Peroxyredoxin 6 Protects RIN-M5F Pancreatic Beta Cells Against Streptozotocin-Induced Senescence.

IF 2.5 Q3 CELL BIOLOGY

Cellular Physiology and Biochemistry Pub Date : 2024-09-23 DOI:10.33594/000000729

Elena G Novoselova, Olga V Glushkova, Maxim O Khrenov, Sergey M Lunin, Tatyana V Novoselova, Mars G Sharapov, Svetlana B Parfenyuk

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Abstract

Background/aims: There are evidences that a decrease in the functional activity of pancreatic β-cells under type 2 diabetes conditions may be associated with their senescence, therefore, senotherapy may be a prospective strategy for the diabetes treatment.

Methods: The senotherapeutic potential of peroxiredoxin 6 (PRDX6) was studied in RIN-m5F pancreatic β-cells with streptozotocin-induced senescence by measuring markers, associated with senescence.

Results: Exposure to streptozotocin (STZ) resulted in the senescence of the β-cells. The addition of PRDX6 to the culture medium of RIN-m5F β-cells before treatment with STZ decreased the levels of the following senescence markers: the percentage of SA-β-Gal-positive cells, the phosphorylation of histone H2AX and p21 proteins, and the secretion of the proinflammatory cytokine IL-6 but not the anti-inflammatory cytokine IL-10. These effects were accompanied by a decrease in the production of reactive oxygen species (ROS) and the restoration of impaired NF-κB activation. In addition, PRDX6 altered the production of the heat shock protein HSP90: the production of the constitutive form of HSP90-beta decreased, while the level of inducible HSP90-alpha increased.

Conclusion: PRDX6 prevented the senescence of RIN-m5F cells in response to the DNA damage-inducing agent streptozotocin, indicating a potential protective role of PRDX6 in type 2 diabetes mellitus.

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过氧化还原酶 6 可保护 RIN-M5F 胰腺β细胞免受链脲佐菌素诱导的衰老。

背景/目的：有证据表明，在2型糖尿病条件下，胰腺β细胞功能活性的降低可能与其衰老有关，因此，衰老疗法可能是糖尿病治疗的一种前瞻性策略：方法：在链脲佐菌素诱导衰老的RIN-m5F胰腺β细胞中，通过测量与衰老相关的标记物，研究过氧化物歧化酶6（PRDX6）的衰老治疗潜力：结果：接触链脲佐菌素（STZ）会导致β细胞衰老。在用 STZ 处理 RIN-m5F β 细胞之前向其培养液中添加 PRDX6 可降低以下衰老标记物的水平：SA-β-Gal 阳性细胞的百分比、组蛋白 H2AX 和 p21 蛋白的磷酸化、促炎细胞因子 IL-6 的分泌，但不包括抗炎细胞因子 IL-10。在产生这些影响的同时，活性氧（ROS）的产生也有所减少，受损的 NF-κB 激活也得到了恢复。此外，PRDX6 还改变了热休克蛋白 HSP90 的产生：组成型 HSP90-beta 的产生减少，而诱导型 HSP90-α 的水平增加：结论：PRDX6能防止RIN-m5F细胞在DNA损伤诱导剂链脲佐菌素作用下衰老，这表明PRDX6在2型糖尿病中具有潜在的保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cellular Physiology and Biochemistry 生物-生理学

CiteScore

5.80

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： Cellular Physiology and Biochemistry is a multidisciplinary scientific forum dedicated to advancing the frontiers of basic cellular research. It addresses scientists from both the physiological and biochemical disciplines as well as related fields such as genetics, molecular biology, pathophysiology, pathobiochemistry and cellular toxicology & pharmacology. Original papers and reviews on the mechanisms of intracellular transmission, cellular metabolism, cell growth, differentiation and death, ion channels and carriers, and the maintenance, regulation and disturbances of cell volume are presented. Appearing monthly under peer review, Cellular Physiology and Biochemistry takes an active role in the concerted international effort to unravel the mechanisms of cellular function.