昆明理工大学学报(自然科学版)
昆明理工大學學報(自然科學版)
곤명리공대학학보(자연과학판)
JOURNAL OF KUNMING UNIVERSITY OF SCIENCE AND TECHNOLOGY(SCIENCE AND TECHNOLOGY)
2015年
2期
108-113
,共6页
孟瑚%周晓萍%徐剑%罗惠民%熊丽焱
孟瑚%週曉萍%徐劍%囉惠民%熊麗焱
맹호%주효평%서검%라혜민%웅려염
CyPA%急性肾损伤%炎症介质%血管紧张素 II%厄贝沙坦
CyPA%急性腎損傷%炎癥介質%血管緊張素 II%阨貝沙坦
CyPA%급성신손상%염증개질%혈관긴장소 II%액패사탄
CyPA%acute kidney injury%inflammatory mediator%AngII%irbesatan
研究亲环素 A(CyPA)在正常人群及急性肾损伤(AKI)患者外周血中的浓度变化,探讨CyPA 是否与急性肾损伤有关及其可能的作用机制.检测急性肾损伤患者外周血中厄贝沙坦治疗前后 CyPA、AngII、TNFα、IL -6、IL -1α、MCP -1水平,并以正常人为对照组.结果发现 AKI 组外周血 CyPA 水平治疗前高于正常对照组.AKI 组 CyPA 与 AngII 及 TNFα、IL -6、IL -1α正相关,与 MCP -1负相关,相关系数分别为0.6,0.539,0.688,0.693,-0.725.说明 CyPA 作为一种炎症细胞介质,可能协同 AngII,参与了 AKI 患者炎性反应,加重肾小管上皮细胞损伤及细胞凋亡.通过选择性地抑制或阻断 CyPA 或 AngII 受体可能为我们提供一条对急性肾损伤的新治疗途径.
研究親環素 A(CyPA)在正常人群及急性腎損傷(AKI)患者外週血中的濃度變化,探討CyPA 是否與急性腎損傷有關及其可能的作用機製.檢測急性腎損傷患者外週血中阨貝沙坦治療前後 CyPA、AngII、TNFα、IL -6、IL -1α、MCP -1水平,併以正常人為對照組.結果髮現 AKI 組外週血 CyPA 水平治療前高于正常對照組.AKI 組 CyPA 與 AngII 及 TNFα、IL -6、IL -1α正相關,與 MCP -1負相關,相關繫數分彆為0.6,0.539,0.688,0.693,-0.725.說明 CyPA 作為一種炎癥細胞介質,可能協同 AngII,參與瞭 AKI 患者炎性反應,加重腎小管上皮細胞損傷及細胞凋亡.通過選擇性地抑製或阻斷 CyPA 或 AngII 受體可能為我們提供一條對急性腎損傷的新治療途徑.
연구친배소 A(CyPA)재정상인군급급성신손상(AKI)환자외주혈중적농도변화,탐토CyPA 시부여급성신손상유관급기가능적작용궤제.검측급성신손상환자외주혈중액패사탄치료전후 CyPA、AngII、TNFα、IL -6、IL -1α、MCP -1수평,병이정상인위대조조.결과발현 AKI 조외주혈 CyPA 수평치료전고우정상대조조.AKI 조 CyPA 여 AngII 급 TNFα、IL -6、IL -1α정상관,여 MCP -1부상관,상관계수분별위0.6,0.539,0.688,0.693,-0.725.설명 CyPA 작위일충염증세포개질,가능협동 AngII,삼여료 AKI 환자염성반응,가중신소관상피세포손상급세포조망.통과선택성지억제혹조단 CyPA 혹 AngII 수체가능위아문제공일조대급성신손상적신치료도경.
CyPA concentration levels in the peripheral blood in the normal subjects and patients with acute kid-ney injury (AKI)are detected to determine whether CyPA is associated with acute kidney injury and its possible mechanism.The level of CyPA,AngII,TNFα,IL -6,IL -1 and MCP -1 are measured in patients with AKI before and after treatment with irbesatan for 4 weeks.The positive control group is composed of normal subjects.It is observed that the level of CyPA in peripheral blood of AKI group is higher than that in the normal control group,The correlation coefficient of CyPA and AngII,IL -6,IL -1,TNF and MCP -1 are 0.6,0.539,0.688, 0.693,-0.725 respectively .The results show that CyPA may act as an inflammatory cell medium which coop-erates with AngII ,promotes AKI patients with inflammatory reaction,and increases renal tubular and interstitial injury.CyPA may be a new marker of inflammation in AKI damage.Through selective inhibition of CyPA or blocking of AngII receptors may provide a new treatment of AKI.