩压最大上升/下降速率(the maximum rising and dropping rates of left ventricular pressure,dp/dtmaxand dp/dtmin),并在相应的时点分别测定冠脉流出液中的超氧化物歧化酶(superoxide dismutase,SOD)活性和丙二醛(malondialdehyde,MDA)的水平。结果:H/R后各时点大鼠心功能各指标均低于缺氧前;GLY处理组复氧后心功能各指标均高于H/R组,并拮抗损伤导致的SOD减少和MDA升高。结论:一定浓度的GLY能显著改善缺氧/复氧心肌的舒缩功能,其机制可能与其提高SOD活性抑制脂质过氧化反应有关。
α-MSH is an endogenous neuropetide that is effective of all categories of expreimental inflammation. The mechanisms underlying the anti-inflammatory influence of α-MSH are reviewed in the article. α-MSH suppresses ...
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α-MSH is an endogenous neuropetide that is effective of all categories of expreimental inflammation. The mechanisms underlying the anti-inflammatory influence of α-MSH are reviewed in the article. α-MSH suppresses inflammation in the CNS and periphery by downregulating the activation of NF-κB, then inhibiting production of proinflammatory cytokines, nitric oxide, chemokines and adhension molecules, and increasing synthesis of anti-inflammatory cytokines. α-MSH is useful in the treatment of many pathological situations in humans.
Over the past ten years studies in animals and human have supported the links between inflammation and tumors. The inflammatory cells and agents found in tumors play an important role in the pathogenesis of malignant ...
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Over the past ten years studies in animals and human have supported the links between inflammation and tumors. The inflammatory cells and agents found in tumors play an important role in the pathogenesis of malignant disease facilitating tumor growth, invasion and metastasis. This article reviewed the molecular mechanism of inflammatory action in promoting tumors and suggested that inflammatory cytokine network is more likely to contribute to immunosuppression than to mount an effective host anti-tumor response. [
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