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黄芩苷减轻体外小梁细胞的氧化应激损伤。

Baicalin alleviates oxidative stress damage in trabecular meshwork cells in vitro.

机构信息

Department of Ophthalmology, Jinan Eighth People's Hospital, No.73 Wenhua Dong Road, Lixia District, Jinan, Shandong, 250000, China.

Department of Ophthalmology, Linyi People's Hospital, No. 48 Jiefang Road, Lanshan District, Linyi, Shandong, 276000, China.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 2018 Jan;391(1):51-58. doi: 10.1007/s00210-017-1433-9. Epub 2017 Oct 28.

DOI:10.1007/s00210-017-1433-9
PMID:29080912
Abstract

Oxidative stress and inflammation play a key role in pathophysiology of glaucoma. Baicalin is known as an anti-oxidative and anti-inflammatory substance, possessing the potential to treat glaucoma. This study was designed to assess the anti-oxidative and anti-inflammatory potentials in culture human trabecular meshwork (hTM) cells. Using hTM cells as the in vitro model, we investigated the effects of baicalin on oxidative stress-induced markers for hTM impairments. We pre-incubated hTM cells with baicalin before hydrogen peroxide stressing or pre- plus co-incubated with baicalin before and during stressing and monitored the cell death, production of intracellular reactive oxygen species (iROS) and inflammatory cytokines, accumulation of carbonylated proteins, and activity of senescence marker. Samples that received pre- plus co-treatment with 10 or 15 μM baicalin showed significantly increased cell survival and decreased iROS production. Further studies demonstrated that pre- plus co-treatment with 15 μM baicalin significantly inhibited proinflammatory factor IL-1α and ELAM-1 production, decreased activities of senescence marker SA-β-gal, and lowered carbonylated protein levels. In contrast, samples that received only pre-treatment did not show any of these protective effects. Baicalin can protect hTM cells against oxidative stress, shedding light on potential treatment for glaucoma.

摘要

氧化应激和炎症在青光眼的病理生理学中起着关键作用。黄芩素是一种抗氧化和抗炎物质,具有治疗青光眼的潜力。本研究旨在评估黄芩素在体外培养的人眼小梁细胞(hTM)中的抗氧化和抗炎潜力。我们使用 hTM 细胞作为体外模型,研究了黄芩素对 hTM 损伤的氧化应激诱导标志物的影响。我们在 hTM 细胞受到过氧化氢应激之前用黄芩素进行预孵育,或者在应激之前和期间与黄芩素进行预孵育和共孵育,并监测细胞死亡、细胞内活性氧(iROS)和炎症细胞因子的产生、羰基化蛋白的积累以及衰老标志物的活性。接受 10 或 15μM 黄芩素预加共处理的样品显示出明显增加的细胞存活率和减少的 iROS 产生。进一步的研究表明,用 15μM 黄芩素预加共处理可显著抑制促炎因子 IL-1α 和 ELAM-1 的产生,降低衰老标志物 SA-β-半乳糖苷酶的活性,并降低羰基化蛋白水平。相比之下,仅接受预处理的样品没有显示出任何这些保护作用。黄芩素可以保护 hTM 细胞免受氧化应激,为治疗青光眼提供了新的思路。

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