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首页> 外文期刊>European journal of ophthalmology >Effects of antiglaucoma drugs GLC756, a novel dopamine D2 agonist and D1 antagonist, and timolol on endotoxin-induced TNF-alpha release in serum of rats.
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Effects of antiglaucoma drugs GLC756, a novel dopamine D2 agonist and D1 antagonist, and timolol on endotoxin-induced TNF-alpha release in serum of rats.

机译：抗青光眼药物GLC756，新型多巴胺D2激动剂和D1拮抗剂以及噻吗洛尔对内毒素诱导的大鼠血清TNF-α释放的影响。

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PURPOSE. Anti-inflammatory activity of an antiglaucoma drug may be an advantage for long-term treatment of glaucoma since it may reduce the risk of treatment-related inflammatory processes in outer compartments of the eye and probably also prevent or delay progression of glaucomatous retinal neurodegeneration. In this study, the effect of GLC756, a novel mixed dopamine D 2 receptor agonist and dopamine D 1 receptor antagonist, and timolol on endo-toxin-induced cytokine tumor necrosis factor- a (TNF-a) release in serum was examined. METHODS. For endotoxin-induced TNF- a release, 8-week-old Lewis rats were intravenously injected with 160 microg lipopolysaccharide (LPS) from Salmonella typhimurium. GLC756, timolol, or betamethasone were either systemically (1 mg/kg SC for 5 days) or topically (0.4%, 0.5%, and 0.1%, respectively, 20 microL eye drops given 16 times over 48 hours in left and right eye) administered. TNF- a was measured in serum 2 and 48 hours after LPS induction. RESULTS. A marked TNF- a increase in serum was found 2 hours after LPS induction. Administration of GLC756 and betamethasone, systemically and topically, decreased TNF-a release. However, due to large scattering of mean values only the effect of systemically administered GLC756 was statistically significant. In contrast, timolol increased TNF-a values stronger than LPS alone. CONCLUSIONS. The significant suppression of LPS-induced TNF-a increase by GLC756 suggests an additional anti-inflammatory potential of the dopaminergic compound in the treatment of glaucoma.
机译：目的。抗青光眼药物的抗炎活性可能是青光眼的长期治疗的一项优势，因为它可以降低眼外层与治疗相关的炎症过程的风险，还可能预防或延迟青光眼性视网膜神经变性的进展。在这项研究中，研究了GLC756（一种新型的多巴胺D 2受体激动剂和多巴胺D 1受体混合拮抗剂）和噻吗洛尔对内毒素诱导的细胞因子肿瘤坏死因子-a（TNF-a）释放的影响。方法。对于内毒素诱导的TNF-α释放，给8周大的Lewis大鼠静脉注射鼠伤寒沙门氏菌160微克脂多糖（LPS）。 GLC756，噻吗洛尔或倍他米松全身给药（1 mg / kg SC，持续5天）或局部给药（分别为0.4％，0.5％和0.1％，分别在20小时内分别在左眼和右眼中滴注20微升滴眼液16次）管理。在LPS诱导后2和48小时，在血清中测量TNF-α。结果。 LPS诱导2小时后，血清TNF显着增加。全身和局部给予GLC756和倍他米松可降低TNF-α的释放。但是，由于平均值的较大分散，只有全身给药的GLC756的效果在统计学上显着。相反，噻吗洛尔增加的TNF-α值比单独使用LPS强。结论。 GLC756对LPS诱导的TNF-α升高的显着抑制表明多巴胺能化合物在治疗青光眼方面具有额外的抗炎潜力。

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