Methamphetamine (METH), an addictive stimulant of neurotransmitters, is associated with cardiovascular and neurological diseases. METH-induced ophthalmic complications are also present but have been insufficiently investigated. The purpose of this study is to investigate the retinal effects of METH. C57BL/6 mice were administrated progressively increasing doses of METH (0-6 mg/kg) by repetitive intraperitoneal injections for 5 days (4 times per day). Retinal degeneration was examined by morphological changes and terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay. Norepinephrine levels were measured by ELISA, protein expression levels were determined by immunoblot and immunostaining, and gelatinase activity was examined by zymography. The thickness of the retina and the number of nuclei in the inner and outer nuclear layers were decreased by METH. Retinal cell death and astrocyte activation by METH treatment were confirmed by TUNEL assay and glial fibrillary acidic protein expression, respectively. Increased tumor necrosis factor-α protein in the retina and elevated norepinephrine levels in plasma were found in METH-treated mice. Platelet endothelial cell adhesion molecule-1 (PECAM-1) protein expression level was decreased in the retina and central retinal artery (CRA) by METH treatment, along with the endothelial proteoglycans glypican-1 and syndecan-1. Moreover, a regulator of the extracellular matrix, matrix metalloproteinase-14 (MMP-14) in the retina, and MMP-2 and MMP-9 in plasma, were increased by METH treatment. In conclusion, METH administration is involved in retinal degeneration with a vascular loss of PECAM-1 and the glycocalyx in the CRA and retina, and an increase of MMPs.

中文翻译：

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甲基苯丙胺可引起视网膜和视网膜中央动脉的急性变化。

甲基苯丙胺（METH）是一种神经递质的成瘾性兴奋剂，与心血管和神经系统疾病有关。还存在甲乙丙胺引起的眼科并发症，但尚未进行充分的研究。这项研究的目的是调查甲基苯丙氨酸甲酯的视网膜作用。通过重复腹膜内注射持续5天（每天4次），向C57BL / 6小鼠逐渐增加剂量的METH（0-6 mg / kg）。通过形态学改变和末端脱氧核苷酸转移酶脱氧尿苷三磷酸缺口末端标记（TUNEL）测定来检查视网膜变性。通过ELISA测量去甲肾上腺素水平，通过免疫印迹和免疫染色确定蛋白表达水平，并通过酶谱检查明胶酶活性。METH减少了视网膜的厚度和内，外核层中的核数。通过TUNEL测定和胶质原纤维酸性蛋白表达分别证实了通过METH处理的视网膜细胞死亡和星形胶质细胞激活。在METH治疗的小鼠中，发现视网膜中的肿瘤坏死因子-α蛋白增加，血浆中去甲肾上腺素水平升高。通过METH处理，视网膜和视网膜中央动脉（CRA）中的血小板内皮细胞粘附分子1（PECAM-1）蛋白表达水平以及内皮蛋白聚糖glypican-1和syndecan-1均降低。此外，通过METH处理可增加细胞外基质的调节剂，视网膜中的基质金属蛋白酶14（MMP-14），血浆中的MMP-2和MMP-9。结论，