Kangxian ruangan keli inhibits hepatic stellate cell proliferation mediated by PDGF

Yang, Ling; Chi-zhi, Zhang; Zhu, Qingjing

doi:10.3748/wjg.v9.i9.2050

Cited by 9 publications

(4 citation statements)

References 24 publications

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“…Considering the phenotype and appearance of HSC-T6 cells, the transformation of quiescent HSC cells into fibrogenic myofibroblasts is the primary indicator of the activation of these cells. Activated cells had spindle-shaped, which were more elongated and converted to myofibroblasts, but inactive cells were virtually round [ 22 , 23 ] . The shape of the control cells treated with PDGF-BB and isorhamnetin are shown in Fig.…”

Section: Resultsmentioning

confidence: 99%

Isorhamnetin Exerts Antifibrotic Effects by Attenuating Platelet-Derived Growth Factor-BB-induced HSC-T6 Cells Activation via Suppressing PI3K-AKT Signaling Pathway

Rashidi,

Matour,

Beheshtinasab

et al. 2023

IBJ

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Background: Currently, liver fibrosis is growing worldwide; unfortunately, there is no definite cure for this disease. Hence, understanding the molecular pathways involved in the development of liver fibrosis can help to find a proper treatment. In this study, we aimed to evaluate the effects of isorhamnetin as an antifibrotic agent on PDGF-BB-activated HSC-T6 cells in a concentration-dependent manner. We have also attempted to assess signaling pathways that may affect liver fibrosis. Methods: PDGF-BB was used to activate the HSC-T6 rat hepatic stellate cell line. The activated cells were treated with Isorhamnetin for 24 h. Finally, we compared the mRNA expression level of COLA1 and α-SMA and also the level of phosphorylated AKT protein with the control group. Results: The obtained data revealed a significant increase in the expression level of the COLA1 and α-SMA genes (p > 0.05), as well as phosphorylated AKT protein, in the cells treated with PDGF-BB. In addition, 75 and 100 µM concentrations of Isorhamnetin markedly declined the COLA1 and α-SMA expression and also the phosphorylated AKT protein level in the HSC-T6 cells. Conclusion: Our findings suggest that Isorhamnetin decreases HSC-T6 activation, the expression of COLA1 and α-SMA , in vitro, which could act as an antifibrotic element to reduce and treat liver fibrosis disease.

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Section: Resultsmentioning

confidence: 99%

Isorhamnetin Exerts Antifibrotic Effects by Attenuating Platelet-Derived Growth Factor-BB-induced HSC-T6 Cells Activation via Suppressing PI3K-AKT Signaling Pathway

Rashidi,

Matour,

Beheshtinasab

et al. 2023

IBJ

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“…During liver injury, they change, become activated, and convert to myo broblast cells, which lead to liver brosis. (23). Akt phosphorylation is with HSC replication increase, mRNA levels, and COLA1 protein levels.…”

Section: Discussionmentioning

confidence: 99%

Isorhamnetin exerts antifibrosis effects by attenuating PDGF-BB--induced HSC-T6 cells activation via suppressing PI3K-AKT Signaling Pathway, a new remedy for liver fibrosis

Rashidi

Matour

Nasab

et al. 2023

Preprint

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Background Liver inflammation and fibrosis are the results of chronic liver injuries, which activated myofibroblasts in the liver to produce more proteins in the extracellular matrix. The origin of myofibroblasts is quiescent hepatic stellate cells. Isorhamnetin as a natural flavonoid widely distributed in fruits and vegetables has anti-inflammatory activity and avoids cell proliferation and migration. Objectives We studied the effect of Isorhamnetin as an antifibrotic following stimulation by PDGF- BB in the HSC-T6 cells, as well as related mechanisms in vitro. Methods First of all, we used PDGF- BB to activate the HSC-T6 cells. After that, we used Isorhamnetin to treat activated cells for 24h. Finally, we compared the mRNA expression amount of collagen1 (COLA1), Alpha Smooth Muscle Actin (α-SMA), and level of phosphorylated AKT protein with our control group. Results The obtained data revealed the expression of the COLA1, α-SMA genes, as well as the amount of phosphorylate-AKT protein in the cells treated with PDGF-BB, significantly rose in comparison with our control. In addition, 75 and 100 µM concentrations of Isorhamnetin markedly declined the COLA1, α-SMA expression, and the phosphorylated AKT protein in the HSC-T6 cells. Conclusions Isorhamnetin significantly decreased HSC-T6 activation by preventing the PI3K-AKT cell signaling and reducing the expression of COLA1, α-SMA within liver fibrosis in vitro, so Isorhamnetin can prohibit liver fibrosis progression. In terms of these data, Isorhamnetin use can be recommended as a helpful therapeutic factor to treat liver fibrosis.

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“…For activating HSC-T6 cells, cells were kept in serum-starved in FBS-free DMEM condition for 24 h, later exposed to 10ng/ml PDGF-BB (22,23).…”

Section: Cell Culture Conditionsmentioning

confidence: 99%

Isorhamnetin exerts antifibrosis effects by attenuating PDGF-BB--induced HSC-T6 cells activation via suppressing PI3K-AKT Signaling Pathway, a new remedy for liver fibrosis

Rashidi

Matour

Nasab

et al. 2022

Preprint

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Background: Liver inflammation and fibrosis are the results of chronic liver injuries, which activated myofibroblasts in the liver to produce more proteins in the extracellular matrix. The origin of myofibroblasts is quiescent hepatic stellate cells. Isorhamnetin as a natural flavonoid widely distributed in fruits and vegetables has anti-inflammatory activity and avoids cell proliferation and migration.Objectives: We studied the effect of Isorhamnetin as an antifibrotic following stimulation by PDGF- BB in the HSC-T6 cells, as well as related mechanisms in vitro.Methods: First of all, we used PDGF- BB to activate the HSC-T6 cells. After that, we used Isorhamnetin to treat activated cells for 24h. Finally, we compared the mRNA expression amount of collagen1 (COLA1), Alpha Smooth Muscle Actin (α-SMA), and level of phosphorylated AKT protein with our control group.Results: The obtained data revealed the expression of the COLA1, α-SMA genes, as well as the amount of phosphorylate-AKT protein in the cells treated with PDGF-BB, significantly rose in comparison with our control. In addition, 75 and 100 µM concentrations of Isorhamnetin markedly declined the COLA1, α-SMA expression, and the phosphorylated AKT protein in the HSC-T6 cells.Conclusions: Isorhamnetin significantly decreased HSC-T6 activation by preventing the PI3K-AKT cell signaling and reducing the expression of COLA1, α-SMA within liver fibrosis in vitro, so Isorhamnetin can prohibit liver fibrosis progression. In terms of these data, Isorhamnetin use can be recommended as a helpful therapeutic factor to treat liver fibrosis.

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Kangxian ruangan keli inhibits hepatic stellate cell proliferation mediated by PDGF

Abstract: Within the dose range used in the present study, KXR preparation shows an inhibitory effect on HSC proliferation induced by PDGF. The mechanism of this process may involve interference with tyrosine phosphorylation mediated by PDGF.

Cited by 9 publications

References 24 publications

Isorhamnetin Exerts Antifibrotic Effects by Attenuating Platelet-Derived Growth Factor-BB-induced HSC-T6 Cells Activation via Suppressing PI3K-AKT Signaling Pathway

Isorhamnetin Exerts Antifibrotic Effects by Attenuating Platelet-Derived Growth Factor-BB-induced HSC-T6 Cells Activation via Suppressing PI3K-AKT Signaling Pathway

Isorhamnetin exerts antifibrosis effects by attenuating PDGF-BB--induced HSC-T6 cells activation via suppressing PI3K-AKT Signaling Pathway, a new remedy for liver fibrosis

Isorhamnetin exerts antifibrosis effects by attenuating PDGF-BB--induced HSC-T6 cells activation via suppressing PI3K-AKT Signaling Pathway, a new remedy for liver fibrosis

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