Basic Science ; The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury
Purpose: Preconditioning due to activation of AMPK might reduce ischemia-reperfusion (I/R) injury in the kidney, based on the key role of AMPK in preserving ATP. To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, be...
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| Veröffentlicht in: | Kidney research and clinical practice 2009-03, Vol.28 (2), p.96 |
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| creator | Sang Ju Lee Yoon Kyoung Chang Ki Rayng Na Kang Wook Lee Kwang Sun Suh Suk Young Kim Yoon Sik Chang Young Tai Shin Byung Kee Bang |
| description | Purpose: Preconditioning due to activation of AMPK might reduce ischemia-reperfusion (I/R) injury in the kidney, based on the key role of AMPK in preserving ATP. To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, before sustained ischemia was investigated. Methods: Adult male Sprague-Dawley rats weighing approximately 220-250 g were used. To induce renal ischemia, a laparotomy was performed under ketamine and xylazine hydrochloride, and the blood supply to both kidneys was interrupted by placement of vessel clamps at the level of the renal pedicles. Reflow was initiated by removing the clamps. The following experimental groups were defined 1. Acute renal ischemia 0 sec, 10 min, 15 min, 2. AICAR treatment, 3. Sham group (S), 4. Ischemia/Reperfusion group (I/R), 5. AICAR+I/R group (A+I/R), 6. AraA (Adenine-9-b-D-arabinofuranoside, an AMPK) inhibitor+AICAR+I/R group (AraA+A+I/R). Results: There was only faint AMPK phosphorylation in the sham group. After 10 minutes of ischemia, or AICAR preconditioning however, Thr172 phosphorylation of AMPK was increased (p |
| format | Article |
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To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, before sustained ischemia was investigated. Methods: Adult male Sprague-Dawley rats weighing approximately 220-250 g were used. To induce renal ischemia, a laparotomy was performed under ketamine and xylazine hydrochloride, and the blood supply to both kidneys was interrupted by placement of vessel clamps at the level of the renal pedicles. Reflow was initiated by removing the clamps. The following experimental groups were defined 1. Acute renal ischemia 0 sec, 10 min, 15 min, 2. AICAR treatment, 3. Sham group (S), 4. Ischemia/Reperfusion group (I/R), 5. AICAR+I/R group (A+I/R), 6. AraA (Adenine-9-b-D-arabinofuranoside, an AMPK) inhibitor+AICAR+I/R group (AraA+A+I/R). Results: There was only faint AMPK phosphorylation in the sham group. After 10 minutes of ischemia, or AICAR preconditioning however, Thr172 phosphorylation of AMPK was increased (p<0.05). The serum levels of BUN and creatinine were significantly decreased in AICAR preconditioning group (A+I/R). (128.0±7.33 mg/dL, 4.18±0.27 mg/dL vs. 90.2±11.13 mg/dL, 2.58±0.7 mg/dL, p<0.05), but these effects were attenuated by AMPK inhibitor, AraA (AraA+A+I/R group). In quantitative analysis of tubular injury, tubular injury score in AICAR preconditioning group significantly decreased (p<0.05). Conclusion: The AMPK activator AICAR has a protective effect against renal I/R injury.</description><identifier>ISSN: 2211-9132</identifier><language>kor</language><publisher>대한신장학회</publisher><subject>AICA ribonucleotide ; AMP-activated protein kinases ; Ischemia ; Reperfusion</subject><ispartof>Kidney research and clinical practice, 2009-03, Vol.28 (2), p.96</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781</link.rule.ids></links><search><creatorcontrib>Sang Ju Lee</creatorcontrib><creatorcontrib>Yoon Kyoung Chang</creatorcontrib><creatorcontrib>Ki Rayng Na</creatorcontrib><creatorcontrib>Kang Wook Lee</creatorcontrib><creatorcontrib>Kwang Sun Suh</creatorcontrib><creatorcontrib>Suk Young Kim</creatorcontrib><creatorcontrib>Yoon Sik Chang</creatorcontrib><creatorcontrib>Young Tai Shin</creatorcontrib><creatorcontrib>Byung Kee Bang</creatorcontrib><title>Basic Science ; The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury</title><title>Kidney research and clinical practice</title><addtitle>Kidney Research and Clinical Practice</addtitle><description>Purpose: Preconditioning due to activation of AMPK might reduce ischemia-reperfusion (I/R) injury in the kidney, based on the key role of AMPK in preserving ATP. To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, before sustained ischemia was investigated. Methods: Adult male Sprague-Dawley rats weighing approximately 220-250 g were used. To induce renal ischemia, a laparotomy was performed under ketamine and xylazine hydrochloride, and the blood supply to both kidneys was interrupted by placement of vessel clamps at the level of the renal pedicles. Reflow was initiated by removing the clamps. The following experimental groups were defined 1. Acute renal ischemia 0 sec, 10 min, 15 min, 2. AICAR treatment, 3. Sham group (S), 4. Ischemia/Reperfusion group (I/R), 5. AICAR+I/R group (A+I/R), 6. AraA (Adenine-9-b-D-arabinofuranoside, an AMPK) inhibitor+AICAR+I/R group (AraA+A+I/R). Results: There was only faint AMPK phosphorylation in the sham group. After 10 minutes of ischemia, or AICAR preconditioning however, Thr172 phosphorylation of AMPK was increased (p<0.05). The serum levels of BUN and creatinine were significantly decreased in AICAR preconditioning group (A+I/R). (128.0±7.33 mg/dL, 4.18±0.27 mg/dL vs. 90.2±11.13 mg/dL, 2.58±0.7 mg/dL, p<0.05), but these effects were attenuated by AMPK inhibitor, AraA (AraA+A+I/R group). In quantitative analysis of tubular injury, tubular injury score in AICAR preconditioning group significantly decreased (p<0.05). Conclusion: The AMPK activator AICAR has a protective effect against renal I/R injury.</description><subject>AICA ribonucleotide</subject><subject>AMP-activated protein kinases</subject><subject>Ischemia</subject><subject>Reperfusion</subject><issn>2211-9132</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><recordid>eNp9jLsKwkAQAK9QUNQvsNkfCOTh48QqBsV0YtLLea5mNbnE2wuSvzeFtdUwDMxAjMMwCLxNEIUjMWOmq7_019FiJeVYlDvFpCHThEYjbCEvEE4WdW1u5Kg2ZB7wIVdAnCbxuU-1Q-0Y4ociww6y9sr4btE4OKNRJaSsC6xI9dqgvbfcTyA1z9Z2UzG8q5Jx9uNEzA_7PDl6L2K-NJYqZbtLuJZyI4Pof_0Cm8NDPQ</recordid><startdate>20090330</startdate><enddate>20090330</enddate><creator>Sang Ju Lee</creator><creator>Yoon Kyoung Chang</creator><creator>Ki Rayng Na</creator><creator>Kang Wook Lee</creator><creator>Kwang Sun Suh</creator><creator>Suk Young Kim</creator><creator>Yoon Sik Chang</creator><creator>Young Tai Shin</creator><creator>Byung Kee Bang</creator><general>대한신장학회</general><scope>HZB</scope><scope>Q5X</scope></search><sort><creationdate>20090330</creationdate><title>Basic Science ; The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury</title><author>Sang Ju Lee ; Yoon Kyoung Chang ; Ki Rayng Na ; Kang Wook Lee ; Kwang Sun Suh ; Suk Young Kim ; Yoon Sik Chang ; Young Tai Shin ; Byung Kee Bang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-kiss_primary_27889813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>kor</language><creationdate>2009</creationdate><topic>AICA ribonucleotide</topic><topic>AMP-activated protein kinases</topic><topic>Ischemia</topic><topic>Reperfusion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sang Ju Lee</creatorcontrib><creatorcontrib>Yoon Kyoung Chang</creatorcontrib><creatorcontrib>Ki Rayng Na</creatorcontrib><creatorcontrib>Kang Wook Lee</creatorcontrib><creatorcontrib>Kwang Sun Suh</creatorcontrib><creatorcontrib>Suk Young Kim</creatorcontrib><creatorcontrib>Yoon Sik Chang</creatorcontrib><creatorcontrib>Young Tai Shin</creatorcontrib><creatorcontrib>Byung Kee Bang</creatorcontrib><collection>Korean Studies Information Service System (KISS)</collection><collection>Korean Studies Information Service System (KISS) B-Type</collection><jtitle>Kidney research and clinical practice</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sang Ju Lee</au><au>Yoon Kyoung Chang</au><au>Ki Rayng Na</au><au>Kang Wook Lee</au><au>Kwang Sun Suh</au><au>Suk Young Kim</au><au>Yoon Sik Chang</au><au>Young Tai Shin</au><au>Byung Kee Bang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Basic Science ; The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury</atitle><jtitle>Kidney research and clinical practice</jtitle><addtitle>Kidney Research and Clinical Practice</addtitle><date>2009-03-30</date><risdate>2009</risdate><volume>28</volume><issue>2</issue><spage>96</spage><pages>96-</pages><issn>2211-9132</issn><abstract>Purpose: Preconditioning due to activation of AMPK might reduce ischemia-reperfusion (I/R) injury in the kidney, based on the key role of AMPK in preserving ATP. To evaluate this possibility, the effect of preconditioning with 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), AMPK activator, before sustained ischemia was investigated. Methods: Adult male Sprague-Dawley rats weighing approximately 220-250 g were used. To induce renal ischemia, a laparotomy was performed under ketamine and xylazine hydrochloride, and the blood supply to both kidneys was interrupted by placement of vessel clamps at the level of the renal pedicles. Reflow was initiated by removing the clamps. The following experimental groups were defined 1. Acute renal ischemia 0 sec, 10 min, 15 min, 2. AICAR treatment, 3. Sham group (S), 4. Ischemia/Reperfusion group (I/R), 5. AICAR+I/R group (A+I/R), 6. AraA (Adenine-9-b-D-arabinofuranoside, an AMPK) inhibitor+AICAR+I/R group (AraA+A+I/R). Results: There was only faint AMPK phosphorylation in the sham group. After 10 minutes of ischemia, or AICAR preconditioning however, Thr172 phosphorylation of AMPK was increased (p<0.05). The serum levels of BUN and creatinine were significantly decreased in AICAR preconditioning group (A+I/R). (128.0±7.33 mg/dL, 4.18±0.27 mg/dL vs. 90.2±11.13 mg/dL, 2.58±0.7 mg/dL, p<0.05), but these effects were attenuated by AMPK inhibitor, AraA (AraA+A+I/R group). In quantitative analysis of tubular injury, tubular injury score in AICAR preconditioning group significantly decreased (p<0.05). Conclusion: The AMPK activator AICAR has a protective effect against renal I/R injury.</abstract><pub>대한신장학회</pub><tpages>7</tpages></addata></record> |
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| subjects | AICA ribonucleotide AMP-activated protein kinases Ischemia Reperfusion |
| title | Basic Science ; The Preconditioning with AICAR Protects Against Subsequent Renal Ischemia Reperfusion Injury |
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