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目的通过构建兔颈动脉粥样硬化(AS)模型,观察全反式维甲酸(ATRA)对AS斑块中转化生长因子-β1(TGF-β1)、兔白介素-6(IL-6)、兔白介素-10(IL-10)和兔白介素-17(IL-17)的表达水平,探讨ATRA的抗AS作用及其机制。方法选取34只纯种雄性新西兰白兔随机分为正常组、模型组、他汀组、ATRA组。正常组给予基础饲料,其余各组给予高脂饲料。实验4周后他汀组予辛伐他汀2 mg/(kg·d)灌胃给药,ATRA组予ATRA 20 mg/d灌胃给药。12周末处死动物,取颈动脉组织观察AS斑块形态及炎症反应情况,并测定血清中血脂、TGF-β、IL-6、IL-10、IL-17的水平。结果模型组颈动脉可见AS斑块形成,内膜断裂。他汀组及ATRA组内皮细胞形态和内膜尚完整。血清中TGF-β1和IL-10水平结果,ATRA组分别为(3 059.49±599.75)ng/L和(46.83±4.56)ng/L,他汀组分别为(2 709.48±601.44)ng/L和(43.13±4.07)ng/L,均比模型组的(2 039.16±638.07)ng/L和(36.39±7.34)ng/L显著增高(P<0.05)。血清中IL-6和IL-17水平结果,ATRA组分别为(64.92±6.64)ng/L和(1 474.88±140.55)ng/L,他汀组分别为(69.54±8.84)ng/L和(1 518.58±136.69)ng/L,均比模型组的(110.00±7.26)ng/L和(2 002.66±195.57)ng/L显著降低(P<0.05)。结论 ATRA具有抗AS的作用,其机制可能与ATRA的炎症免疫调节作用有关。
Objective To investigate the effects of all-trans retinoic acid (ATRA) on the expression of transforming growth factor-β1 (TGF-β1), interleukin-6 (IL-6) (IL-10) and interleukin-17 (IL-17) in rabbits and explore the anti-AS effect of ATRA and its mechanism. Methods Thirty-four male New Zealand white rabbits were randomly divided into normal group, model group, statin group and ATRA group. The normal group given basic feed, the rest of the group given high-fat feed. Four weeks after the experiment, simvastatin 2 mg / (kg · d) was administered intragastrically in the statin group and ATRA 20 mg / d in the ATRA group. Animals were sacrificed on the 12th week. Carotid artery was used to observe the morphology and inflammatory response of AS plaques. Serum levels of lipids, TGF-β, IL-6, IL-10 and IL-17 were measured. Results The carotid artery in the model group showed AS plaque formation and rupture of the intima. The statin group and ATRA group endothelial cell morphology and intima is still intact. The levels of TGF-β1 and IL-10 in the serum were (3 059.49 ± 599.75) ng / L and (46.83 ± 4.56) ng / L in the ATRA group and (2 709.48 ± 601.44) ng / L and (43.13 ± 4.07) ng / L, both of which were significantly higher than those of the model group (2039.16 ± 638.07 ng / L and 36.39 ± 7.34 ng / L, P <0.05). Serum levels of IL-6 and IL-17 in the ATRA group were (64.92 ± 6.64) ng / L and (1447.88 ± 140.55) ng / L, respectively, and those in the statin group were (69.54 ± 8.84) ng / L and 518.58 ± 136.69 ng / L, both were significantly lower than those in model group (110.00 ± 7.26 ng / L and (2 002.66 ± 195.57) ng / L, P <0.05). Conclusion ATRA has the anti-AS effect and its mechanism may be related to the immunoregulatory effect of ATRA.