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TMS prevents DOCA-salt-induced endothelial dysfunction in rats. Endothelial function was examined by measuring the response of the aorta (A) and mesenteric arteries (B) to increasing concentrations of ACh (10−9–10−5 mol/l) following constriction with PE (10−5 mol/l). Endothelium-independent vasodilation was examined by measuring the relaxation response to sodium nitroprusside (SNP; 10−9–10−5 mol/l) after the vessels were constricted with PE (10−5 mol/l). C: to determine the contribution of endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the response to ACh (10−9–10−5 mol/l) was determined in the presence of indomethacin (10−5 mol/l) and <t>NG-nitro-l-arginine</t> methyl ester (l-NAME; 10−4 mol/l). A combination of indomethacin and l-NAME was added to the myograph chamber ∼10 min before constriction with PE. Relaxation is expressed as a percentage of the contraction by PE. Data are means ± SE (n = 5). *P < 0.05, UNX vs. DOCA-salt. †P < 0.05, DOCA-salt vs. DOCA-salt + TMS.
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TMS prevents DOCA-salt-induced endothelial dysfunction in rats. Endothelial function was examined by measuring the response of the aorta (A) and mesenteric arteries (B) to increasing concentrations of ACh (10−9–10−5 mol/l) following constriction with PE (10−5 mol/l). Endothelium-independent vasodilation was examined by measuring the relaxation response to sodium nitroprusside (SNP; 10−9–10−5 mol/l) after the vessels were constricted with PE (10−5 mol/l). C: to determine the contribution of endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the response to ACh (10−9–10−5 mol/l) was determined in the presence of indomethacin (10−5 mol/l) and <t>NG-nitro-l-arginine</t> methyl ester (l-NAME; 10−4 mol/l). A combination of indomethacin and l-NAME was added to the myograph chamber ∼10 min before constriction with PE. Relaxation is expressed as a percentage of the contraction by PE. Data are means ± SE (n = 5). *P < 0.05, UNX vs. DOCA-salt. †P < 0.05, DOCA-salt vs. DOCA-salt + TMS.
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TMS prevents DOCA-salt-induced endothelial dysfunction in rats. Endothelial function was examined by measuring the response of the aorta (A) and mesenteric arteries (B) to increasing concentrations of ACh (10−9–10−5 mol/l) following constriction with PE (10−5 mol/l). Endothelium-independent vasodilation was examined by measuring the relaxation response to sodium nitroprusside (SNP; 10−9–10−5 mol/l) after the vessels were constricted with PE (10−5 mol/l). C: to determine the contribution of endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the response to ACh (10−9–10−5 mol/l) was determined in the presence of indomethacin (10−5 mol/l) and <t>NG-nitro-l-arginine</t> methyl ester (l-NAME; 10−4 mol/l). A combination of indomethacin and l-NAME was added to the myograph chamber ∼10 min before constriction with PE. Relaxation is expressed as a percentage of the contraction by PE. Data are means ± SE (n = 5). *P < 0.05, UNX vs. DOCA-salt. †P < 0.05, DOCA-salt vs. DOCA-salt + TMS.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester <t>(L-NAME,</t> dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.
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TMS prevents DOCA-salt-induced endothelial dysfunction in rats. Endothelial function was examined by measuring the response of the aorta (A) and mesenteric arteries (B) to increasing concentrations of ACh (10−9–10−5 mol/l) following constriction with PE (10−5 mol/l). Endothelium-independent vasodilation was examined by measuring the relaxation response to sodium nitroprusside (SNP; 10−9–10−5 mol/l) after the vessels were constricted with PE (10−5 mol/l). C: to determine the contribution of endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the response to ACh (10−9–10−5 mol/l) was determined in the presence of indomethacin (10−5 mol/l) and NG-nitro-l-arginine methyl ester (l-NAME; 10−4 mol/l). A combination of indomethacin and l-NAME was added to the myograph chamber ∼10 min before constriction with PE. Relaxation is expressed as a percentage of the contraction by PE. Data are means ± SE (n = 5). *P < 0.05, UNX vs. DOCA-salt. †P < 0.05, DOCA-salt vs. DOCA-salt + TMS.

Journal: American Journal of Physiology - Heart and Circulatory Physiology

Article Title: 2,3?,4,5?-Tetramethoxystilbene prevents deoxycorticosterone-salt-induced hypertension: contribution of cytochrome P -450 1B1

doi: 10.1152/ajpheart.00655.2010

Figure Lengend Snippet: TMS prevents DOCA-salt-induced endothelial dysfunction in rats. Endothelial function was examined by measuring the response of the aorta (A) and mesenteric arteries (B) to increasing concentrations of ACh (10−9–10−5 mol/l) following constriction with PE (10−5 mol/l). Endothelium-independent vasodilation was examined by measuring the relaxation response to sodium nitroprusside (SNP; 10−9–10−5 mol/l) after the vessels were constricted with PE (10−5 mol/l). C: to determine the contribution of endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation, the response to ACh (10−9–10−5 mol/l) was determined in the presence of indomethacin (10−5 mol/l) and NG-nitro-l-arginine methyl ester (l-NAME; 10−4 mol/l). A combination of indomethacin and l-NAME was added to the myograph chamber ∼10 min before constriction with PE. Relaxation is expressed as a percentage of the contraction by PE. Data are means ± SE (n = 5). *P < 0.05, UNX vs. DOCA-salt. †P < 0.05, DOCA-salt vs. DOCA-salt + TMS.

Article Snippet: Materials TMS and N G -nitro- l -arginine methyl ester ( l -NAME) were obtained from Cayman Chemical (Ann Arbor, MI).

Techniques: Derivative Assay

Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester (L-NAME, dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Enteric Glia Mediate Neuron Death in Colitis Through Purinergic Pathways That Require Connexin-43 and Nitric Oxide

doi: 10.1016/j.jcmgh.2015.08.007

Figure Lengend Snippet: Enteric glia contribute to oxidative stress by producing nitric oxide (NO) during inflammation. ( A – C ) In situ NO imaging with the NO sensitive dye 4-amino-5-methylamino-2′,7′-difluorofluorescein (DAF-FM). ( A ) Representative traces of mean glial NO responses after treatment with the NO donor propylamine propylamine NONOate (PAPA NONOate, solid green line, 100 μM) or the pan-nitric oxide synthase (NOS) inhibitor N ω -nitro- l -arginine methyl ester (L-NAME, dashed black line, 100 μM). ( B ) Representative images of DAF-FM fluorescence in myenteric ganglia from healthy (saline) or inflamed (dinitrobenzene sulfonic acid [DNBS] colitis) mice. Arrows point to representative glial cells and representative neurons (or the lack thereof) are denoted by asterisks (scale bar: 30 μM). ( C ) Quantification of DAF-FM fluorescence in observable myenteric neurons and glia in the healthy (saline) or inflamed colon at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 5–10 animals; * P < .05, t test compared to glia-saline). ( D ) Percentage of nitrotyrosine immunoreactive (nT + ve) ganglia in the myenteric plexus of saline and DNBS-treated animals at 6 hours ( left ) and 48 hours ( right ) after the initiation of DNBS-colitis (n = 3–5 animals; * P < .05, unpaired t test). ( E ) Representative myenteric ganglion showing immunoreactivity for nitrated proteins (nTYR; magenta ). Enteric glia are labeled with the glial cell marker GFAP ( green ) and yellow arrowheads highlight areas of colocalization (scale bar: 20 μM). The boxed region in the overlay image is shown at a higher magnification to highlight immunoreactivity of nitrated proteins on glial processes.

Article Snippet: We purchased 1400W [ N -([3-(aminomethyl)phenyl]methyl)ethanimidamide dihydrochloride], L-NAME ( N ω -nitro- l -arginine methyl ester) and propylamine propylamine NONOate (PAPA NONOate) from Cayman Chemical (Ann Arbor, MI).

Techniques: In Situ, Imaging, Fluorescence, Labeling, Marker