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Heat Shock Protein 72 Protects Retinal Ganglion Cells in Rat Model of Acute Glaucoma

机译：热休克蛋白72保护急性青光眼大鼠模型中的视网膜神经节细胞

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摘要

Purpose: To investigate whether the induction of heat shock protein (HSP)72 by heat stress (HS) or zinc (Zn~(2+)) administration can increase survival of retinal ganglion cells (RGC) in rat model of acute experimental glaucoma. Methods: Acute glaucoma model was made by intracameral irrigation with BSS at 10~2 mmHg for two hours in right eyes of male Wistar rats. Glaucoma model rats were treated with HS once a week (six rats) or intraperitoneal injection of zinc sulfate (24.6 mg/kg) every two weeks (six rats), and were referred to as HS group and zinc group, respectively. Untreated model rats served as damage group (six rats). In control groups, querc-etin (400 mg/kg) was intraperitoneally injected to inhibit the induction of heat shock proteins 6 hours before HS or zinc administration, and were referred to as HS+que group (six rats) and zinc+que group (six rats), respectively. Subsequent to 16 days of IOP elevation, the rats were sacrificed. Eyes were quickly enucleated, and the retinas were dissected. RGC were labeled with Nissl staining and counted under microscope. Results: The average RGC density in normal Wistar rats was (2504±181) cells/mm~2. In damage group, it decreased to (2015±111) cells/mm~2. The RGC densities at 1, 2, and 3 mm from the center of the optic nerve head were (2716±215), (2496±168), and (2317±171) cells/mm~2, respectively, for normal rats and (2211±133), (1969±154), and (1872±68) cells/mm~2, respectively, for damage group. The latter was significantly lower at all locations compared with the former (P=0.027 for each, Mann-Whitney test). The average RGC densities were (2207±200) cells/mm~2 for HS group, (2272±155) cells/mm~2 for zinc group, (1964±188) cells/mm~2 for HS+que group, (2051±214) cells/mm~2 for zinc+que group and (2015±111) cells/mm~2 for damage group. There were significant differences in density of labeled RGCs among the five groups (P=0.040, Kruskal-Wallis test). Both HS and zinc group had higher RGC densities than damage group (P = 0.036 between HS and damage group, P = 0.019 between zinc and damage group, Mann-Whitney test). There was no significant difference in RGC densitiy between control groups and damage group (P = 0.260 between HS+que and damage group, P = 0.748 between zinc+que and damage group, Mann-Whitney test). Conclusions: The results demonstrated that the induction of HSP72 in RGCs by HS or zinc administration plays an important role in the survival of RGCs in rat model of acute glaucoma. A novel therapeutic approach to glaucoma through an enhanced induction of endogenous HSP72 could be possible.
机译：目的：研究热应激（HS）或锌（Zn〜（2+））诱导的热休克蛋白（HSP）72是否可以增加急性实验性青光眼大鼠视网膜神经节细胞（RGC）的存活率。方法：雄性Wistar大鼠右眼经10〜2 mmHg BSS前房内冲洗2小时，制成急性青光眼模型。青光眼模型大鼠每周一次用HS治疗（六只大鼠）或每两周一次腹膜内注射硫酸锌（24.6 mg / kg）（六只大鼠），分别称为HS组和锌组。未治疗的模型大鼠作为损伤组（六只大鼠）。在对照组中，在施用HS或锌前6小时腹膜内注射槲皮素（400 mg / kg）以抑制热休克蛋白的诱导，被称为HS + que组（六只大鼠）和锌+ que组。 （六只大鼠）。 IOP升高16天后，处死大鼠。迅速摘除眼球，并解剖视网膜。用Nissl染色标记RGC，并在显微镜下计数。结果：正常Wistar大鼠的平均RGC密度为（2504±181）个细胞/ mm〜2。损伤组降至（2015±111）cells / mm〜2。正常大鼠和距视神经头中心1、2和3 mm处的RGC密度分别为（2716±215），（2496±168）和（2317±171）细胞/ mm〜2。损伤组分别为（2211±133），（1969±154）和（1872±68）个/ mm〜2。与前者相比，后者在所有位置上均显着降低（每个P = 0.027，Mann-Whitney检验）。 HS组的平均RGC密度为（2207±200）细胞/ mm〜2，锌组的平均RGC密度为（2272±155）细胞/ mm〜2，HS + que组的平均RGC密度为（1964±188）细胞/ mm〜2，（锌+ que组为2051±214细胞/ mm〜2，损伤组为（2015±111）细胞/ mm〜2。五组之间标记的RGC的密度存在显着差异（P = 0.040，Kruskal-Wallis检验）。 HS和锌组的RGC密度均高于损伤组（HS与损伤组之间的P = 0.036，锌与损伤组之间的P = 0.019，Mann-Whitney检验）。对照组和损伤组之间的RGC密度无显着差异（HS + que和损伤组之间的P = 0.260，锌+ que和损伤组之间的P = 0.748，Mann-Whitney检验）。结论：研究结果表明，HS或锌的诱导在RGCs中诱导HSP72在急性青光眼大鼠模型中对RGCs的存活起着重要作用。通过增强内源性HSP72的诱导来治疗青光眼的新方法是可能的。

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