中国医药
中國醫藥
중국의약
CHINA MEDICINE
2013年
2期
151-153
,共3页
孙常青%李卫华%陈庆福%郭丽蓉
孫常青%李衛華%陳慶福%郭麗蓉
손상청%리위화%진경복%곽려용
动脉粥样硬化%磷脂酶A2,分泌型%白细胞介素6%辛伐他汀
動脈粥樣硬化%燐脂酶A2,分泌型%白細胞介素6%辛伐他汀
동맥죽양경화%린지매A2,분비형%백세포개소6%신벌타정
Atherosclerosis%Phospholipase A2,secretory%Interleukin-6%Simvastatin
目的 了解分泌型磷脂酶A2Ⅱa型(sPLA2Ⅱa)在动脉粥样硬化大鼠模型主动脉的表达及分布,通过测定肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)等相关细胞因子探讨sPLA2Ⅱa的作用机制,并了解他汀类药物对sPLA2Ⅱa的影响.方法 将雄性Wistar大鼠30只完全随机分为正常对照组、高脂饮食组、辛伐他汀组,各10只.正常对照组喂食基础饲料,高脂饮食组喂食高脂饲料,辛伐他汀组喂食高脂饲料及辛伐他汀悬液(5 mg/kg)灌胃,正常对照组和高脂饮食组大鼠给予等容积的0.9％氯化钠注射液灌胃,连续6周,取材.采用免疫组织化学SP法检测主动脉组织中sPLA2Ⅱa的表达及分布,酶联免疫吸附测定法检测血清IL-6、TNF-α水平.结果 ①与正常对照组相比,高脂饮食组大鼠血清TC、TG、LDL-C含量明显升高[TG:(1.9±0.5)mmol/L比(1.5±0.6)mmol/L,TC:(5.82±1.13) mmol/L比(1.98±0.26) mmol/L,LDL-C:(3.97±0.78) mmol/L比(0.50±0.16) mmol/L,均P＜0.01]；与高脂饮食组比较,辛伐他汀组血清TC、TG、LDL-C[TC:(3.78±0.59)mmoL/L,TG:(0.8±0.4) mmol/L,LDL-C:(1.49±0.62) mmol/L]明显降低(均P＜0.05).②高脂饮食组大鼠血清TNF-α、IL-6水平明显高于正常对照组[TNF-α:(15.48±1.03)ng/L比(8.40±0.28) ng/L,IL-6:(72.0±7.5) ng/L比(25.1±2.3)ng/L,均P＜0.01]；辛伐他汀组TNF-α、IL-6水平[TNF-α:(10.54±1.96) ng/L,IL-6:(40.2±20.2)ng/L]明显低于高脂饮食组(均P＜0.05).③高脂饮食组sPLA2Ⅱa呈强阳性表达,主要位于血管壁动脉粥样硬化斑块区域无定形物质,与正常对照组比较表达均明显升高；辛伐他汀组sPLA2Ⅱa表达较高脂饮食组明显下调.结论 动脉粥样硬化大鼠主动脉sPLA2Ⅱa表达明显升高,可能与TNF-α、IL-6共同参与动脉粥样硬化斑块的形成及发展过程,辛伐他汀可以降低sPLA2Ⅱa表达水平.
目的 瞭解分泌型燐脂酶A2Ⅱa型(sPLA2Ⅱa)在動脈粥樣硬化大鼠模型主動脈的錶達及分佈,通過測定腫瘤壞死因子α(TNF-α)、白細胞介素6(IL-6)等相關細胞因子探討sPLA2Ⅱa的作用機製,併瞭解他汀類藥物對sPLA2Ⅱa的影響.方法 將雄性Wistar大鼠30隻完全隨機分為正常對照組、高脂飲食組、辛伐他汀組,各10隻.正常對照組餵食基礎飼料,高脂飲食組餵食高脂飼料,辛伐他汀組餵食高脂飼料及辛伐他汀懸液(5 mg/kg)灌胃,正常對照組和高脂飲食組大鼠給予等容積的0.9％氯化鈉註射液灌胃,連續6週,取材.採用免疫組織化學SP法檢測主動脈組織中sPLA2Ⅱa的錶達及分佈,酶聯免疫吸附測定法檢測血清IL-6、TNF-α水平.結果 ①與正常對照組相比,高脂飲食組大鼠血清TC、TG、LDL-C含量明顯升高[TG:(1.9±0.5)mmol/L比(1.5±0.6)mmol/L,TC:(5.82±1.13) mmol/L比(1.98±0.26) mmol/L,LDL-C:(3.97±0.78) mmol/L比(0.50±0.16) mmol/L,均P＜0.01]；與高脂飲食組比較,辛伐他汀組血清TC、TG、LDL-C[TC:(3.78±0.59)mmoL/L,TG:(0.8±0.4) mmol/L,LDL-C:(1.49±0.62) mmol/L]明顯降低(均P＜0.05).②高脂飲食組大鼠血清TNF-α、IL-6水平明顯高于正常對照組[TNF-α:(15.48±1.03)ng/L比(8.40±0.28) ng/L,IL-6:(72.0±7.5) ng/L比(25.1±2.3)ng/L,均P＜0.01]；辛伐他汀組TNF-α、IL-6水平[TNF-α:(10.54±1.96) ng/L,IL-6:(40.2±20.2)ng/L]明顯低于高脂飲食組(均P＜0.05).③高脂飲食組sPLA2Ⅱa呈彊暘性錶達,主要位于血管壁動脈粥樣硬化斑塊區域無定形物質,與正常對照組比較錶達均明顯升高；辛伐他汀組sPLA2Ⅱa錶達較高脂飲食組明顯下調.結論 動脈粥樣硬化大鼠主動脈sPLA2Ⅱa錶達明顯升高,可能與TNF-α、IL-6共同參與動脈粥樣硬化斑塊的形成及髮展過程,辛伐他汀可以降低sPLA2Ⅱa錶達水平.
목적 료해분비형린지매A2Ⅱa형(sPLA2Ⅱa)재동맥죽양경화대서모형주동맥적표체급분포,통과측정종류배사인자α(TNF-α)、백세포개소6(IL-6)등상관세포인자탐토sPLA2Ⅱa적작용궤제,병료해타정류약물대sPLA2Ⅱa적영향.방법 장웅성Wistar대서30지완전수궤분위정상대조조、고지음식조、신벌타정조,각10지.정상대조조위식기출사료,고지음식조위식고지사료,신벌타정조위식고지사료급신벌타정현액(5 mg/kg)관위,정상대조조화고지음식조대서급여등용적적0.9％록화납주사액관위,련속6주,취재.채용면역조직화학SP법검측주동맥조직중sPLA2Ⅱa적표체급분포,매련면역흡부측정법검측혈청IL-6、TNF-α수평.결과 ①여정상대조조상비,고지음식조대서혈청TC、TG、LDL-C함량명현승고[TG:(1.9±0.5)mmol/L비(1.5±0.6)mmol/L,TC:(5.82±1.13) mmol/L비(1.98±0.26) mmol/L,LDL-C:(3.97±0.78) mmol/L비(0.50±0.16) mmol/L,균P＜0.01]；여고지음식조비교,신벌타정조혈청TC、TG、LDL-C[TC:(3.78±0.59)mmoL/L,TG:(0.8±0.4) mmol/L,LDL-C:(1.49±0.62) mmol/L]명현강저(균P＜0.05).②고지음식조대서혈청TNF-α、IL-6수평명현고우정상대조조[TNF-α:(15.48±1.03)ng/L비(8.40±0.28) ng/L,IL-6:(72.0±7.5) ng/L비(25.1±2.3)ng/L,균P＜0.01]；신벌타정조TNF-α、IL-6수평[TNF-α:(10.54±1.96) ng/L,IL-6:(40.2±20.2)ng/L]명현저우고지음식조(균P＜0.05).③고지음식조sPLA2Ⅱa정강양성표체,주요위우혈관벽동맥죽양경화반괴구역무정형물질,여정상대조조비교표체균명현승고；신벌타정조sPLA2Ⅱa표체교고지음식조명현하조.결론 동맥죽양경화대서주동맥sPLA2Ⅱa표체명현승고,가능여TNF-α、IL-6공동삼여동맥죽양경화반괴적형성급발전과정,신벌타정가이강저sPLA2Ⅱa표체수평.
Objective To detect the expression of group Ⅱ a secretory phospholipase A2 (sPLA2 Ⅱ a) inthe aorta of atherosclerosis (AS) rat model and to investigate its relation to tumor necrosis factor α (TNF-α) andinterleukin 6 (IL-6).To study the influence of simvastatin on sPLA2 Ⅱ a.Methods The athemsclerosis model inrats was set up by feeding with high cholesterol diet for six week.Meanwhile animals were randomized to receiveeither no treatment or simvastatin [5 mg/(kg · d)].The expression of sPLA2 Ⅱ a was studied by immunohisto-chemistry.The levels of TNF-α and IL-6 in serum were measured by enzyme linked immunosorbent assay.ResultsThe total cholesterol (TC),triglyceride (TG) and low-density lipoprotein cholesterol (LDL-C) level of high fatdiet group [(TG:(1.9 ± 0.5) mmol/L,TC:(5.82 ± 1.13) mmol/L,LDL-C:(3.97 ± 0.78) mmol/L] wassignificantly higher than those in control group[TG:(1.5 ± 0.6)mmol/L,TC:(1.98 ± 0.26) mmol/L,LDL-C:(0.50 ± 0.16) mmol/L,P ＜ 0.01],simvastatin decrease the level of TC,TG and LDL-C [TC:(3.78 ±0.59) mmol/L,TG:(0.8 ± 0.4) mmol/L,LDL-C:(1.49 ± 0.62) mmol/L,P ＜ 0.05].It showed that the levelsof TNF-α and IL-6 in serum in high fat diet group[TNF-α:(15.48 ± 1.03) ng/L,IL-6:(72.0 ±7.5)ng/L] weresignificantly higher than those in control group [TNF-α:(8.40 ± 0.28) ng/L,IL-6:(25.1 ± 2.3)ng/L,P ＜0.01]; simvastatin decreased the levels of TNF-α and IL-6 [TNF-α:(10.54 ± 1.96)ng/L,IL-6:(40.2 ±20.2) ng/L,P ＜0.01].sPLA2 Ⅱ a was present in smooth muscle cell and plaque of aorta.In contrast,sPLA2 Ⅱ aexpression in aorta was much higher in high fat diet group than those in control group,expression of the enzyme inaorta was decreased in simvastatin group compared to high fat diet group.Conclusions This result supports thehypothesis that sPLA2 Ⅱ a may play a significant role in the pathogenesis of AS.Simvastatin could relieve theprocess of AS by decreasing the expression level of sPLA2 Ⅱ a.
