Anti-inflammatory effects of fimasartan via Akt, ERK, and NFκB pathways on astrocytes stimulated by hemolysate View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2015-11-25

AUTHORS

Xiu-Li Yang, Chi Kyung Kim, Tae Jung Kim, Jing Sun, Doeun Rim, Young-Ju Kim, Sang-Bae Ko, Hyunduk Jang, Byung-Woo Yoon

ABSTRACT

ObjectiveThe aim of this study was to investigate whether fimasartan, a novel angiotensin II receptor blocker, modulates hemolysate-induced inflammation in astrocytes.MethodsWe stimulated astrocytes with hemolysate to induce hemorrhagic inflammation in vitro. Astrocytes were pretreated with fimasartan and then incubated with hemolysate at different durations. Anti-inflammatory cell signaling molecules including Akt, extracellular signal regulated kinase (ERK), NFκB and cyclooxygenase-2 (COX-2) were assessed by western blotting. Pro-inflammatory mediators were evaluated by real-time RT-PCR and ELISA.ResultsThe stimulation by hemolysate generated a robust activation of inflammatory signaling pathways in astrocytes. Hemolysate increased the phosphorylation of Akt at 1 h, and ERK1/2 at 20 min compared with the control group and promoted the degradation of IκBα. Pretreated fimasartan significantly decreased hemolysate-induced phosphorylation of Akt and ERK1/2. In addition, fimasartan also suppressed NFκB-related inflammatory pathways induced by hemolysate, including reduction of the gene expression of NFκB, and decreased nuclear translocation of NFκB and degradation of IκB. This reduction of inflammatory upstream pathways decreased the expression of inflammatory end-products: COX-2 and interleukin-1 (IL-1β). Furthermore, the expression of COX-2 was attenuated by both Akt inhibitor (LY294002) and ERK inhibitor (U0126), and IκBα degradation was suppressed by LY294002.ConclusionsThese results demonstrate that pretreatment with fimasartan to astrocytes suppresses the inflammatory responses induced by hemolysate. Akt, ERK and NFκB were associated with hemolysate-induced COX-2 and IL-1β expression. Based on these mechanisms, fimasartan could be a candidate anti-inflammatory regulator for the treatment of intracerebral hemorrhage. More... »

PAGES

115-123

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00011-015-0895-9

DOI

http://dx.doi.org/10.1007/s00011-015-0895-9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1037644294

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26608500


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35 schema:description ObjectiveThe aim of this study was to investigate whether fimasartan, a novel angiotensin II receptor blocker, modulates hemolysate-induced inflammation in astrocytes.MethodsWe stimulated astrocytes with hemolysate to induce hemorrhagic inflammation in vitro. Astrocytes were pretreated with fimasartan and then incubated with hemolysate at different durations. Anti-inflammatory cell signaling molecules including Akt, extracellular signal regulated kinase (ERK), NFκB and cyclooxygenase-2 (COX-2) were assessed by western blotting. Pro-inflammatory mediators were evaluated by real-time RT-PCR and ELISA.ResultsThe stimulation by hemolysate generated a robust activation of inflammatory signaling pathways in astrocytes. Hemolysate increased the phosphorylation of Akt at 1 h, and ERK1/2 at 20 min compared with the control group and promoted the degradation of IκBα. Pretreated fimasartan significantly decreased hemolysate-induced phosphorylation of Akt and ERK1/2. In addition, fimasartan also suppressed NFκB-related inflammatory pathways induced by hemolysate, including reduction of the gene expression of NFκB, and decreased nuclear translocation of NFκB and degradation of IκB. This reduction of inflammatory upstream pathways decreased the expression of inflammatory end-products: COX-2 and interleukin-1 (IL-1β). Furthermore, the expression of COX-2 was attenuated by both Akt inhibitor (LY294002) and ERK inhibitor (U0126), and IκBα degradation was suppressed by LY294002.ConclusionsThese results demonstrate that pretreatment with fimasartan to astrocytes suppresses the inflammatory responses induced by hemolysate. Akt, ERK and NFκB were associated with hemolysate-induced COX-2 and IL-1β expression. Based on these mechanisms, fimasartan could be a candidate anti-inflammatory regulator for the treatment of intracerebral hemorrhage.
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41 schema:keywords Akt
42 Akt inhibitor
43 ELISA
44 ERK
45 ERK inhibitor
46 ERK1/2
47 II receptor blockers
48 IL-1β expression
49 IκBα
50 IκBα degradation
51 MethodsWe
52 NFκB
53 NFκB pathway
54 RT-PCR
55 Western blotting
56 activation
57 addition
58 aim
59 angiotensin II receptor blockers
60 anti-inflammatory cells
61 anti-inflammatory effects
62 anti-inflammatory regulator
63 astrocytes
64 blockers
65 blotting
66 cells
67 control group
68 cyclooxygenase-2
69 degradation
70 degradation of IκBα
71 different durations
72 duration
73 effect
74 expression
75 extracellular signals
76 fimasartan
77 gene expression
78 group
79 hemolysate
80 hemorrhage
81 hemorrhagic inflammation
82 inflammation
83 inflammatory pathways
84 inflammatory response
85 inflammatory signaling pathways
86 inhibitors
87 interleukin-1
88 intracerebral hemorrhage
89 kinase
90 mechanism
91 mediators
92 min
93 molecules
94 novel angiotensin II receptor blocker
95 nuclear translocation
96 pathway
97 phosphorylation
98 phosphorylation of Akt
99 pretreatment
100 pro-inflammatory mediators
101 real-time RT-PCR
102 receptor blockers
103 reduction
104 regulator
105 response
106 results
107 robust activation
108 signaling pathways
109 signals
110 stimulation
111 study
112 translocation
113 treatment
114 upstream pathways
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