2013
DOI: 10.1007/s10620-013-2800-0
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Apamin Attenuated Cerulein-Induced Acute Pancreatitis by Inhibition of JNK Pathway in Mice

Abstract: These results could suggest that apamin could protect against AP by inhibition of JNK activation.

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Cited by 16 publications
(18 citation statements)
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References 26 publications
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“…Bae et al [20] explored the possibility that apamin suppresses AP on acinal cells via SK channel regulation and the role of SK channels in AP in acinar cells. Bae et al [20] demonstrated evidence that apamin inhibits the development of AP by cerulein, a well-known substance that stimulates smooth muscles and induces digestion. Treatment with apamin in mice reduces serum amylase, lipase, cytokine, and myeloid oxidase activities.…”
Section: Pancreatitismentioning
confidence: 99%
See 1 more Smart Citation
“…Bae et al [20] explored the possibility that apamin suppresses AP on acinal cells via SK channel regulation and the role of SK channels in AP in acinar cells. Bae et al [20] demonstrated evidence that apamin inhibits the development of AP by cerulein, a well-known substance that stimulates smooth muscles and induces digestion. Treatment with apamin in mice reduces serum amylase, lipase, cytokine, and myeloid oxidase activities.…”
Section: Pancreatitismentioning
confidence: 99%
“…Treatment with apamin in mice reduces serum amylase, lipase, cytokine, and myeloid oxidase activities. Based on Bae et al's study [20], the inhibitory effects of apamin have been demonstrated through c-Jun N-terminal kinases (JNK) inactivation in a cerulein-induced AP model in vivo. The administration of apamin inhibits the development of cerulein-induced AP, reducing inflammation, edema, cytokine production, and neutrophil infiltration in the pancreas.…”
Section: Pancreatitismentioning
confidence: 99%
“…Following exposure to several stimulants, a series of the downstream molecules of NF-κB are activated, such as TNF-α, IL-10, IL-6, IL-1b, and iNOS. Studies have reported that cerulein induces NF-κB activation, thereby causing AP in vitro and in vivo [ 27 29 ]. In the present study, we found that cerulein stimulation promoted the phosphorylation of p65 and thus caused the activation of NF-κB in AR42J cells.…”
Section: Discussionmentioning
confidence: 99%
“…Through functional enrichment analysis, significant functions related to miR-24 were predicted: 'Positive regulation of calcium-mediated signaling', 'activation of JUN kinase activity', 'calcium ion transport', 'regulation of Rho protein signal transduction', 'negative regulation of protein kinase B signaling cascade', and 'T cell receptor signaling pathway'. Previous studies suggested that the dose-dependent inhibition of Rho-kinase had protective effects on AP, whereas bee venom could prevent AP and inhibit pancreatic acinar cell death through the inhibition of c-Jun N-terminal kinase activation (40,41). The phosphoinositide 3-kinase and protein kinase B signal transduction pathways may participate in the pathological process of lung injury in severe AP through the upregulation of NF-κB, tumor necrosis factor-α, and IL-lβ (18).…”
Section: Discussionmentioning
confidence: 99%