长期噪声暴露对大鼠心脏肾素-血管紧张素系统的影响及替米沙坦的干预

目的观察长期噪声暴露对大鼠心脏肾素-血管紧张素系统(renin-angiotensin system,RAS)主要成分的影响及替米沙坦(Telmisartan)的干预作用,为噪声损伤心脏的机制研究提供依据。方法将成年SD大鼠随机分为正常对照组、噪声组、噪声+替米沙坦组、单纯替米沙坦组,每组6只。噪声组和噪声+替米沙坦组暴露于100 dB(SPL)白噪声,6 h/d;噪声+替米沙坦组及单纯替米沙坦组用10 mg/(kg.d)盐酸替米沙坦水溶液灌胃,均连续12周。采用ELISA法测定大鼠血浆、心肌组织血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)含量,采用SYBRGreen实时荧光定量RT-PCR法测定心肌组织血管紧张素原(angiotensinogen,AGT)和血管紧张素Ⅱ受体1A亚型(AT1A)的基因表达。结果暴露12周后,噪声组血浆、心肌AngⅡ分别为(172.246±31.314)pg/ml、(22.250±2.438)pg/ng prot,明显高于正常组〔分别为(127.640±29.773)pg/ml、(17.484±1.022)pg/ng prot〕(P<0.05,P<0.01);噪声+替米沙坦组心肌AngⅡ含量为(13.002±2.457)pg/ng prot,明显低于正常组和噪声组(P<0.01);噪声组AT1A基因表达明显高于对照组(P<0.05);噪声+替米沙坦组AGT、AT1A基因表达明显低于噪声组(P<0.05,P<0.01)。结论噪声暴露可兴奋RAS,RAS兴奋可能是噪声致心肌损伤的途径之一。

EFFECTS OF LONG-TERM NOISE EXPOSURE ON CARDIAC RENIN-ANGIOTENSIN SYSTEM AND INTERVENTION BY TELMISARTAN

Objective To study the effects of long-term noise exposure on cardiac renin-angiotensin system （RAS） and the intervention by Telmisartan in rats, so as to provide the evidence for studying the mechanisms of heart damage by noise exposure. Methods Twenty-four SD rats were divided intd four groups：control group（ C group）, noise ex- posure group（ N group）, noise exposure plus Telmisartan group（N ＋ T group）, and Telmisartan group（T group）, with six rats per group. The N group and N ＋ T group were exposed to the white noise 100 dB（SPL） 6 h/day;the N ＋ T group and T group were administered Telmisartan（ 10 mg/kg per day） for 12 weeks. Angiotensin ]] （Ang 11 ） content in plasma, and cardiac muscle were measured by ELISA. Angiotensinogen （AGT）and angiotensin II AT1 receptor（ATiA） mRNA were determined by SYBR green RT-PCR. Results After 12 week treatment, Ang Ⅱ content in plasma, and cardiac muscle in N group （ 172. 246 ±31. 314）pg/ml, （22. 250 ±2.438）pg/ng prot respectively were higher than in C group （ 127. 640 ± 29.773）pg/ml, （17.484 ± 1. 022） pg/ng prot] （P 〈 0.05, P 〈 0.01）,whereas that in cardiac muscle in N ＋ T group （ 13. 002 ± 2. 457）pg/ng prot3was lower than in C and N group（ P 〈 0.01 ）. Expression of AT1A mRNA in N group was higher than in C group（ P 〈 0.01 ）. Expression of AGT and AT1A mRNA in N ＋ T group was lower than those in N group （ P 〈 0.01 ）. Conclusion Noise exposure may excite the cardiac renin-angiotensin system, which may be one of the mechanisms of heart damage induced by noise exposure.