谷胱甘肽抑制TRPM7可通过下调胶质母细胞瘤细胞中Ca2+和Zn2+来降低顺铂的氧化和凋亡作用。

IF 2.6 4区医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL

Advances in medical sciences Pub Date : 2025-01-30 DOI:10.1016/j.advms.2025.01.008

Kemal Ertilav , Mustafa Nazıroğlu

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引用次数: 0

摘要

目的：顺铂（CiSP）介导的TRPM7刺激可能通过上调胶质母细胞瘤（DBTRG-05MG）细胞中的Ca2+、凋亡和活性氧（ROS）来诱导氧化和凋亡活性，而抗氧化剂谷胱甘肽（GSH）抑制TRPM7可能会减少DBTRG-05MG的增加。该研究的目的是研究TRPM7激活如何刺激DBTRG-05MG细胞死亡，以及它如何通过改变ROS毒性和细胞凋亡来抑制TRPM7拮抗剂（GSH和carvacrol， CRV）的作用。方法：在DBTRG-05MG中建立5组：对照组、GSH （10 mM, 2h）、CiSP （25 μM, 24h）、CiSP+GSH、CiSP+CRV （200 mM, 24h）。结果：CiSP组胞质游离Ca2+的数量在TRPM7（钠triben）的刺激下进一步增加，尽管GSH和CRV处理导致它们在细胞中减少。细胞中线粒体膜超极化、ROS、死亡细胞、凋亡、游离锌离子和caspase-3、-8、-9的数量在CiSP中高于对照和GSH，但CiSP+GSH和CiSP+CRV的数量低于CiSP。GSH孵育后，cisp诱导的细胞活力和GSH浓度下降。结论：刺激TRPM7可增强CiSP的抗癌作用，但其抑制作用通过GSH和CRV的治疗降低了CiSP诱导的氧化应激和DBTRG-05MG死亡的数量。通过CiSP引起的氧化性胶质母细胞瘤损伤，TRPM7刺激可被认为是一个潜在的肿瘤杀伤通道。

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Inhibition of TRPM7 by glutathione decreases oxidant and apoptotic action of cisplatin through the downregulation of Ca2+ and Zn2+ in glioblastoma cells

Purpose

Cisplatin (CiSP)-mediated stimulation of TRPM7 may induce oxidant and apoptotic activities through the upregulation of Ca²⁺, apoptosis, and reactive oxygen species (ROS) in glioblastoma (DBTRG-05MG) cells, whereas inhibition of TRPM7 by the antioxidant glutathione (GSH) may reduce the observed increases in DBTRG-05MG. The aim of the study was to examine how TRPM7 activation stimulates DBTRG-05MG cell death but also how it inhibits the effects of TRPM7 antagonists (GSH and carvacrol, CRV) via altering ROS toxicity and apoptosis.

Method

In the DBTRG-05MG, 5 groups were established: control, GSH (10 mM for 2 h), CiSP (25 μM for 24 h), CiSP + GSH, and CiSP + CRV (200 μM for 24 h).

Results

The amounts of cytosolic free Ca²⁺ were further increased in the CiSP group by the stimulation of TRPM7 (naltriben), even though the GSH and CRV treatments caused them to decrease in the cells. The amounts of mitochondrial membrane dysfunction, ROS, death cell, apoptosis, free zinc ion, and caspase-3, -8, and -9 in the cells were higher in the CiSP than in the control and GSH, although their amounts were lower in the CiSP + GSH and CiSP + CRV than in the CiSP only. The CiSP-induced decreases in cell viability and GSH concentrations were increased by GSH incubation.

Conclusions

The stimulation of TRPM7 increased the anticancer action of CiSP, although its inhibition decreased the amount of CiSP-induced oxidative stress and DBTRG-05MG deaths through the treatment of GSH and CRV. TRPM7 stimulation could be considered a potential tumor killer channel through oxidative glioblastoma damage caused by CiSP.

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来源期刊

Advances in medical sciences 医学-医学：研究与实验

CiteScore

5.00

自引率

0.00%

发文量

审稿时长

25 days

期刊介绍： Advances in Medical Sciences is an international, peer-reviewed journal that welcomes original research articles and reviews on current advances in life sciences, preclinical and clinical medicine, and related disciplines. The Journal’s primary aim is to make every effort to contribute to progress in medical sciences. The strive is to bridge laboratory and clinical settings with cutting edge research findings and new developments. Advances in Medical Sciences publishes articles which bring novel insights into diagnostic and molecular imaging, offering essential prior knowledge for diagnosis and treatment indispensable in all areas of medical sciences. It also publishes articles on pathological sciences giving foundation knowledge on the overall study of human diseases. Through its publications Advances in Medical Sciences also stresses the importance of pharmaceutical sciences as a rapidly and ever expanding area of research on drug design, development, action and evaluation contributing significantly to a variety of scientific disciplines. The journal welcomes submissions from the following disciplines: General and internal medicine, Cancer research, Genetics, Endocrinology, Gastroenterology, Cardiology and Cardiovascular Medicine, Immunology and Allergy, Pathology and Forensic Medicine, Cell and molecular Biology, Haematology, Biochemistry, Clinical and Experimental Pathology.