Age-induced augmentation of p38 MAPK phosphorylation in mouse lung
Age-induced augmentation of p38 MAPK phosphorylation in mouse lung
复制标题
年龄诱导的小鼠肺中 p38 MAPK 磷酸化增强
DOI：
10.1016/j.exger.2011.04.005
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发表时间：
2011-08-01
影响因子：
3.9
通讯作者：
Huang, Kewu
中科院分区：
文献类型：
--
作者：
Li, Zongli;Li, Junfa;Huang, Kewu
p38丝裂原活化蛋白激酶（p38 MAPK）通路是促炎细胞因子生物合成的关键调节因子，这可能有助于随着衰老观察到的慢性低度炎症。我们假设衰老上调小鼠肺中p38 MAPK以及促炎细胞因子肿瘤坏死因子-α（TNF-α）、白细胞介素-1 β（IL-1 β）和白细胞介素-6（IL-6）的活化，并伴有氧化-抗氧化状态的紊乱。为了验证这一假设，使用Western印迹分析测定了年轻（2月龄）和老年（20月龄）雄性C57 BL/6 J小鼠的肺、脑、心脏、脾、肾和肌肉中磷酸化p38 MAPK的蛋白水平。结果显示，磷酸化p38 MAPK蛋白水平，而不是总p38 MAPK水平，显著增加（p
The p38 mitogen-activated protein kinase (p38 MAPK) pathway is a key regulator of pro-inflammatory cytokine biosynthesis, which may contribute to the chronic low-grade inflammation observed with aging. We hypothesize that aging up-regulates the activation of p38 MAPK as well as the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in mouse lung, and is accompanied by disturbances in oxidant-antioxidant status. In addition, the elevated protein levels of phosphorylated active form of p38 MAPK (phospho-p38 MAPK) with age are tissue-specific.To test this hypothesis, protein levels of phospho-p38 MAPK were determined using Western blot analysis in isolated lung, brain, heart, spleen, kidney and muscle of young (2-month-old) and aged (20-month-old) male C57BL/6J mice. Results show that phospho-p38 MAPK protein levels, not total-p38 MAPK, increased significantly (p