中文摘要：

目的观察白发性高血压大鼠（spontaneously hypertensive rats，SHR）脑组织（皮质、纹体、小脑）炎症状态和过氧化物酶体增殖物激活受体（peroxisome proliferator-activated receptors，PPARs）三个亚型PPARct、PPARD／8和PPARγ表达的变化。方法 以Wistar—Kyoto大鼠为对照，SHR为研究对象。紫外分光光度法检测脑组织髓过氧化物酶（myeloperoxidase，MPO）活性和蛋白质羰基化水平；RT—PCR法和Westernblot法观察炎性因子（IL-1β、TNFα、ICAM-1、iNOS）和PPARs各亚型表达。结果与Wistar—Kyoto大鼠相比，SHR除血压显著升高外，皮质、纹体、小脑组织中（1）MPO活性显著增高，炎性因子IL-1β、TNFα、ICAM-1、iNOS表达增强，除IL-1β在纹体、小脑和TNFα在小脑未检测到明显改变外，其余差异均有统计学意义；蛋白质羰基化水平明显增加，分别为（3、27±0．43）nmol／mg和（11．87±1．11）nmol／mg、（4．02±1．04）nmol／mg和（14、06±1．36）nmol／mg、（5．94±0．71）nmol／mg和（14.95±1.82）nmol／mg，差异具有统计学意义（t=17．70、14、36、11．30，均为P〈0．05）。（2）PPARct、PPAR13／8和PPA脚三亚型的基因和蛋白表达被显著诱导。在皮质、纹体和小脑PPARα蛋白表达分别增加644．78％、791．95％和42．85％（t=13．53、9．86、3．14）；PPAR13／8增加106．72％、94．12％和161、44％（t=7．17、9、07、7．95）；PPAR3,增加2700．16％、790．81％和875．00％（t=16．25、11．60、12．77），差异均有统计学意义（P〈0．05）。结论SHR大鼠脑组织（皮质、纹体、小脑）存在明显的炎症反应，同时PPARs各亚型表达增加。炎症可能在高血压及其脑组织并发症的病理改变中起重要作用，而PPARs代偿不足可能参与了高血压所致炎症反应的发生和发展。

英文摘要：

Objective To evaluate the inflammatory response and the expressions of peroxisome proliferator-activated receptor （PPAR） isoforms （PPARet, PPARβ/δ, and PPARγ,） in the brain （cortex, striatum, cerebellum） of spontaneously hypertensive rats （SHR） . Methods Brain tissues （ cortex, striatum, and cerebellum） were dissected from SHR and age-matched control Wistar-Kyoto rats. Myeloperoxidase （MPO） activity was measured in brain tissues as an index of neutrophil accumulation and the carbonyl protein content was analyzed by spectrophotometry to evaluate the protein oxidation. RT-PCR and Western blotting were performed to examine the expressions of inflammatory mediators （ IL-1β, TNFα, ICAM-1, and iNOS） and nuclear factor PPARs （PPARet, PPARα, and PPARγ,）, respectively. Results （ 1 ） Systolic blood pressure of SHR was significantly higher than that of Wistar-Kyoto rats, （205.4 ± 9.4） mm Hg versus （ 130.4 ± 7.9） mm Hg （t = 14. 96, P 〈 0. 01 ）. （2） MPO activity of cortex, striatum, and cerebellum were markedly higher in SHR than in Wistar-Kyoto rats. Carbonyl protein levels of cortex, striatum, and cerebellum in Wistar-Kyoto rats and SHR were （3. 27 ± 0. 43） nmol/mg versus （11.87 ± 1.11） nmol/mg, （4.02 ± 1.04） nmol/mg versus （14.06 ± 1.36） nmol/mg, （5.94±0.71） nmol/mg versus （ 14. 95± 1.82 ） nmol/mg, indicating significantly higher levels of protein oxidation in SHR than Wistar-Kyoto rats （ t = 17.70, 14. 36, 11.30, P 〈 0.05）. Consistently, the expression of pro-inflammatorymediators （IL-1β, TNFα, ICAM-1, and iNOS） was upregulated when compared with Wistar-Kyoto rats. The difference between SHR and control Wistar-Kyoto rats was statistically significant except the mRNA expression of IL-1β in striatum, cerebellum and TNFα in cerebellum of SHR. All the above experimental data indicated the occurrence of inflammatory status in the brain tissue of hypertension. （3） mRNA and protein levels of brain PPAR isoforms （ PPAR