Abstract：
This study explored the possibility of highlighting early retinal neurovascular alterations of diabetic retinopathy (DR) by monitoring in DR patients the serum levels of microglial biomarkers ionized calcium-binding adapter molecule 1 (Iba-1), glucose transporter 5 (GLUT5), and translocator protein (TSPO), along with serum changes of the endothelial dysfunction marker arginase-1.
Serum markers were determined by enzyme-linked immunosorbent assay in 50 patients: 12 non-diabetic subjects, 14 diabetic patients without DR, 13 patients with non-proliferative DR (NPDR), and 11 patients with proliferative DR (PDR). The results were correlated with hyperreflective retinal spots (HRS), observed with optical coherence tomography (OCT).
Although HRS were absent in diabetic patients without DR, NPDR patients showed an average of 4 ± 1 HRS, whereas the highest presence was detected in PDR patients, with 8 ± 1 HRS (P < 0.01 vs. NPDR). HRS were positively correlated (P < 0.01) with serum levels of arginase-1 (r = 0.91), Iba-1 (r = 0.96), GLUT5 (r = 0.94), and TSPO (r = 0.88). Moreover, serum proinflammatory cytokines and chemokines showed a positive correlation (P < 0.01) with HRS number and the serum markers analyzed.
Serum markers of microglial activation positively correlate with retinal HRS in NPDR and PDR patients.
These data corroborate the possibility of highlighting early retinal neurovascular changes due to diabetes by monitoring circulating microglial markers.
Serum markers were determined by enzyme-linked immunosorbent assay in 50 patients: 12 non-diabetic subjects, 14 diabetic patients without DR, 13 patients with non-proliferative DR (NPDR), and 11 patients with proliferative DR (PDR). The results were correlated with hyperreflective retinal spots (HRS), observed with optical coherence tomography (OCT).
Although HRS were absent in diabetic patients without DR, NPDR patients showed an average of 4 ± 1 HRS, whereas the highest presence was detected in PDR patients, with 8 ± 1 HRS (P < 0.01 vs. NPDR). HRS were positively correlated (P < 0.01) with serum levels of arginase-1 (r = 0.91), Iba-1 (r = 0.96), GLUT5 (r = 0.94), and TSPO (r = 0.88). Moreover, serum proinflammatory cytokines and chemokines showed a positive correlation (P < 0.01) with HRS number and the serum markers analyzed.
Serum markers of microglial activation positively correlate with retinal HRS in NPDR and PDR patients.
These data corroborate the possibility of highlighting early retinal neurovascular changes due to diabetes by monitoring circulating microglial markers.
摘要：
本研究通过监测糖尿病视网膜病变（DR）患者的小胶质细胞生物标志物离子化钙结合接头分子1（Iba-1）的血清水平，探索了突出糖尿病视网膜神经血管早期改变的可能性。葡萄糖转运蛋白5（GLUT5），和转运蛋白（TSPO），随着内皮功能障碍标志物精氨酸酶-1的血清变化。
通过酶联免疫吸附试验测定了50例患者的血清标志物：12例非糖尿病受试者，14例糖尿病患者无DR，13例非增殖性DR（NPDR），11例增殖性DR(PDR)患者。结果与高反射视网膜斑点（HRS）相关，用光学相干断层扫描（OCT）观察。
虽然没有DR的糖尿病患者没有HRS，NPDR患者显示平均4±1HRS，而在PDR患者中检测到最高的存在，8±1HRS（P<0.01vs.NPDR）。HRS与血清精氨酸酶-1水平呈正相关(P<0.01)(r=0.91)。Iba-1（r=0.96），GLUT5（r=0.94），和TSPO(r=0.88)。此外，血清促炎细胞因子和趋化因子与HRS数和血清标志物呈正相关(P<0.01)。
NPDR和PDR患者小胶质细胞活化的血清标志物与视网膜HRS呈正相关。
这些数据证实了通过监测循环小胶质细胞标志物来突出糖尿病引起的早期视网膜神经血管变化的可能性。
通过酶联免疫吸附试验测定了50例患者的血清标志物：12例非糖尿病受试者，14例糖尿病患者无DR，13例非增殖性DR（NPDR），11例增殖性DR(PDR)患者。结果与高反射视网膜斑点（HRS）相关，用光学相干断层扫描（OCT）观察。
虽然没有DR的糖尿病患者没有HRS，NPDR患者显示平均4±1HRS，而在PDR患者中检测到最高的存在，8±1HRS（P<0.01vs.NPDR）。HRS与血清精氨酸酶-1水平呈正相关(P<0.01)(r=0.91)。Iba-1（r=0.96），GLUT5（r=0.94），和TSPO(r=0.88)。此外，血清促炎细胞因子和趋化因子与HRS数和血清标志物呈正相关(P<0.01)。
NPDR和PDR患者小胶质细胞活化的血清标志物与视网膜HRS呈正相关。
这些数据证实了通过监测循环小胶质细胞标志物来突出糖尿病引起的早期视网膜神经血管变化的可能性。
