Prevention of in vitro hepatic stellate cells activation by the adenosine derivative compound IFC305

Velasco-Loyden, Gabriela; Pérez‐Carreón, Julio Isael; Agüero, José; Romero, Pilar Cabrales; Vidrio-Gómez, Susana; Martínez-Pérez, Lidia; Yáñez-Maldonado, Lucia; Hernández‐Muñoz, Rolando; Macı́as-Silva, Marina; Sánchez, Victoria Chagoya de

doi:10.1016/j.bcp.2010.08.017

Cited by 20 publications

(21 citation statements)

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“…Furthermore, telmisartan, an angiotensin II type 1 receptor antagonist, prevented liver fibrogenesis and pre-neoplastic lesions by a mechanism involving an increase in MMP-13 expression [10]. In addition, Velasco-Loyden et al [20] revealed that the aspartate salt of adenosine IFC305 suppresses the activation of hepatic stellate cells, the main extracellular matrixproducing cells in the fibrotic liver, by inhibiting the production of collagen α 1 (I) mRNA, and increasing the expression of MMP-13 mRNA, which may result in an important decrease of collagen deposition. Besides, collagen-I degradation is critical to hepatic stellate cell apoptosis and hepatocyte regeneration during recovery from liver fibrosis [8].…”

Section: Discussionmentioning

confidence: 97%

Protective effects of curcumin, α-lipoic acid, and N-acetylcysteine against carbon tetrachloride-induced liver fibrosis in rats

et al. 2011

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Liver fibrosis is a major health problem that can lead to the development of liver cirrhosis and hepatocellular carcinoma. On the other hand, several antioxidants have been shown to possess protective effect against liver fibrosis. Therefore, in the present work, the effectiveness of curcumin, α-lipoic acid, and N-acetylcysteine in protecting against carbon tetrachloride (CCl(4))-induced liver fibrosis as well as the mechanism(s) implicated in this protective effect was studied. The antioxidants used in this study resulted in hepatoprotective effect as evident by substantial decreases in collagen deposition in histopathological examinations in addition to significant decrease in serum levels of alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transpeptidase, bilirubin, and transforming growth factor-alpha (TGF-α) as well as hepatic malondialdehyde concentration, with a concurrent increase in serum matrix metalloproteinase-13 (MMP-13) and hepatic reduced glutathione (GSH) levels as compared to CCl(4) fibrotic group. In conclusion, curcumin, α-lipoic acid, and N-acetylcysteine protect rats against CCl(4)-induced liver fibrosis most possibly through their antioxidant activities and their capacities to induce MMP-13 and to inhibit TGF-α levels.

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Section: Discussionmentioning

confidence: 97%

Protective effects of curcumin, α-lipoic acid, and N-acetylcysteine against carbon tetrachloride-induced liver fibrosis in rats

et al. 2011

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“…In fact, in this study we found that the overexpression of the A2a receptor protein during cirrhosis decreases in the presence of IFC-305 (Figure 7), suggesting a role of this receptor in the described effect. Previously, we showed that the inhibitory effect of IFC305 in hepatic stellate cells activation was not mediated by adenosine receptors, but it was related with adenosine transport and intracellular AMP formation [42], neither in the adenosine acceleration of the cell cycle after one-third hepatectomy [19]. Possibly, a diminution of A2a receptor expression induced by the IFC305 increases adenosine transport into the cell promoting their effects in DNA repair and maintaining the energetic equilibrium.…”

Section: Discussionmentioning

confidence: 99%

Recovery of the Cell Cycle Inhibition inCCl4-Induced Cirrhosis by the Adenosine Derivative IFC-305

Sánchez

Martínez-Pérez

Hernández‐Muñoz

et al. 2012

International Journal of Hepatology

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Introduction. Cirrhosis is a chronic degenerative illness characterized by changes in normal liver architecture, failure of hepatic function, and impairment of proliferative activity. The aim of this study is to know how IFC-305 compound induces proliferation of the liver during reversion of cirrhosis. Methods. Once cirrhosis has been installed by CCl4 treatment for 10 weeks in male Wistar rats, they were divided into four groups: two received saline and two received the compound; all were euthanized at 5 and 10 weeks of treatment. Liver homogenate, mitochondria, and nucleus were used to measure cyclins, CDKs, and cell cycle regulatory proteins PCNA, pRb, p53, E2F, p21, p27, HGF, liver ATP, and mitochondrial function. Results. Diminution and small changes were observed in the studied proteins in the cirrhotic animals without treatment. The IFC-305-treated rats showed a clear increase in most of the proteins studied mainly in PCNA and CDK6, and a marked increased in ATP and mitochondrial function. Discussion/Conclusion. IFC-305 induces a recovery of the cell cycle inhibition promoting recovery of DNA damage through the action of PCNA and p53. The increase in energy and preservation of mitochondrial function contribute to recovering the proliferative function.

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“…HSCs were isolated from the livers of female Sprague–Dawley rats (486 ± 23 g) as described previously . Freshly isolated HSCs activated spontaneously and transdifferentiated from a quiescent to an MFB phenotype in a process similar to that observed in vivo . After 24 h of isolation, HSCs were cultured in Dulbecco's modified Eagle's medium—10% fetal bovine serum with DPN (at a final concentration of 10 −7 mol/L) and/or PHTPP (at a final concentration of 10 −7 mol/L).…”

Section: Methodsmentioning

confidence: 99%

Estrogen receptor β selective agonist ameliorates liver cirrhosis in rats by inhibiting the activation and proliferation of hepatic stellate cells

Zhang

et al. 2018

J of Gastro and Hepatol

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Prevention of in vitro hepatic stellate cells activation by the adenosine derivative compound IFC305

Cited by 20 publications

References 52 publications

Protective effects of curcumin, α-lipoic acid, and N-acetylcysteine against carbon tetrachloride-induced liver fibrosis in rats

Protective effects of curcumin, α-lipoic acid, and N-acetylcysteine against carbon tetrachloride-induced liver fibrosis in rats

Recovery of the Cell Cycle Inhibition inCCl4-Induced Cirrhosis by the Adenosine Derivative IFC-305

Estrogen receptor β selective agonist ameliorates liver cirrhosis in rats by inhibiting the activation and proliferation of hepatic stellate cells

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