Ren Le-Meng, Zhang Ying-Hui
The First Clinical Medical College, Lanzhou University, Lanzhou 730000, Gansu Province, China.
Medical Record Room, the Second Hospital of Shandong University, Shandong University, Jinan 250033, Shandong Province, China.
Int J Ophthalmol. 2020 Dec 18;13(12):1880-1886. doi: 10.18240/ijo.2020.12.06. eCollection 2020.
To determine whether Houttuynia cordata Thunb (HCT) can increase the survival of the retinal ganglion cells (RGCs) and inhibit microglia activation following retinal ischemia-reperfusion (RIR) injury.
Rat model of RIR was induced by transient elevation of the intraocular pressure (IOP). HCT was orally administered for 2d before the performance of retinal RIR model and once a day for the next 14d. After 14d of RIR injury, the rats were sacrificed for further analysis. Survival RGCs were stained with haematoxylin and eosin (H&E). Apoptosis of RGCs was detected by TUNEL staining. Retinal function was examined by flash-electroretinography (F-ERG). Retinal microglia were labeled using Iba-1, one specific marker for microglia. The mRNA expression levels of inducible nitric oxide synthase (iNOS), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β) were assessed by quantitative real time reverse transcription polymerase chain reaction (qRT-PCR).
Systemic HCT treatment significantly reduced RGCs death by H&E staining and exhibited an anti-apoptotic effect as assessed by TUNEL staining at day 14 after RIR injury. HCT greatly improved the retinal function as examined by F-ERG. The number of activated microglia significantly increased after RIR injury, which was significantly attenuated by HCT treatment. Besides, RIR injury induced a strong upregulation of pro-inflammatory genes TNF-α, iNOS and IL-1β mRNAs at day 14 post injury, which was suppressed by HCT.
Neuroprotective effects of HCT encourage the survival of RGCs through inhibiting microglia activation due to RIR injury. Together these results support the use of HCT as promising therapy for the ischemic events of the retina diseases.
确定鱼腥草（HCT）能否提高视网膜神经节细胞（RGCs）的存活率，并抑制视网膜缺血再灌注（RIR）损伤后的小胶质细胞激活。
通过短暂升高眼压（IOP）诱导大鼠RIR模型。在建立视网膜RIR模型前2天口服给予HCT，随后14天每天给药1次。RIR损伤14天后，处死大鼠进行进一步分析。存活的RGCs用苏木精和伊红（H&E）染色。通过TUNEL染色检测RGCs的凋亡。用闪光视网膜电图（F-ERG）检查视网膜功能。使用小胶质细胞的特异性标志物离子钙结合衔接分子1（Iba-1）标记视网膜小胶质细胞。通过定量实时逆转录聚合酶链反应（qRT-PCR）评估诱导型一氧化氮合酶（iNOS）、肿瘤坏死因子α（TNF-α）和白细胞介素1β（IL-1β）的mRNA表达水平。
全身给予HCT治疗通过H&E染色显著减少了RIR损伤后14天RGCs的死亡，并且TUNEL染色显示其具有抗凋亡作用。F-ERG检查显示HCT显著改善了视网膜功能。RIR损伤后活化的小胶质细胞数量显著增加，而HCT治疗可使其显著减少。此外，RIR损伤在损伤后14天诱导促炎基因TNF-α、iNOS和IL-1β mRNA强烈上调，而HCT可抑制这种上调。
HCT的神经保护作用通过抑制RIR损伤引起的小胶质细胞激活来促进RGCs的存活。这些结果共同支持将HCT作为视网膜疾病缺血事件的一种有前景的治疗方法。
