Antioxidative effect and mechanism of tert-butyl hydroquinone on rat retinal Müller cells under high glucose condition
10.3760/cma.j.issn.2095-0160.2020.01.004
- VernacularTitle: 叔丁基对苯二酚对高糖环境下大鼠视网膜Müller细胞的抗氧化应激作用及其机制
- Author:
Wei HE
1
;
Min TIAN
2
;
Xi YU
3
;
Yang CAO
2
;
Wenli ZHENG
4
;
Hongbin LYU
2
Author Information
1. Department of Ophthalmology, the People＇s Hospital of Chengdu Wenjiang District, Chengdu 611130, China
2. Department of Ophthalmology, the Affiliated Hospital of Southwest Medical University, Luzhou 646099, China
3. Department of Ophthalmology, The Second People＇s Hospital of Luzhou
4. The Affiliated Hospital Eye Hospital of Panzhihua College, Panzhihua 617000, China
- Publication Type:Journal Article
- Keywords:
Diabetic retinopathy;
Müller cells;
Teniary butyl hydroquinone;
Oxidative stress;
Protective mechanism
- From:
Chinese Journal of Experimental Ophthalmology
2020;38(1):16-22
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To expore the impact of teniary butyl hydroquinone (tBHQ) on Müller cells in SD rats retina under high glucose condition, and discuss the mechanism of tBHQ.
Methods:The Müller cells of SD rats were cultured in vitro and the experiment was divided into normal control group, high glucose group and tBHQ intervention group.Western blot and quantitative real time PCR were used to determine the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), hemeoxygenase-1 (HO-1), hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) protein and mRNA in each group.
Results:Müller cells cultured in vitro were flat with irregularly sharp.The nucleus was oval, while the cytoplasm was abundant.Adjacent cells were interwoven to a network.Western blot assay showed the overall expression of Nrf2, HO-1, HIF-1α, and VEGF in Müller cells of normal control group, high glucose group, and tBHQ intervention group were significantly different (F=73.831, 148.618, 152.269, 91.217, all at P<0.001); Among them, the relative expressions of Nrf2, HO-1, HIF-1α and VEGF proteins in the high glucose group were 0.17±0.02, 0.47±0.02, 0.67±0.07, and 0.6±0.05, which were increased in comparion with 0.06±0.01, 0.19±0.03, 0.06±0.00 and 0.07±0.02 in the normal control group, with statistically significant differences (t=4.114, 9.275, 16.479, 13.353, all at P<0.001); the relative expressions of Nrf2 and HO-1 proteins in the tBHQ intervention group were 0.40±0.06 and 0.72±0.05, which were increased by comparion with those in the higher glucose group, with statistically significant differences (t=7.847, 7.947, both at P<0.001); the relative expressions of HIF-1α and VEGF proteins in the tBHQ intervention group were 0.18±0.04, 0.26±0.07, which were decreased in comparion with those in the higher glucose group, but were increased in comparion with those in normal control group, with statistically significant differences (t=13.215, 8.444, both at P<0.001). Quantitative real time PCR showed that the relative mRNA expressions of Nrf2, HO-1, HIF-1α, and VEGF in Müller cells of normal control group, high glucose group, and tBHQ intervention group were significantly different (F=340.317, 1 582.911, 488.852, 185.699, all at P<0.001); the relative mRNA expressions of Nrf2, HO-1, HIF-1α, and VEGF proteins in the high-glucose group were 1.53±0.06, 1.50±0.04, 2.56±0.09, and 3.04±0.19, which were increased in comparion with 1.07±0.07, 0.95±0.05, 0.99±0.02, and 1.09±0.08 in the normal control group, with statistically significant differences (t=7.292, 15.014, 30.550, 18.573, all at P<0.001); The relative mRNA expressions of Nrf2 and HO-1 proteins in the tBHQ intervention group were 2.68±0.09 and 2.94±0.05, which were increased in comparion with those in the high-glucose group, with statistically significant differences (t=18.046, 39.458, both at P<0.001); The relative mRNA expression of HIF-1α and VEGF protein in the tBHQ intervention group were 1.48±0.05 and 1.6±0.08, which were decreased by comparion with those in the higher glucose group were increased in comparion with those in normal control group, with statistically significant differences (t=21.036, 13.739, both at P<0.001).
Conclusions:tBHQ protects Müller cells from damage in high glucose condition by activating anti-oxidative stress signaling pathway of Nrf2/ARE.
