P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice
Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by th...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kakinohana, Manabu [verfasserIn] |
|---|
| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2014transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways - Gao, Ying ELSEVIER, 2013, biology and chemistry : the official journal of the Nitric Oxide Society, Orlando, Fla |
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| Übergeordnetes Werk: |
volume:39 ; year:2014 ; day:30 ; month:05 ; pages:28 |
| Links: |
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| DOI / URN: |
10.1016/j.niox.2014.03.089 |
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| 520 | |a Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. | ||
| 520 | |a Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. | ||
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10.1016/j.niox.2014.03.089 doi GBVA2014018000007.pica (DE-627)ELV02833440X (ELSEVIER)S1089-8603(14)00109-8 DE-627 ger DE-627 rakwb eng 570 540 570 DE-600 540 DE-600 570 VZ 670 VZ 51.60 bkl 58.45 bkl Kakinohana, Manabu verfasserin aut P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice 2014transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Kida, Kotaro oth Ichinose, Fumito oth Enthalten in Acad. Press Gao, Ying ELSEVIER Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways 2013 biology and chemistry : the official journal of the Nitric Oxide Society Orlando, Fla (DE-627)ELV017091187 volume:39 year:2014 day:30 month:05 pages:28 https://doi.org/10.1016/j.niox.2014.03.089 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 39 2014 30 0530 28 39.2014, S28- 045F 570 |
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10.1016/j.niox.2014.03.089 doi GBVA2014018000007.pica (DE-627)ELV02833440X (ELSEVIER)S1089-8603(14)00109-8 DE-627 ger DE-627 rakwb eng 570 540 570 DE-600 540 DE-600 570 VZ 670 VZ 51.60 bkl 58.45 bkl Kakinohana, Manabu verfasserin aut P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice 2014transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Kida, Kotaro oth Ichinose, Fumito oth Enthalten in Acad. Press Gao, Ying ELSEVIER Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways 2013 biology and chemistry : the official journal of the Nitric Oxide Society Orlando, Fla (DE-627)ELV017091187 volume:39 year:2014 day:30 month:05 pages:28 https://doi.org/10.1016/j.niox.2014.03.089 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 39 2014 30 0530 28 39.2014, S28- 045F 570 |
| allfields_unstemmed |
10.1016/j.niox.2014.03.089 doi GBVA2014018000007.pica (DE-627)ELV02833440X (ELSEVIER)S1089-8603(14)00109-8 DE-627 ger DE-627 rakwb eng 570 540 570 DE-600 540 DE-600 570 VZ 670 VZ 51.60 bkl 58.45 bkl Kakinohana, Manabu verfasserin aut P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice 2014transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Kida, Kotaro oth Ichinose, Fumito oth Enthalten in Acad. Press Gao, Ying ELSEVIER Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways 2013 biology and chemistry : the official journal of the Nitric Oxide Society Orlando, Fla (DE-627)ELV017091187 volume:39 year:2014 day:30 month:05 pages:28 https://doi.org/10.1016/j.niox.2014.03.089 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 39 2014 30 0530 28 39.2014, S28- 045F 570 |
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10.1016/j.niox.2014.03.089 doi GBVA2014018000007.pica (DE-627)ELV02833440X (ELSEVIER)S1089-8603(14)00109-8 DE-627 ger DE-627 rakwb eng 570 540 570 DE-600 540 DE-600 570 VZ 670 VZ 51.60 bkl 58.45 bkl Kakinohana, Manabu verfasserin aut P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice 2014transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Kida, Kotaro oth Ichinose, Fumito oth Enthalten in Acad. Press Gao, Ying ELSEVIER Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways 2013 biology and chemistry : the official journal of the Nitric Oxide Society Orlando, Fla (DE-627)ELV017091187 volume:39 year:2014 day:30 month:05 pages:28 https://doi.org/10.1016/j.niox.2014.03.089 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 39 2014 30 0530 28 39.2014, S28- 045F 570 |
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10.1016/j.niox.2014.03.089 doi GBVA2014018000007.pica (DE-627)ELV02833440X (ELSEVIER)S1089-8603(14)00109-8 DE-627 ger DE-627 rakwb eng 570 540 570 DE-600 540 DE-600 570 VZ 670 VZ 51.60 bkl 58.45 bkl Kakinohana, Manabu verfasserin aut P39 Inhaled hydrogen sulfide can prevent delayed neuronal death after spinal cord ischemia in mice 2014transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. Kida, Kotaro oth Ichinose, Fumito oth Enthalten in Acad. Press Gao, Ying ELSEVIER Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways 2013 biology and chemistry : the official journal of the Nitric Oxide Society Orlando, Fla (DE-627)ELV017091187 volume:39 year:2014 day:30 month:05 pages:28 https://doi.org/10.1016/j.niox.2014.03.089 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 51.60 Keramische Werkstoffe Hartstoffe Werkstoffkunde VZ 58.45 Gesteinshüttenkunde VZ AR 39 2014 30 0530 28 39.2014, S28- 045F 570 |
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Enthalten in Enhancement of (−)-epigallocatechin-3-gallate and theaflavin-3-3′-digallate induced apoptosis by ascorbic acid in human lung adenocarcinoma SPC-A-1 cells and esophageal carcinoma Eca-109 cells via MAPK pathways Orlando, Fla volume:39 year:2014 day:30 month:05 pages:28 |
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Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. |
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Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. |
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Transient spinal cord ischemia (SCI) can produce delayed neuronal death inducing paraplegia in mice. In the present study, we investigated the effect of inhaled hydrogen sulfide (H2S) therapy on delayed neuronal death after SCI in mice. Under general anesthesisa in C57BL6 mice, SCI was induced by the clips placed on the left subclavian artery and aortic arch for 5min. Mice breath air alone (Control) or air mixed with H2S (80ppm) for 5h (H2S group), starting at 23h after 5min of SCI. Neurological function was assessed by Basso-mouse scale (BMS) at 8, 24, 48 and 72h of reperfusion. Inflammatory cytokine RNA transcript levels in the spinal cord were measured rt-PCR. Although mice subjected to 5min SCI showed mild and transient motor dysfunction at 24h after reperfusion, the motor function of hindlimbs in Control exhibited completely paraplegia by 48h of reperfusion. In contrast, six of nine mice in H2S goup did not show any developments of neurological dysfunction from 48h after 5min SCI. 5min SCI did not affect gene expression of IL-6 or TNFalpha at 8h of reperfusion. Whereas those gene expression in control group increased starting at 30h after reperfusion and significantly higher at 48h than preischemia, inahled H2S (H2S group) significantly suppressed gene expression of inflammatory cytokine at 48h after ischemia compared with Control group. According to our data, inhaled H2S potentially protected delayed neuronal death in after SCI via its anti-inflammatory effects. |
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