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The effects of intravitreal H2 S application on apoptosis in the retina and cornea in experimental glaucoma model.
International Journal of Experimental Pathology ( IF 3 ) Pub Date : 2019-11-27 , DOI: 10.1111/iep.12334 Zuleyha Erisgin 1 , Murat Atabey Ozer 2 , Murat Tosun 3 , Serkan Ozen 2 , Selcuk Takir 4
International Journal of Experimental Pathology ( IF 3 ) Pub Date : 2019-11-27 , DOI: 10.1111/iep.12334 Zuleyha Erisgin 1 , Murat Atabey Ozer 2 , Murat Tosun 3 , Serkan Ozen 2 , Selcuk Takir 4
Affiliation
One of the most important causes of visual loss (blindness) is glaucoma, which occurs due to the degeneration of the ganglion cells in retina. It has been shown that hydrogen sulphide (H2S) acts an antioxidant, neuroprotective and neuromodulator and provides protection against oxidative stress and apoptosis. This study aims to examine through which apoptotic pathway H2S acts in experimental glaucoma model. Twenty‐two male wistar albino rats were used in this study. Group 1 (n = 6, control group): Intravitreal saline was given in the third week without inducing ocular hypertension (OHT) with laser photocoagulation. Group 2 (n = 8): After the induction of OHT with laser photocoagulation, intravitreal saline was given in the third week. Group 3 (n = 8): After the induction of OHT with laser photocoagulation, intravitreal H2S’s donor sodium hydrosulphide (NaSH) 100 nmol/L was given in the third week. At the end of the 6th week, the eyes of the rats were sacrified under anaesthesia and extracted and then routine tissue follow‐up was undertaken. Besides haematoxylin & eosin (H&E) staining, Bax, Bcl‐2, p53 and caspase‐3 activation were examined immunohistochemically in the retina and the cornea. This showed that ocular hypertension caused apoptosis through the intrinsic pathway, due to Bax and caspase‐3 activation, in both retina and cornea, and that this led to DNA damage due to p53 activation. Also, we found that H2S exposure in glaucoma distinctly suppressed Bax, caspase‐3 and p53 activations in retina but that it has a limited effect on the cornea. According to these results, glaucoma caused apoptosis in the retina through intrinsic pathway, and the damage to the retina could be compensated partially by H2S but would have limited on the cornea.
中文翻译:
玻璃体内硫化氢对实验性青光眼模型视网膜和角膜细胞凋亡的影响。
视力丧失(失明)的最重要原因之一是青光眼,这是由于视网膜中神经节细胞变性引起的。已经表明,硫化氢(H 2 S)起到抗氧化剂,神经保护剂和神经调节剂的作用,并提供针对氧化应激和细胞凋亡的保护作用。这项研究旨在检查通过哪个凋亡途径H 2S在实验性青光眼模型中起作用。本研究使用了22只雄性Wistar白化病大鼠。第1组(n = 6,对照组):在第三周给予玻璃体盐水,而激光光凝不诱发高眼压(OHT)。第2组(n = 8):激光光凝诱导OHT后,第三周给予玻璃体内盐水。第3组(n = 8):激光光凝诱导OHT后,玻璃体内H 2在第三周给予S的供体氢硫化钠(NaSH)100 nmol / L。在第6周结束时,在麻醉下将大鼠的眼睛牺牲并取出,然后进行常规的组织随访。除苏木精和曙红(H&E)染色外,还对视网膜和角膜中的Bax,Bcl-2,p53和caspase-3活化进行了免疫组织化学检查。这表明高眼压通过视网膜和角膜中的Bax和caspase-3激活通过内在途径引起凋亡,并且由于p53激活导致DNA损伤。此外,我们发现H 2青光眼中的S暴露可明显抑制视网膜中的Bax,caspase-3和p53活化,但对角膜的作用有限。根据这些结果,青光眼通过内在途径引起视网膜细胞凋亡,并且对视网膜的损害可以部分被H 2 S补偿,但会限制角膜。
更新日期:2019-11-27
中文翻译:
玻璃体内硫化氢对实验性青光眼模型视网膜和角膜细胞凋亡的影响。
视力丧失(失明)的最重要原因之一是青光眼,这是由于视网膜中神经节细胞变性引起的。已经表明,硫化氢(H 2 S)起到抗氧化剂,神经保护剂和神经调节剂的作用,并提供针对氧化应激和细胞凋亡的保护作用。这项研究旨在检查通过哪个凋亡途径H 2S在实验性青光眼模型中起作用。本研究使用了22只雄性Wistar白化病大鼠。第1组(n = 6,对照组):在第三周给予玻璃体盐水,而激光光凝不诱发高眼压(OHT)。第2组(n = 8):激光光凝诱导OHT后,第三周给予玻璃体内盐水。第3组(n = 8):激光光凝诱导OHT后,玻璃体内H 2在第三周给予S的供体氢硫化钠(NaSH)100 nmol / L。在第6周结束时,在麻醉下将大鼠的眼睛牺牲并取出,然后进行常规的组织随访。除苏木精和曙红(H&E)染色外,还对视网膜和角膜中的Bax,Bcl-2,p53和caspase-3活化进行了免疫组织化学检查。这表明高眼压通过视网膜和角膜中的Bax和caspase-3激活通过内在途径引起凋亡,并且由于p53激活导致DNA损伤。此外,我们发现H 2青光眼中的S暴露可明显抑制视网膜中的Bax,caspase-3和p53活化,但对角膜的作用有限。根据这些结果,青光眼通过内在途径引起视网膜细胞凋亡,并且对视网膜的损害可以部分被H 2 S补偿,但会限制角膜。