中华临床医师杂志（电子版）
中華臨床醫師雜誌（電子版）
중화림상의사잡지（전자판）
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2014年
12期
2303-2306
,共4页
常乐%赵明月%马振华%马艳琴
常樂%趙明月%馬振華%馬豔琴
상악%조명월%마진화%마염금
PM2.5%系统性炎症%黏附分子%荧光定量PCR
PM2.5%繫統性炎癥%黏附分子%熒光定量PCR
PM2.5%계통성염증%점부분자%형광정량PCR
PM2.5%Systemic inflammation%Adhesion molecules%QRT-PCR
目的：研究PM2.5短期暴露对大鼠系统性炎症及主动脉细胞间黏附分子-1（ICAM-1）及血管细胞黏附分子-1（VCAM-1）基因表达的影响，初步探讨PM2.5心血管毒性损伤机制。方法采集空气中PM2.5样本并制备成20 mg/ml的混悬液。24只SD大鼠随机分为对照组、低剂量染毒组和高剂量染毒组，每组8只，分别给予气管内灌注生理盐水或不同浓度混悬液，每日1次，连续染毒7 d。采用ELISA技术检测各组大鼠血清中炎症因子白细胞介素-6（IL-6）和单核细胞趋化蛋白-1（MCP-1）的水平；采用荧光定量PCR技术检测大鼠主动脉VCAM-1、ICAM-1基因表达水平。结果 PM2.5暴露显著增加了血清MCP-1和IL-6水平。对照组、低剂量组和高剂量组血清MCP-1浓度分别为（5.28±0.24）pg/ml、（7.00±0.55）pg/ml 和（11.02±1.00）pg/ml（P＜0.01）；各组血清IL-6浓度分别为（40.17±1.79）pg/ml、（56.08±4.39）pg/ml（P＜0.05）和（76.15±4.60）pg/ml （P＜0.01）。低剂量组和高剂量组动脉组织ICAM-1 mRNA水平分别为对照组的1.8倍和4.1倍；VCAM-1 mRNA水平分别为对照组的4.0倍和4.6倍。结论暴露于PM2.5可引起大鼠血清炎症因子水平及动脉组织相关黏附分子表达增加，且呈剂量依赖性。诱导系统性炎症可能是 PM2.5心血管毒性机制之一。
目的：研究PM2.5短期暴露對大鼠繫統性炎癥及主動脈細胞間黏附分子-1（ICAM-1）及血管細胞黏附分子-1（VCAM-1）基因錶達的影響，初步探討PM2.5心血管毒性損傷機製。方法採集空氣中PM2.5樣本併製備成20 mg/ml的混懸液。24隻SD大鼠隨機分為對照組、低劑量染毒組和高劑量染毒組，每組8隻，分彆給予氣管內灌註生理鹽水或不同濃度混懸液，每日1次，連續染毒7 d。採用ELISA技術檢測各組大鼠血清中炎癥因子白細胞介素-6（IL-6）和單覈細胞趨化蛋白-1（MCP-1）的水平；採用熒光定量PCR技術檢測大鼠主動脈VCAM-1、ICAM-1基因錶達水平。結果 PM2.5暴露顯著增加瞭血清MCP-1和IL-6水平。對照組、低劑量組和高劑量組血清MCP-1濃度分彆為（5.28±0.24）pg/ml、（7.00±0.55）pg/ml 和（11.02±1.00）pg/ml（P＜0.01）；各組血清IL-6濃度分彆為（40.17±1.79）pg/ml、（56.08±4.39）pg/ml（P＜0.05）和（76.15±4.60）pg/ml （P＜0.01）。低劑量組和高劑量組動脈組織ICAM-1 mRNA水平分彆為對照組的1.8倍和4.1倍；VCAM-1 mRNA水平分彆為對照組的4.0倍和4.6倍。結論暴露于PM2.5可引起大鼠血清炎癥因子水平及動脈組織相關黏附分子錶達增加，且呈劑量依賴性。誘導繫統性炎癥可能是 PM2.5心血管毒性機製之一。
목적：연구PM2.5단기폭로대대서계통성염증급주동맥세포간점부분자-1（ICAM-1）급혈관세포점부분자-1（VCAM-1）기인표체적영향，초보탐토PM2.5심혈관독성손상궤제。방법채집공기중PM2.5양본병제비성20 mg/ml적혼현액。24지SD대서수궤분위대조조、저제량염독조화고제량염독조，매조8지，분별급여기관내관주생리염수혹불동농도혼현액，매일1차，련속염독7 d。채용ELISA기술검측각조대서혈청중염증인자백세포개소-6（IL-6）화단핵세포추화단백-1（MCP-1）적수평；채용형광정량PCR기술검측대서주동맥VCAM-1、ICAM-1기인표체수평。결과 PM2.5폭로현저증가료혈청MCP-1화IL-6수평。대조조、저제량조화고제량조혈청MCP-1농도분별위（5.28±0.24）pg/ml、（7.00±0.55）pg/ml 화（11.02±1.00）pg/ml（P＜0.01）；각조혈청IL-6농도분별위（40.17±1.79）pg/ml、（56.08±4.39）pg/ml（P＜0.05）화（76.15±4.60）pg/ml （P＜0.01）。저제량조화고제량조동맥조직ICAM-1 mRNA수평분별위대조조적1.8배화4.1배；VCAM-1 mRNA수평분별위대조조적4.0배화4.6배。결론폭로우PM2.5가인기대서혈청염증인자수평급동맥조직상관점부분자표체증가，차정제량의뢰성。유도계통성염증가능시 PM2.5심혈관독성궤제지일。
Objective To investigate the effect of exposure to PM2.5 on the systemic inflammation and the mRNA expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1(ICAM-1) in the rat aorta.MethodsFine particles were collected and made into suspension of 20 mg/ml. 24 SD rats were randomly categorized into 3 groups (n=8): control group, low-dosed group and high-dosed group, which were submitted to instillation of different dose of fine particle for 7 days.Biomarkers of systemic inflammation (MCP-1 and IL-6) in serum were analyzed by ELISA. Real-time PCR was applied to investigate the mRNA expression of VCAM-1 and ICAM-1 in the aorta.Results The serum levels of MCP-1 and IL-6 increased significantly in rats exposed to low-dose or high-dose PM2.5 in comparison with that of the control group. MCP-1 levels in the serum of the three groups were (5.28±0.24) pg/ml, (7.00±0.55) pg/ml and (11.02±1.00) pg/ml(P<0.01) respectively. And the IL-6 levels were (40.17±1.79)pg/ml, (56.08±4.39)pg/ml(P<0.05) and (76.15±4.60)pg/ml(P<0.01) respectively. Exposure to low dose or high dose PM2.5 significantly upregulated the expression of VCAM-1 and ICAM-1 in the aorta of rats. The levels of ICAM-1 mRNA of low-dose exposed rats and high-dose exposed rats were 1.8 and 4.1 times compared with that of the control group. The same trends were shown in the levels of VCAM-1 mRNA, which were 4.0 and 4.6 times in the two experimental groups compared with the control group. ConclusionExposure to PM2.5can increase the levels of inflammation biomarkers in rat serum. Also, the expression of the adhesion molecules in the aorta was increased which showed dose-effect relationship. In conclusion, PM2.5 exposure could cause systemic inflammation, which may be one of the pathophysiological mechanisms linking PM2.5 and cardiovascular diseases.
