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目的观察LED红光照射对早期糖尿病大鼠视网膜电生理及氧化应激的影响,探讨光生物调节作用(photobiomodulation,PBM)对糖尿病大鼠视网膜病变的防治作用及其机制。方法 2014年9月—2015年10月选取健康雄性SD大鼠40只,随机分为正常对照组、糖尿病组、50秒LED治疗组、240秒LED治疗组各10只,后三组采用链脲佐菌素诱导糖尿病大鼠模型,50秒LED治疗组及240秒LED治疗组分别给予LED照射治疗。9周后检测大鼠视网膜电图(electroretinogram,ERG)a波、b波的潜伏期和振幅,黄嘌呤氧化酶法检测视网膜锰超氧化物歧化酶(Mn SOD)活性,实时荧光定量聚合酶链反应(PCR)法检测Mn SOD m RNA表达水平。计量资料采用方差分析,两两比较采用LSD-t检验,P<0.05为差异有统计学意义。结果 240秒LED治疗组ERG b波的潜伏期和振幅分别为(64.8±4.9)ms、(406.9±59.9)u V,与糖尿病组和50秒LED治疗组的(85.1±8.6)ms、(182.5±56.3)u V(84.9、±8.9)ms、(183.1±55.9)u V比较差异均有统计学意义(均P<0.05)。240秒LED治疗组ERG a波潜伏期为(23.0±1.8)ms,与糖尿病组和50秒LED治疗组的(31.0±3.7)、(30.9±3.7)ms比较差异均有统计学意义(均P<0.05)。240秒LED治疗组视网膜Mn SOD活性及其m RNA表达水平分别为(45.919±6.834)U/mg、(0.899±0.091),与糖尿病组和50秒LED治疗组的(20.045±6.786)U/mg、(0.257±0.056)、(21.096±6.798)U/mg、(0.289±0.049)比较差异均有统计学意义(均P<0.05)。结论 240秒LED治疗能逆转大鼠视觉电生理异常,提高其视网膜Mn SOD m RNA表达水平和Mn SOD活性,减轻视网膜氧化应激损伤,对糖尿病视网膜病变大鼠视网膜早期病变具有保护作用。
Objective To observe the effect of red LED irradiation on retinal electrophysiological and oxidative stress in early diabetic rats and to explore the preventive and therapeutic effects of photobiomodulation (PBM) on diabetic retinopathy and its mechanism. Methods From September 2014 to October 2015, 40 healthy male SD rats were randomly divided into normal control group, diabetes group, 50 seconds LED treatment group and 240 seconds LED treatment group, 10 rats in each group. ZOU induced diabetic rat model, 50 seconds LED treatment group and 240 seconds LED treatment group were given LED irradiation treatment. After 9 weeks, the a-wave and b-wave latency and amplitude of electroretinogram (ERG) in rats were detected. The activities of retinal manganese superoxide dismutase (Mn SOD) were detected by xanthine oxidase method. Real-time fluorescence quantitative polymerase chain reaction (PCR) method to detect the expression level of Mn SOD m RNA. Measurement data were analyzed by ANOVA, pairwise comparisons using LSD-t test, P <0.05 for the difference was statistically significant. Results The latency and amplitude of ERG b wave in the 240-second LED treatment group were (64.8 ± 4.9) ms and (406.9 ± 59.9) μV, respectively, which were significantly lower than those in the DM group and the 50-second LED treatment group 56.3) uV (84.9, ± 8.9) ms, (183.1 ± 55.9) uV, respectively. All the differences were statistically significant (all P <0.05). The latency of ERG a wave in 240 seconds LED group was (23.0 ± 1.8) ms, which was significantly different from that in diabetic group and 50 seconds LED group (31.0 ± 3.7) and (30.9 ± 3.7) ms respectively (all P < 0.05). The activities of Mn SOD and the expression of m RNA in retina of 240 s LED treatment group were (45.919 ± 6.834) U / mg and (0.899 ± 0.091), respectively, which were significantly higher than those in diabetic group and 50 s LED treatment group (20.045 ± 6.786) U / mg , (0.257 ± 0.056), (21.096 ± 6.798) U / mg and (0.289 ± 0.049) respectively (all P <0.05). Conclusion 240 s LED treatment can reverse the visual electrophysiological abnormalities in rats, increase the expression level of Mn SOD m RNA in retina and Mn SOD activity, reduce the damage of retinal oxidative stress and protect the early retina of diabetic retinopathy rats.