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奥美拉唑诱导红细胞收缩

Induction of Erythrocyte Shrinkage by Omeprazole.

作者信息

Naveed Ayesha, Jilani Kashif, Siddique Abu Bakar, Akbar Muhammad, Riaz Muhammad, Mushtaq Zahid, Sikandar Muhammad, Ilyas Sajida, Bibi Ismat, Asghar Asma, Rasool Ghulam, Irfan Muhammad

机构信息

Department of Biochemistry, University of Agriculture, Faisalabad, Pakistan.

Department of Zoology, Wildlife and Fisheries, University of Agriculture, Faisalabad, Pakistan.

出版信息

Dose Response. 2020 Aug 3;18(3):1559325820946941. doi: 10.1177/1559325820946941. eCollection 2020 Jul-Sep.

DOI:10.1177/1559325820946941
PMID:32863802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7432979/
Abstract

Omeprazole, a proton pump inhibitor blocks the H/K-ATPase channels of gastric parietal cells. It is used for the treatment of peptic ulcer. Prolonged use of omeprazole may involve in inducing anemia. The key marker of eryptosis includes membrane blebbing, cell shrinkage and phosphatidylserine (PS) exposure at the cell surface. In current study, the eryptotic, oxidative as well as hemolytic effects of therapeutical doses (0.5, 1 and 1.5 µM) of omeprazole were investigated after exposing erythrocytes for 48 hours. Investigation of eryptosis was done by cell size measurement, PS exposure determination and calcium channel inhibition. As a possible mechanism of omeprazole induced eryptosis, oxidative stress was investigated by determining the catalase, glutathione peroxidase and superoxide dismutase activities. Similarly, necrotic effect of omeprazole on erythrocytes was also evaluated through hemolysis measurement. Results of our study illustrated that 1.5 µM of omeprazole may induce significant decrease in superoxide dismutase, glutathione peroxidase and catalase activities as well as triggered the erythrocytes shrinkage, PS exposure and hemolysis. Role of calcium was also confirmed in inducing erythrocyte shrinkage. It is concluded that the exposure of erythrocytes with 1.5 µM omeprazole may enhance the rate of eryptosis and hemolysis by inducing oxidative stress.

摘要

奥美拉唑是一种质子泵抑制剂,可阻断胃壁细胞的H/K-ATP酶通道。它用于治疗消化性溃疡。长期使用奥美拉唑可能会导致贫血。红细胞凋亡的关键标志物包括细胞膜泡化、细胞皱缩和细胞表面磷脂酰丝氨酸(PS)暴露。在本研究中,将红细胞暴露48小时后,研究了治疗剂量(0.5、1和1.5μM)的奥美拉唑的红细胞凋亡、氧化及溶血作用。通过测量细胞大小、测定PS暴露和抑制钙通道来研究红细胞凋亡。作为奥美拉唑诱导红细胞凋亡的一种可能机制,通过测定过氧化氢酶、谷胱甘肽过氧化物酶和超氧化物歧化酶的活性来研究氧化应激。同样,通过溶血测量评估奥美拉唑对红细胞的坏死作用。我们的研究结果表明,1.5μM的奥美拉唑可能会导致超氧化物歧化酶、谷胱甘肽过氧化物酶和过氧化氢酶的活性显著降低,并引发红细胞皱缩、PS暴露和溶血。钙在诱导红细胞皱缩中的作用也得到了证实。结论是,用1.5μM奥美拉唑处理红细胞可能通过诱导氧化应激提高红细胞凋亡和溶血的速率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/ea4bf26c2bb8/10.1177_1559325820946941-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/db45672fe44d/10.1177_1559325820946941-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/9b2e5e7bb4f5/10.1177_1559325820946941-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/97ffbff9090b/10.1177_1559325820946941-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/e63a2df3d46a/10.1177_1559325820946941-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/ea4bf26c2bb8/10.1177_1559325820946941-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/db45672fe44d/10.1177_1559325820946941-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/9b2e5e7bb4f5/10.1177_1559325820946941-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/97ffbff9090b/10.1177_1559325820946941-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/e63a2df3d46a/10.1177_1559325820946941-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e319/7432979/ea4bf26c2bb8/10.1177_1559325820946941-fig5.jpg

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