The Effects of Seleno-Methionine in Cadmium-Challenged Human Primary Chondrocytes

Pharmaceuticals Pub Date : 2024-07-12 DOI:10.3390/ph17070936
Valentina Urzì Brancati, Federica Aliquò, J. Freni, Alice Pantano, Erika Galipò, Domenico Puzzolo, L. Minutoli, Herbert Ryan Marini, Giuseppe Maurizio Campo, Angela D'Ascola
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Abstract

Cadmium (Cd) is a potentially toxic element able to interfere with cellular functions and lead to disease or even death. Cd accumulation has been demonstrated in cartilage, where it can induce damage in joints. The aim of this study was to evaluate the effect of CdCl2 on primary cultures of human chondrocytes and the possible protective effect of seleno-methionine (Se-Met). Human primary articular chondrocytes were cultured and treated as follows: control groups, cells challenged with 7.5 μM and 10 μM CdCl2 alone, and cells pretreated with 10 and 20 μM Se-Met and then challenged with 7.5 μM and 10 μM CdCl2. Twenty-four hours after incubation, cell viability, histological evaluation with hematoxylin–eosin stain, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay were performed. Furthermore, reverse transcription-PCR was carried out to evaluate mRNA levels of BAX, BAK1, CASP-3, and CASP-9. After CdCl2 challenge at both doses, a reduced cell viability and an overexpression of BAX, BAK1, CASP-3, and CASP-9 genes, as well as a high number of TUNEL-positive cells, were demonstrated, all parameters becoming higher as the dose of CdCl2 was increased. The pretreatment with Se-Met lowered the expression of all considered genes, improved cell viability and morphological changes, and reduced the number of TUNEL-positive cells. It was concluded that Se-Met plays a protective role against CdCl2-induced structural and functional changes in chondrocytes in vitro, as it improved cell viability and showed a positive role in the context of the apoptotic pathways. It is therefore suggested that a translational, multifaceted approach, with plant-based diets, bioactive functional foods, nutraceuticals, micronutrients, and drugs, is possibly advisable in situations of environmental pollution caused by potentially toxic elements.
硒蛋氨酸对镉挑战人原代软骨细胞的影响
镉(Cd)是一种潜在的有毒元素,能够干扰细胞功能,导致疾病甚至死亡。镉在软骨中的蓄积已得到证实,它可诱发关节损伤。本研究旨在评估氯化镉对人类软骨细胞原代培养物的影响以及硒蛋氨酸(Se-Met)可能产生的保护作用。人类原代关节软骨细胞的培养和处理方法如下:对照组、单独用 7.5 μM 和 10 μM CdCl2 处理的细胞、用 10 和 20 μM Se-Met 预处理后再用 7.5 μM 和 10 μM CdCl2 处理的细胞。培养 24 小时后,进行细胞存活率、苏木精-伊红染色组织学评估和末端脱氧核苷酸转移酶 dUTP 缺口标记(TUNEL)检测。此外,还进行了逆转录-PCR,以评估BAX、BAK1、CASP-3和CASP-9的mRNA水平。两种剂量的氯化镉都会导致细胞存活率降低,BAX、BAK1、CASP-3 和 CASP-9 基因过度表达,以及大量 TUNEL 阳性细胞,随着氯化镉剂量的增加,所有参数都会升高。用 Se-Met 进行预处理可降低所有上述基因的表达,改善细胞活力和形态变化,并减少 TUNEL 阳性细胞的数量。结论是,Se-Met 对氯化镉诱导的体外软骨细胞的结构和功能变化具有保护作用,因为它能提高细胞活力,并在细胞凋亡途径中发挥积极作用。因此,建议在潜在有毒元素造成环境污染的情况下,最好采用转化的、多方面的方法,包括以植物为基础的膳食、生物活性功能食品、营养保健品、微量元素和药物。
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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