Title : MAPKs and Hsc70 are critical to the protective effect of molecular hydrogen during the early phase of acute pancreatitis.

Pub. Date : 2016 Feb

PMID : 26683671






4 Functional Relationships(s)
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1 The subsequent in vitro experiments showed that H2 treatment inhibited the phosphorylation of extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK, and activated NF-kappaB and the expression of tumor necrosis factor alpha and interleukin-1beta, while simultaneously preventing the translocation of phospho-ERK, phospho-JNK, and phospho-p38 from the cytoplasm to the nucleus. Hydrogen mitogen-activated protein kinase 1 Homo sapiens
2 The subsequent in vitro experiments showed that H2 treatment inhibited the phosphorylation of extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK, and activated NF-kappaB and the expression of tumor necrosis factor alpha and interleukin-1beta, while simultaneously preventing the translocation of phospho-ERK, phospho-JNK, and phospho-p38 from the cytoplasm to the nucleus. Hydrogen mitogen-activated protein kinase 1 Homo sapiens
3 The subsequent in vitro experiments showed that H2 treatment inhibited the phosphorylation of extracellular signal-regulated kinase (ERK), c-jun N-terminal kinase (JNK), and p38 MAPK, and activated NF-kappaB and the expression of tumor necrosis factor alpha and interleukin-1beta, while simultaneously preventing the translocation of phospho-ERK, phospho-JNK, and phospho-p38 from the cytoplasm to the nucleus. Hydrogen mitogen-activated protein kinase 1 Homo sapiens
4 In conclusion, H2 treatment can ameliorate the inflammatory response and reduce the expression of inflammatory mediators during the early phase of AP by inhibiting the MAPK pathways and increasing Hsc70 expression. Hydrogen mitogen-activated protein kinase 1 Homo sapiens