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Effect of dietary fiber on inflammatory response after cerebral ischemia in rats |
LI Haitao1 QU Bo2 YANG Shida2▲ |
1.Department of Laboratory Medicine, Jinqiu Hospital of Liaoning Province, Liaoning Province, Shenyang 110016, China;
2.Department of Laboratory Medicine, the People′s Hospital of Liaoning Province, Liaoning Province, Shenyang 110015, China |
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Abstract Objective To investigate the effect of dietary fiber on inflammatory response after cerebral ischemia in rats. Methods Thirty-four adult male rats were divided into sham group (n = 10), ischemic group (n = 12), ischemic+dietary fiber group (n = 12) according to the principle of random distribution. Endothelin was injected into the brain of the ischemia group and ischemic+dietary fiber group to make the cerebral ischemia model, 4 rats died; while sham operation group was injected with isovolume normal saline, all the rats survived. Finally, 10 rats in sham operation group, 10 rats in ischemia group, and 10 rats in ischemia+dietary fiber group. Normal diet was added to the sham group and ischemia group, dietary fiber was added to the ischemia+dietary fiber group. The infarct volume was measured and the number of Iba-1/BrdU and GFAP/BrdU double staining positive cells in the infarct peripheral cortex of each group was observed by immunofluorescence staining. Results There was no significant difference in infarct volume between ischemia group and ischemia+dietary fiber group (P > 0.05). The number of Iba-1/BrdU double staining positive cells, GFAP/BrdU double staining positive cells in ischemia group were more than those in sham operation group, while the number of Iba-1/BrdU double staining positive cells, GFAP/BrdU double staining positive cells in ischemia+dietary fiber group were less than those in ischemia group, and the differences were all highly statistically significant (all P < 0.05). Conclusion Dietary fiber can inhibit the activation of new microglia and astrocytes around the infarct in the recovery period of cerebral infarction, and thus inhibit the inflammatory response after cerebral infarction.
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