ArticleFrontiers in neurology
MAPK signaling pathway contributes to regulating the Nrf2 expression and compensation for hypoxia in hypoglossal nucleus induced by chronic intermittent hypoxia in rats.
Article in Frontiers in neurology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: To investigate the expression of classic markers of oxidative stress and the possible triggers, the expression of Nrf2, Keap1, and MAPK pathway-related proteins (JNK, p38MAPK, ERK) were evaluated in the hypoglossal nucleus under a rat model of chronic intermittent hypoxia (CIH). Methods: A total of 18 adult male Sprague-Dawley rats were randomly divided into 3 groups, including 2 CIH groups (3 weeks and 8 weeks, respectively) and a control group. The CIH groups were fed in low oxygen cabins, in which the fraction of oxygen volume circulated between 5% and 21%, while the control group was fed in atmospheric environment cabins. After 3 and 8 weeks, the expressions of Keap1, Nrf2, JNK, p38MAPK, and ERK in the hypoglossal nucleus of each group were observed by immunohistochemistry. Results: Immunohistochemical analysis showed that Nrf2 expression in the CIH groups increased as the duration of hypoxia was prolonged. However, the Keap1 expression remained the same after 3 and 8 weeks of CIH. The expressions of JNK, p38MAPK, and ERK in the hypoglossal nucleus of the CIH groups were higher than those of the control group. The expressions of JNK, p38MAPK, and ERK in the CIH-8w group were higher than those of the CIH-3w group. The expressions of p-JNK and p-p38MAPK in the ventral nucleus were significantly higher than those in the dorsal nucleus in the CIH groups. Discussion: MAPK pathway is activated by CIH and may lead to the accumulation of Nrf2 in the hypoglossal nucleus. The different reactions of the ventral and dorsal nucleus to CIH may relate to their regulating effect on the upper airway muscle groups.
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