CN108836971B - Ws6对小梁网细胞肌动蛋白形成的影响 - Google Patents
Ws6对小梁网细胞肌动蛋白形成的影响 Download PDFInfo
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Abstract
本发明公开了WS6对小梁网细胞肌动蛋白形成的影响。WS6为促胰岛β细胞增殖活性化合物。WS6对小梁网细胞的细胞毒性。WS6抑制小梁网细胞肌动蛋白的形成。本发明的有益效果是揭示了WS6能够显著抑制TRPV4激动剂GSK101引起的小梁网细胞肌动蛋白的形成。这有助于降低眼压,对眼压升高引起的青光眼有潜在的治疗意义。
Description
技术领域
本发明属于医学技术领域,涉及WS6(促胰岛细胞增殖药物)对小梁网细胞肌动蛋白形成的影响。
背景技术
青光眼(Glaucomas)是一种视网膜神经节细胞退变引起的一种视神经疾病,能够导致视盘凹陷、视野缺损,最终可以导致失明。
研究表明,高眼压是青光眼的重要治病因素。每降低1mm Hg眼压,能减少大约10%青光眼进程。高眼压主要由眼前节房水循环失衡而导致。房水产生于睫状体,通过位于虹膜与晶状体之间的狭小缝隙而进入眼前节的房水循环中,随后通过房水外排途径排出眼睛。房水外排的阻力主要来自于小梁网外排途径,原发性开角型青光眼患者的房水外排途径通常会出现异常,从而导致高眼压的产生。
小梁网是定位于角膜基部毗邻睫状体的筛板状组织,其正常功能的维持对房水循环的平衡以及眼内压的维持具有至关重要的作用。青光眼眼压升高80-90%的阻力来自小梁网细胞房水外排的不畅,而这与肌动蛋白的增加有密切关系。研究表明,TRPV4离子通道能够调节钙离子平衡、肌动蛋白形成、细胞骨架重构、房水外排、降低眼压。
发明内容
本发明的目的在于提供WS6对小梁网细胞肌动蛋白形成的影响。
本发明所采用的技术方案是WS6对小梁网细胞肌动蛋白形成的影响。
进一步,WS6为促胰岛β细胞增殖活性化合物。
进一步,WS6对小梁网细胞的细胞毒性。
进一步,WS6抑制小梁网细胞肌动蛋白的形成。
本发明的有益效果是揭示了WS6能够显著抑制TRPV4激动剂GSK101引起的小梁网细胞肌动蛋白的形成。这有助于降低眼压,对眼压升高引起的青光眼有潜在的治疗意义。
附图说明
图1是WS6作用于小梁网细胞后的激光共聚焦图像
图2是WS6作用于小梁网细胞后对肌动蛋白形成的抑制作用统计图
具体实施方式
下面结合具体实施方式对本发明进行详细说明。
1WS6对小梁网细胞的细胞毒性
首先,我们选取了10μM、100μM、200μM、300μM等4个梯度浓度的WS6进行其对小梁网细胞的毒性试验。结果表明,经过24h后,随着WS6浓度的增加,小梁网细胞死亡率逐渐增加,到200μM时,死亡率达到了约50%。因此,我们首先选取了10μM的WS6进行药效学试验。
2WS6抑制小梁网细胞肌动蛋白的形成
我们通过鬼笔环肽特异荧光染色技术与激光共聚焦技术,研究了WS6对小梁网细胞肌动蛋白形成的抑制作用。如图1、图2所示结果显示,TRPV4激动剂GSK101能够显著增强小梁网细胞激动蛋白的荧光强度,而加入10uM WS6后小梁网细胞激动蛋白的荧光强度显著降低。
本发明研究利用鬼笔环肽特异荧光染色技术与激光共聚焦技术,研究了WS6对小梁网细胞肌动蛋白形成的抑制作用。结果表明,10μM WS6能够显著抑制TRPV4激动剂GSK101引起的小梁网细胞肌动蛋白的形成。这有助于降低眼压,对眼压升高引起的青光眼有潜在的治疗意义。
以上所述仅是对本发明的较佳实施方式而已,并非对本发明作任何形式上的限制,凡是依据本发明的技术实质对以上实施方式所做的任何简单修改,等同变化与修饰,均属于本发明技术方案的范围内。
Claims (4)
1.WS6在制备用于肌动蛋白增加导致的青光眼治疗药物中的用途。
2.如权利要求1所述的用途,其特征在于:所述WS6为促胰岛β细胞增殖活性化合物。
3.如权利要求1所述的用途,其特征在于:所述WS6对小梁网细胞具有细胞毒性。
4.如权利要求3所述的用途,所述WS6对小梁网细胞的毒性耐受浓度为10μM。
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