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胆固醇、棕榈酸和葡萄糖对人肝星状细胞激活以诱导肝纤维化的作用比较。

Comparison of the effects of cholesterol, palmitic acid, and glucose on activation of human hepatic stellate cells to induce liver fibrosis.

作者信息

Mohammadzadeh Ghorban, Afarin Reza, Bavarsad Samaneh Salehipour, Aslani Fereshteh, Zadeh Shahla Asadi, Shakerian Elham

机构信息

Hyperlipidemia Research Center, Department of Clinical Biochemistry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

Cellular and Molecular Research Center, Medical Basic Science Research Institute, Department of Laboratory Sciences, School of ParaMedicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.

出版信息

J Diabetes Metab Disord. 2022 Jul 19;21(2):1531-1538. doi: 10.1007/s40200-022-01095-z. eCollection 2022 Dec.

Abstract

BACKGROUND

In hepatic damage, Hepatic stellate cells (HSCs) become active, proliferate, and change to myofibroblasts. Increasing the fibrogenic genes, such as Transforming growth factor-β (TGF-β), Alpha Smooth Muscle Actin (α-SMA), and Collagen1 α (COL 1α) show that the activation of HSCs can lead to hepatic fibrosis.

PURPOSE

These days people consume much cholesterol, palmitic acid, and glucose which can have adverse effects on an individuals' health, but their influences on activating human HSCs and inducing liver fibrosis have not been assessed. Our purpose is to investigate the effects of these three main and abundant ingredients in the diet on the activation of human HSCs and inducing liver fibrosis.

METHODS

To measure cholesterol, palmitic acid, and glucose cytotoxic effects on the viability of the cells, the MTT technique was used. Then the treated cells were incubated in media containing cholesterol, palmitic acid, and glucose with different concentrations for 24 h. At last, the α-SMA, COL 1α, and TGF-β, genes mRNA expression were measured by real-time PCR.

RESULTS AND CONCLUSIONS

Our results demonstrated that high concentrations of cholesterol and palmitic acid can activate human HSCs that lead to an increase in the mRNA expressions of fibrogenic genes. Thus, controlling fat intaking and knowing its mechanism is crucial to prevent and attenuate hepatic fibrosis.

摘要

背景

在肝损伤过程中,肝星状细胞(HSCs)会被激活、增殖并转变为肌成纤维细胞。转化生长因子-β(TGF-β)、α平滑肌肌动蛋白(α-SMA)和胶原蛋白1α(COL 1α)等促纤维化基因的增加表明,肝星状细胞的激活可导致肝纤维化。

目的

如今人们摄入大量胆固醇、棕榈酸和葡萄糖,这些物质可能对个体健康产生不利影响,但它们对激活人肝星状细胞和诱导肝纤维化的影响尚未得到评估。我们的目的是研究饮食中这三种主要且含量丰富的成分对人肝星状细胞激活和诱导肝纤维化的影响。

方法

为了检测胆固醇、棕榈酸和葡萄糖对细胞活力的细胞毒性作用,采用了MTT技术。然后将处理后的细胞在含有不同浓度胆固醇、棕榈酸和葡萄糖的培养基中孵育24小时。最后,通过实时PCR检测α-SMA、COL 1α和TGF-β基因的mRNA表达。

结果与结论

我们的结果表明,高浓度的胆固醇和棕榈酸可激活人肝星状细胞,导致促纤维化基因的mRNA表达增加。因此,控制脂肪摄入并了解其机制对于预防和减轻肝纤维化至关重要。

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