Minocyclineameliorates hypoxia-inducedblood-brain barrier damage by inhibition of HIF-1t through SIR

来源 :中华医学会第七次全国高原医学学术会议暨中国病理生理学会第九次全国缺氧和呼吸病理生理学术会议 | 被引量 : 0次 | 上传用户:lnnyhonyy
下载到本地 , 更方便阅读
声明 : 本文档内容版权归属内容提供方 , 如果您对本文有版权争议 , 可与客服联系进行内容授权或下架
论文部分内容阅读
  Severe hypoxia can induce the blood-brain barrier (BBB) disruption and cerebral edema, even cerebral hernia and death.Hypoxia-inducible factor-1α (HIF-1α) is one of the most important factors for the cellular response to hypoxia.Inhibition ofHIF-1αean amelioratethe BBB dysfunction and reduce the permeability of vascular endothelial cells in hypoxia.Recent researches showed that Minocycline was not only a kind of antibiotics, but also able to promote HIF-1α degradation and inhibit angiogenesis when a lack of oxygen.Forsurveying theeffect of Minocycline to highvascular permeability and HIF-1α induced by hypoxia.UsingTrans Epithelial Electric Resistance(TEER), Evans blue and Transmission electron microscopy (TEM), we firstlyfound that Minocycline decreasedthe vascular permeability of brain induced by hypoxia in vitro (1% O2) and in vivo (8000 m).Meanwhile, we discovered that Minocycline regulated HIF-1α in protein level rather than in genetic level, while Minocyclinedecreased the expression of matrix metallproteinases (MMP-2 and MMP-9) and up-regulated tight junction proteins (TJS) both in protein and genetic level.
其他文献
目的:模拟阻塞性睡眠呼吸暂停综合征(OSAS)大鼠模型,研究OSAS继发高血压血管重构的病理形态改变.方法:①将32只SD雄性大鼠按随机列表法分为:慢性间歇低氧组(CIH),实验过程中置于低压氧舱中行间歇低氧模式;②常氧对照组(NC),置于同样规格氧舱中常氧对照.每两周监测尾动脉血压一次,于低氧时程6、12周末对腹主动脉进行HE染色、Masson染色观察其病理形态学改变,采用免疫组化检测腹主动脉α
目的:探讨JNK信号通路抑制剂SP600125逆转OSAS继发高血压大鼠腹主动脉重构的作用。方法:SD大鼠随机分为(n=6):①OSAS组(A组),②OSAS+SP600125干预组(B组),③常氧对照组(C组),④常氧对照+ SP600125干预组(D组),采用间歇性低氧舱建立动物模型,每日监测大鼠血压,12周后无菌取出大鼠腹主动脉,HE及免疫组化染色鉴定腹主动脉病理形态学改变,RT-PCR及W
良性气道狭窄以瘢痕性气道狭窄为主,目前呼吸介入治疗方法短期有效,但远期仍容易出现再狭窄,需要反复多次治疗且疗效不佳。当损伤、炎症等因素刺激下成纤维细胞向肌成纤维母细胞转化,这种细胞表型的转变引起气道成纤维细胞在增生性瘢痕中出现异常的增殖、凋亡减少以及细胞外基质的过度分泌沉积等功能改变,但具体机制未完全明确。成纤维细胞可能通过蛋白质功能的改变引起细胞表型及功能的变化在瘢痕性气道狭窄发病中起重要作用。
会议
High-altitude cerebral hypoxia (HACE) is a fatal acute mountain sickness (AMS).Publications implicate hypoxia-elicited inflammation, but if it correlates to HACE remains unclear.We have reported that
会议