H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress.
The aim of this study was to examine the effect of ACS14, a hydrogen sulfide (H(2)S)-releasing derivative of aspirin (Asp), on Asp-induced gastric injury. Gastric hemorrhagic lesions were induced by intragastric administration of Asp (200 mg/kg, suspended in 0.5% carboxymethyl cellulose solutions) i...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2012-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3460860?pdf=render |
| _version_ | 1818049141365800960 |
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| author | Lei Liu Jie Cui Cheng-Jie Song Jin-Song Bian Anna Sparatore Piero Del Soldato Xin-Yu Wang Chang-Dong Yan |
| author_facet | Lei Liu Jie Cui Cheng-Jie Song Jin-Song Bian Anna Sparatore Piero Del Soldato Xin-Yu Wang Chang-Dong Yan |
| author_sort | Lei Liu |
| collection | DOAJ |
| description | The aim of this study was to examine the effect of ACS14, a hydrogen sulfide (H(2)S)-releasing derivative of aspirin (Asp), on Asp-induced gastric injury. Gastric hemorrhagic lesions were induced by intragastric administration of Asp (200 mg/kg, suspended in 0.5% carboxymethyl cellulose solutions) in a volume of 1 ml/100 g body weight. ACS14 (1, 5 or 10 mg/kg) was given 30 min before the Asp administration. The total area of gastric erosions, H(2)S concentration and oxidative stress in gastric tissues were measured three hours after administration of Asp. Treatment with Asp (200 mg/kg), but not ACS14 (430 mg/kg, at equimolar doses to 200 mg/kg Asp), for 3 h significantly increased gastric mucosal injury. The damage caused by Asp was reversed by ACS14 at 1-10 mg/kg in a concentration-dependent manner. ACS14 abrogated Asp-induced upregulation of COX-2 expression, but had no effect on the reduced PGE(2) level. ACS14 reversed the decreased H(2)S concentrations and blood flow in the gastric tissue in Asp-treated rats. Moreover, ACS14 attenuated Asp-suppressed superoxide dismutase-1 (SOD-1) expression and GSH activity, suggesting that ACS14 may stimulate antioxidants in the gastric tissue. ACS14 also obviously inhibited Asp-induced upregulation of protein expression of oxidases including XOD, p47(phox) and p67(phox). In conclusion, ACS14 protects Asp induced gastric mucosal injury by inhibiting oxidative stress in the gastric tissue. |
| first_indexed | 2024-12-10T10:32:52Z |
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| id | doaj.art-c98069e4e1bf4a4c83a621f941563387 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-10T10:32:52Z |
| publishDate | 2012-01-01 |
| publisher | Public Library of Science (PLoS) |
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| series | PLoS ONE |
| spelling | doaj.art-c98069e4e1bf4a4c83a621f9415633872022-12-22T01:52:32ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-0179e4630110.1371/journal.pone.0046301H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress.Lei LiuJie CuiCheng-Jie SongJin-Song BianAnna SparatorePiero Del SoldatoXin-Yu WangChang-Dong YanThe aim of this study was to examine the effect of ACS14, a hydrogen sulfide (H(2)S)-releasing derivative of aspirin (Asp), on Asp-induced gastric injury. Gastric hemorrhagic lesions were induced by intragastric administration of Asp (200 mg/kg, suspended in 0.5% carboxymethyl cellulose solutions) in a volume of 1 ml/100 g body weight. ACS14 (1, 5 or 10 mg/kg) was given 30 min before the Asp administration. The total area of gastric erosions, H(2)S concentration and oxidative stress in gastric tissues were measured three hours after administration of Asp. Treatment with Asp (200 mg/kg), but not ACS14 (430 mg/kg, at equimolar doses to 200 mg/kg Asp), for 3 h significantly increased gastric mucosal injury. The damage caused by Asp was reversed by ACS14 at 1-10 mg/kg in a concentration-dependent manner. ACS14 abrogated Asp-induced upregulation of COX-2 expression, but had no effect on the reduced PGE(2) level. ACS14 reversed the decreased H(2)S concentrations and blood flow in the gastric tissue in Asp-treated rats. Moreover, ACS14 attenuated Asp-suppressed superoxide dismutase-1 (SOD-1) expression and GSH activity, suggesting that ACS14 may stimulate antioxidants in the gastric tissue. ACS14 also obviously inhibited Asp-induced upregulation of protein expression of oxidases including XOD, p47(phox) and p67(phox). In conclusion, ACS14 protects Asp induced gastric mucosal injury by inhibiting oxidative stress in the gastric tissue.http://europepmc.org/articles/PMC3460860?pdf=render |
| spellingShingle | Lei Liu Jie Cui Cheng-Jie Song Jin-Song Bian Anna Sparatore Piero Del Soldato Xin-Yu Wang Chang-Dong Yan H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. PLoS ONE |
| title | H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. |
| title_full | H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. |
| title_fullStr | H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. |
| title_full_unstemmed | H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. |
| title_short | H(2)S-releasing aspirin protects against aspirin-induced gastric injury via reducing oxidative stress. |
| title_sort | h 2 s releasing aspirin protects against aspirin induced gastric injury via reducing oxidative stress |
| url | http://europepmc.org/articles/PMC3460860?pdf=render |
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