PPARγ agonist pioglitazone rescues neuronal cell damage after transient global cerebral ischemia through matrix metalloproteinase inhibition
Previous studies have demonstrated that pioglitazone, a peroxisome proliferator‐activated receptor gamma (PPARγ) agonist, inhibits ischemia‐induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is kn...
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| Published in: | The European journal of neuroscience Vol. 27; no. 2; pp. 334 - 342 |
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| Main Authors: | , , , , |
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| Language: | English |
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01-01-2008
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| Abstract | Previous studies have demonstrated that pioglitazone, a peroxisome proliferator‐activated receptor gamma (PPARγ) agonist, inhibits ischemia‐induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is known to play a major role in the pathophysiology of brain ischemia, the present study was undertaken to test whether pioglitazone attenuates ischemic neuronal damage through MMP inhibition. C57BL/6 mice were subjected to global brain ischemia for 20 min. Animals were killed 72 h after ischemia. Oral pioglitazone (40 mg/kg/day, as a suspension in 0.5% carboxymethylcellulose) was administered to mice twice daily for 3 days before ischemia and twice daily after ischemia until the animals were killed. We investigated gelatinase activity by zymography and laminin immunohistochemistry. Histological analysis was also performed to test the protective effect of pioglitazone on neuronal damage. Mice treated with pioglitazone had attenuated gelatinase activity. Gelatin gel and in situ zymography showed up‐regulation of gelatinase activity after ischemia. Pioglitazone significantly inhibited ischemia‐induced elevation of the active form of MMP‐9. Pioglitazone also reduced up‐regulation of in situ gelatinase activity and laminin breakdown induced by ischemia in the hippocampus. There was marked neuronal damage in the CA1 and CA2 areas after ischemia. Neuronal damage in mice was significantly decreased by pioglitazone treatment, compared with vehicle‐treated mice. Pioglitazone also inhibited TdT‐mediated dUTP nick end labeling staining in CA1 and CA2 areas. Pioglitazone, a PPARγ agonist, reduces delayed neuronal damage induced by global ischemia through inhibition of MMP‐9 activity. |
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| AbstractList | Previous studies have demonstrated that pioglitazone, a peroxisome proliferator‐activated receptor gamma (PPARγ) agonist, inhibits ischemia‐induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is known to play a major role in the pathophysiology of brain ischemia, the present study was undertaken to test whether pioglitazone attenuates ischemic neuronal damage through MMP inhibition. C57BL/6 mice were subjected to global brain ischemia for 20 min. Animals were killed 72 h after ischemia. Oral pioglitazone (40 mg/kg/day, as a suspension in 0.5% carboxymethylcellulose) was administered to mice twice daily for 3 days before ischemia and twice daily after ischemia until the animals were killed. We investigated gelatinase activity by zymography and laminin immunohistochemistry. Histological analysis was also performed to test the protective effect of pioglitazone on neuronal damage. Mice treated with pioglitazone had attenuated gelatinase activity. Gelatin gel and
in situ
zymography showed up‐regulation of gelatinase activity after ischemia. Pioglitazone significantly inhibited ischemia‐induced elevation of the active form of MMP‐9. Pioglitazone also reduced up‐regulation of
in situ
gelatinase activity and laminin breakdown induced by ischemia in the hippocampus. There was marked neuronal damage in the CA1 and CA2 areas after ischemia. Neuronal damage in mice was significantly decreased by pioglitazone treatment, compared with vehicle‐treated mice. Pioglitazone also inhibited TdT‐mediated dUTP nick end labeling staining in CA1 and CA2 areas. Pioglitazone, a PPARγ agonist, reduces delayed neuronal damage induced by global ischemia through inhibition of MMP‐9 activity. Previous studies have demonstrated that pioglitazone, a peroxisome proliferator‐activated receptor gamma (PPARγ) agonist, inhibits ischemia‐induced injury in various tissues including neural tissue. Pioglitazone has also been shown to reduce matrix metalloproteinase (MMP) activity. Because MMP is known to play a major role in the pathophysiology of brain ischemia, the present study was undertaken to test whether pioglitazone attenuates ischemic neuronal damage through MMP inhibition. C57BL/6 mice were subjected to global brain ischemia for 20 min. Animals were killed 72 h after ischemia. Oral pioglitazone (40 mg/kg/day, as a suspension in 0.5% carboxymethylcellulose) was administered to mice twice daily for 3 days before ischemia and twice daily after ischemia until the animals were killed. We investigated gelatinase activity by zymography and laminin immunohistochemistry. Histological analysis was also performed to test the protective effect of pioglitazone on neuronal damage. Mice treated with pioglitazone had attenuated gelatinase activity. Gelatin gel and in situ zymography showed up‐regulation of gelatinase activity after ischemia. Pioglitazone significantly inhibited ischemia‐induced elevation of the active form of MMP‐9. Pioglitazone also reduced up‐regulation of in situ gelatinase activity and laminin breakdown induced by ischemia in the hippocampus. There was marked neuronal damage in the CA1 and CA2 areas after ischemia. Neuronal damage in mice was significantly decreased by pioglitazone treatment, compared with vehicle‐treated mice. Pioglitazone also inhibited TdT‐mediated dUTP nick end labeling staining in CA1 and CA2 areas. Pioglitazone, a PPARγ agonist, reduces delayed neuronal damage induced by global ischemia through inhibition of MMP‐9 activity. |
| Author | Jang, Young-Ho Yoo, Ho-Sang Lee, Seong-Ryong Lee, Hyung Lee, Kyung-Jae |
| Author_xml | – sequence: 1 givenname: Kyung-Jae surname: Lee fullname: Lee, Kyung-Jae organization: Department of Pharmacology – sequence: 2 givenname: Young-Ho surname: Jang fullname: Jang, Young-Ho organization: Department of Anesthesiology – sequence: 3 givenname: Hyung surname: Lee fullname: Lee, Hyung organization: Department of Neurology, School of Medicine, Keimyung University, Taegu, 700-712 South Korea – sequence: 4 givenname: Ho-Sang surname: Yoo fullname: Yoo, Ho-Sang organization: School of Kinesiology, Yeungnam University, Gyeongsan, Gyeongbuk, South Korea – sequence: 5 givenname: Seong-Ryong surname: Lee fullname: Lee, Seong-Ryong organization: Department of Pharmacology |
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| Title | PPARγ agonist pioglitazone rescues neuronal cell damage after transient global cerebral ischemia through matrix metalloproteinase inhibition |
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