生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2006年
4期
318-323
,共6页
孙莉%高月红%田登科%郑建普%朱春赟%可燕%卞卡
孫莉%高月紅%田登科%鄭建普%硃春赟%可燕%卞卡
손리%고월홍%전등과%정건보%주춘빈%가연%변잡
自发性高血压大鼠%炎症%肾%肝%心%脑
自髮性高血壓大鼠%炎癥%腎%肝%心%腦
자발성고혈압대서%염증%신%간%심%뇌
spontaneously hypertensive rat%inflammation%kidney%liver%heart%brain
高血压是一种慢性血管性疾病,易累及肾、肝、心、脑等组织,引起脑卒中和心、肾损害等并发症.本研究对高血压时肾、肝、心、脑等组织的炎症状态进行了观察.实验采用自发性高血压大鼠(spontaneously hypertensive rat,SHR)和正常血压的Wistar-Kyoto(WKY)大鼠,用RT-PCR和Western blot法观察肾、肝、心、脑等组织炎症相关因子IL-1p、TNFα、ICAM-1、iNOS、C/EBPδ和PPARγ的基因表达;紫外分光光度法观察蛋白质羰基化水平和FRAP法检测组织总抗氧化能力.结果显示:(1)SHR组织炎症相关因子表达较对照WKY增强,除IL-1βmRNA在肝和脑的增加不明显外,其余均有显著性差异(P<0.05);(2)SHR和WKY大鼠肾、心、脑蛋白质羰基化水平(nmol/mg蛋白)分别为8.93±1.08和2.27±0.43、2.23±0.23和0.17±0.02、13.42±1.10和5.72±1.01,SHR明显增加(P<0.05);而肝脏蛋白质羰基化水平无明显变化;(3)SHR肾、肝、心、脑总抗氧化能力水平显著低于WKY大鼠(P<0.05).以上结果表明,SHR多个组织(肾、肝、心和脑)均存在炎症因子被诱导和氧化应激反应等明显的炎症状态,提示炎症可能在高血压及其并发症的病理改变中起重要作用.
高血壓是一種慢性血管性疾病,易纍及腎、肝、心、腦等組織,引起腦卒中和心、腎損害等併髮癥.本研究對高血壓時腎、肝、心、腦等組織的炎癥狀態進行瞭觀察.實驗採用自髮性高血壓大鼠(spontaneously hypertensive rat,SHR)和正常血壓的Wistar-Kyoto(WKY)大鼠,用RT-PCR和Western blot法觀察腎、肝、心、腦等組織炎癥相關因子IL-1p、TNFα、ICAM-1、iNOS、C/EBPδ和PPARγ的基因錶達;紫外分光光度法觀察蛋白質羰基化水平和FRAP法檢測組織總抗氧化能力.結果顯示:(1)SHR組織炎癥相關因子錶達較對照WKY增彊,除IL-1βmRNA在肝和腦的增加不明顯外,其餘均有顯著性差異(P<0.05);(2)SHR和WKY大鼠腎、心、腦蛋白質羰基化水平(nmol/mg蛋白)分彆為8.93±1.08和2.27±0.43、2.23±0.23和0.17±0.02、13.42±1.10和5.72±1.01,SHR明顯增加(P<0.05);而肝髒蛋白質羰基化水平無明顯變化;(3)SHR腎、肝、心、腦總抗氧化能力水平顯著低于WKY大鼠(P<0.05).以上結果錶明,SHR多箇組織(腎、肝、心和腦)均存在炎癥因子被誘導和氧化應激反應等明顯的炎癥狀態,提示炎癥可能在高血壓及其併髮癥的病理改變中起重要作用.
고혈압시일충만성혈관성질병,역루급신、간、심、뇌등조직,인기뇌졸중화심、신손해등병발증.본연구대고혈압시신、간、심、뇌등조직적염증상태진행료관찰.실험채용자발성고혈압대서(spontaneously hypertensive rat,SHR)화정상혈압적Wistar-Kyoto(WKY)대서,용RT-PCR화Western blot법관찰신、간、심、뇌등조직염증상관인자IL-1p、TNFα、ICAM-1、iNOS、C/EBPδ화PPARγ적기인표체;자외분광광도법관찰단백질탄기화수평화FRAP법검측조직총항양화능력.결과현시:(1)SHR조직염증상관인자표체교대조WKY증강,제IL-1βmRNA재간화뇌적증가불명현외,기여균유현저성차이(P<0.05);(2)SHR화WKY대서신、심、뇌단백질탄기화수평(nmol/mg단백)분별위8.93±1.08화2.27±0.43、2.23±0.23화0.17±0.02、13.42±1.10화5.72±1.01,SHR명현증가(P<0.05);이간장단백질탄기화수평무명현변화;(3)SHR신、간、심、뇌총항양화능력수평현저저우WKY대서(P<0.05).이상결과표명,SHR다개조직(신、간、심화뇌)균존재염증인자피유도화양화응격반응등명현적염증상태,제시염증가능재고혈압급기병발증적병리개변중기중요작용.
The hypertension is one of chronic vascular diseases, which often implicates multiple tissues causing stroke, cardiac hypertrophy, and renal failure. A growing body of evidence suggests that inflammatory mechanisms are important participants in the pathophysiology of hypertension. In this study, the inflammatory status of these tissues (kidney, liver, heart, and brain) in spontaneously hypertensive rats (SHR) was analyzed and its molecular mechanism was explored. The tissues were dissected from SHR and agematched control Wistar-Kyoto (WKY) rats to investigate the abundance of inflammation-related mediators (IL-1β, TNFα, ICAM-1,iNOS, C/EBPδ and PPARγ). mRNA levels were determined by reverse transcription-polymerase chain reaction and protein expression was evaluated by Western blot. To evaluate the oxidative stress of tissues, carbonyl protein content and total antioxidant capacity of tissues were detected by spectrophotometry and ferric reduction ability power (FRAP) method. The results suggest that: (1)Expressions of inflammation-related mediators (IL-1β, TNFα, ICAM-1, iNOS, C/EBPδ and PPARγ) in SHR were higher compared with those in WKY rats except no evident increase of IL-1β mRNA in liver and brain in SHR. (2) Tissues in SHR contained obviously increased carbonyl protein (nmol/mg protein) compared to that in WKY rats (8.93±1.08 vs 2.27±0.43 for kidney, 2.23±0.23 vs 0.17±0.02 for heart, 13.42± 1.10 vs 5.72± 1.01 for brain, respectively, P<0.05). However, no evident difference in the amount of carbonyl protein in liver was detected between SHR and WKY rats. (3) Total antioxidant capacities of kidney, liver, heart and brain were markedly lower in SHR than that in WKY rats (P<0.05). Thus, the present data reveal a higher inflammatory status in the important tissues in SHR and indicate that inflammation might play a potential role in pathogencsis of hypertension and secondary organ complications.