Case Western Reserve University, Cleveland, OH 44106, USA.
Invest Ophthalmol Vis Sci. 2013 May 1;54(5):3681-90. doi: 10.1167/iovs.12-11018.
Treatment with light in the far-red to near-infrared region of the spectrum (photobiomodulation [PBM]) has beneficial effects in tissue injury. We investigated the therapeutic efficacy of 670-nm PBM in rodent and cultured cell models of diabetic retinopathy.
Studies were conducted in streptozotocin-induced diabetic rats and in cultured retinal cells. Diabetes-induced retinal abnormalities were assessed functionally, biochemically, and histologically in vivo and in vitro.
We observed beneficial effects of PBM on the neural and vascular elements of retina. Daily 670-nm PBM treatment (6 J/cm(2)) resulted in significant inhibition in the diabetes-induced death of retinal ganglion cells, as well as a 50% improvement of the ERG amplitude (photopic b wave responses) (both P < 0.01). To explore the mechanism for these beneficial effects, we examined physiologic and molecular changes related to cell survival, oxidative stress, and inflammation. PBM did not alter cytochrome oxidase activity in the retina or in cultured retinal cells. PBM inhibited diabetes-induced superoxide production and preserved MnSOD expression in vivo. Diabetes significantly increased both leukostasis and expression of ICAM-1, and PBM essentially prevented both of these abnormalities. In cultured retinal cells, 30-mM glucose exposure increased superoxide production, inflammatory biomarker expression, and cell death. PBM inhibited all of these abnormalities.
PBM ameliorated lesions of diabetic retinopathy in vivo and reduced oxidative stress and cell death in vitro. PBM has been documented to have minimal risk. PBM is noninvasive, inexpensive, and easy to administer. We conclude that PBM is a simple adjunct therapy to attenuate the development of diabetic retinopathy.
光谱远红至近红外区域的光治疗（光生物调节[PBM]）对组织损伤具有有益的影响。我们研究了 670nm PBM 在糖尿病性视网膜病变的啮齿动物和培养细胞模型中的治疗效果。
在链脲佐菌素诱导的糖尿病大鼠和培养的视网膜细胞中进行了研究。在体内和体外评估了糖尿病诱导的视网膜异常的功能、生化和组织学。
我们观察到 PBM 对视网膜的神经和血管元素有有益的影响。每日 670nm PBM 治疗（6J/cm2）可显著抑制糖尿病诱导的视网膜神经节细胞死亡，并使 ERG 幅度（明视 b 波反应）提高 50%（均 P<0.01）。为了探索这些有益效果的机制，我们检查了与细胞存活、氧化应激和炎症相关的生理和分子变化。PBM 没有改变视网膜或培养的视网膜细胞中的细胞色素氧化酶活性。PBM 抑制了糖尿病诱导的超氧化物产生，并在体内保留了 MnSOD 的表达。糖尿病显著增加了白细胞停滞和 ICAM-1 的表达，而 PBM 基本上防止了这两种异常。在培养的视网膜细胞中，30mM 葡萄糖暴露增加了超氧化物的产生、炎症生物标志物的表达和细胞死亡。PBM 抑制了所有这些异常。
PBM 改善了糖尿病性视网膜病变的病变，减少了体外的氧化应激和细胞死亡。PBM 已被证明风险极小。PBM 是非侵入性的、廉价的、易于管理的。我们得出结论，PBM 是一种简单的辅助治疗方法，可以减轻糖尿病性视网膜病变的发展。
