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- Title
大鼠脑缺血再灌注早期过氧化物酶体增殖物激活受体γ 活化与细胞焦亡的关系
- Authors
刘海颖; 冯子人; 孙辉; 孟爱国; 赵俊暕; 张文婷
- Abstract
Objective To investigate the relationship between peroxisome proliferator activated receptor γ (PPARγ) activation and pyroptosis in rat model of cerebral ischemia-reperfusion injury. Methods Forty male SD rats of SPF were randomly divided into sham operation group, MCAO model group, pioglitazone group and pioglitazone+GW9662 group, 10 rats for each group. Neurological deficits were measured by Zea-Longa score, and infarct sizes were measured by TTC staining. The expressions of PPARγ, caspase-1, Gasdermin D (GSDMD), interleukin (IL) - 1β and IL-18 in ischemic penumbra were observed by Western blot assay. Results The expression level of PPARγ protein was significantly lower 24- h after cerebral ischemia-reperfusion injury in MCAO group than that of sham group (P<0.05). The values of caspase-1, GSDMD, IL-1β and IL-18 were significantly higher in MCAO group than those in sham operation group (P<0.05). Meanwhile, the neurological deficits and infarct sizes were significantly higher in MCAO group than those of sham operation group (P<0.01). The level of PPARγ was significantly increased in PGZ group compared with that of MCAO group (P< 0.05), while the caspase-1, GSDMD, IL-1β and IL-18 decreased (P<0.05). And neurological deficits and infarct sizes decreased significantly (P<0.01). However, in PGZ+GW9662 group, the effect of PPARγ was reversed. Conclusion At the early stage of rat cerebral ischemia/reperfusion, the activation of PPARγ inhibits the pyroptosis to reduce neuron injury.
- Publication
Tianjin Medical Journal, 2020, Vol 48, Issue 1, p34
- ISSN
0253-9896
- Publication type
Article
- DOI
10.11958/20192153