Taipei Medical University

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Wen-Ta Chiu
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------>journal_name=Chinese Medical Journal (Taipei).
------>paper_name=Neurogenic pulmonary edema.
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------>fullAbstract=BACKGROUND AND PURPOSE: We examined the effects of a caspase-1 inhibitor, N-Ac-Tyr-Val-Ala-Asp-chloromethyl ketone (Ac-YVAD-CMK), on neurogenic pulmonary edema in the endovascular perforation model of subarachnoid hemorrhage (SAH) in mice. METHODS: Ninety-seven mice were assigned to sham, SAH+vehicle, SAH+Ac-YVAD-CMK (6 or 10 mg/kg), and SAH+Z-Val-Ala-Asp-fluoromethylketone (Z-VAD-FMK, 6 mg/kg) groups. Drugs were intraperitoneally injected 1 hour post-SAH. Pulmonary edema measurements, Western blot for interleukin-1beta, interleukin-18, myeloperoxidase, matrix metalloproteinase (MMP)-2, MMP-9, cleaved caspase-3 and zona occludens-1, MMP zymography, terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling staining, and immunostaining were performed on the lung at 24 hours post-SAH. RESULTS: Ten- but not 6-mg/kg of Ac-YVAD-CMK significantly inhibited a post-SAH increase in the activation of interleukin-1beta and caspase-3 and the number of terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling-positive pulmonary endothelial cells, preventing neurogenic pulmonary edema. Another antiapoptotic drug, Z-VAD-FMK, also reduced neurogenic pulmonary edema. SAH did not change interleukin-18, myeloperoxidase, MMP-2, MMP-9, zona occludens-1 levels, or MMP activity. CONCLUSIONS: We report for the first time that Ac-YVAD-CMK prevents lung cell apoptosis and neurogenic pulmonary edema after SAH in mice.
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------>authors2=Chun-Jen Shih
------>authors3=Hsin-Ying Chen
------>authors4=Lieh-Sheng Lin:
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------>authors=Wen-Ta Chiu
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------>updateTitle=Caspase-1 Inhibitor Prevents Neurogenic Pulmonary Edema After Subarachnoid Hemorrhage in Mice.
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------>publish_year=1987
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A B C D E F G H I J K L M N O P Q R S T U V W X Y Z