In vitro activation of human HSCs with cholesterol, palmitic acid, and glucose (Three main and abundant ingredients in the diet) to induce liver fibrosis and compare their effects on the expression of liver fibrosis main genes

Elham Shakerian ©, Reza Afarin

In vitro activation of human HSCs with cholesterol, palmitic acid, and glucose (Three main and abundant ingredients in the diet) to induce liver fibrosis and compare their effects on the expression of liver fibrosis main genes

کد: G-97834

نویسندگان: Elham Shakerian ©, Reza Afarin

زمان بندی: زمان بندی نشده!

برچسب: بیوشیمی

دانلود: دانلود پوستر

خلاصه مقاله:

Background and Aim

Hepatic fibrosis is the result of chronic liver damage and causes by the activation of hepatic stellate cells (HSCs). In liver damage, HSCs are activated and changed to myofibroblasts. Increasing the genes expression, such as beta-converting growth factor (TGF-β), actin-alpha smooth muscle (α-SMA) and collagen1α (fibrogenic genes) shows the activation of HSCs which leads to hepatic fibrosis. Intaking much cholesterol, palmitic acid, and glucose have harmful effects on human health but their influence in activating human HSCs has not been studied. Aim: In this study, we investigated the effect of cholesterol, palmitic acid, and glucose on human HSCs activation by measuring the mRNA expression level of TGF-β, α-SMA, and collagen1α genes involved in hepatic fibrosis.

Methods

Methods and Materials The cytotoxic effects of cholesterol, palmitic acid, and glucose on the cell viability of Human HSCs were determined by MTT assay. Then the Cells were incubated in media containing different concentrations of cholesterol, palmitic acid, and glucose for 24 h. At last, the mRNA expression of TGF-β, α-SMA, and collagen1α genes were measured using real-time PCR

Results

Results Our data indicated that the mRNA expression of TGF-β, α-SMA, and collagen1α genes was significantly elevated by treating with cholesterol and palmitic acid, but glucose had no effects.

Conclusion

Conclusion The progression of the disease is fatal, and no definitive cure has been found. Therefore, it is important to know the causes of this disease to prevent its development and progression. The results demonstrated that cholesterol and palmitic acid, in high concentrations, could activate HSCs and elevate the mRNA expression level of fibrogenic genes. Thus, controlling fat intaking and knowing its mechanism is crucial to treat and attenuate hepatic fibrosis.

Keywords

Keywords; hepatic fibrosis; Cholesterol; Palmitic acid; Glucose; fibrogenic genes

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