Modulation of extracellular matrix by nutritional hepatotrophic factors in thioacetamide-induced liver cirrhosis in the rat

Guerra, Ricardo Romão; Trotta, Milagros; Parra, Osório Miguel; Avanzo, José Luís; Bateman, Andrew; Aloia, Thiago Pinheiro Arrais; Dagli, M.L.; Hernandez‐Blazquez, Francisco Javier

doi:10.1590/s0100-879x2009005000027

Cited by 22 publications

(42 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A similar reduction in the gene expression level of Col-a1 has been shown in the rats with cirrhotic livers that were treated with NHF (Guerra et al 2009), thereby indicating that the reduction in new collagen deposition together with an increase in liver parenchyma are the primary effects of the NHF treatment. In contrast to previous studies, no differences were observed in the expression of other profibrotic genes involved in cirrhosis.…”

Section: Discussionsupporting

confidence: 64%

“…In fact, it has been demonstrated that the in vivo administration of NHF has a strong ability to accelerate and augment cellular proliferation as well as the growth of normal (Parra et al 1994(Parra et al , 1995, fibrotic (Cogliati et al 2010), and cirrhotic (Guerra et al 2009) liver tissues. Moreover, in fibrotic or cirrhotic livers, NHF treatment causes a reduction in the amount of tissue collagen and an improvement in the liver morphology and function (Cogliati et al 2010;Guerra et al 2009;Parra et al 1996). Furthermore, hepatocyte regeneration often results in the regression of liver cirrhosis (Kawada 2011).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Parenteral Solution of Nutritional Hepatotrophic Factors Improves Regeneration in Thioacetamide-induced Cirrhotic Livers after Partial Hepatectomy

et al. 2013

View full text Add to dashboard Cite

Liver resection is a suitable option for the treatment of certain hepatic conditions, particularly hepatocarcinomas, in patients with cirrhosis. However, this disease impairs liver regeneration, which increases the risk of liver failure and postoperative death. Supportive treatments for regeneration of the remaining liver may be useful for the recovery of these patients. We demonstrated that nutritional hepatotrophic factors (NHF) is an effective regenerative stimulus for cirrhotic livers in rats subjected to partial hepatectomy (PH). The rats with thioacetamide-induced cirrhosis were subjected to PH, and they were divided into 2 groups. One group received intraperitoneal administration of NHF, and the other group received saline solution. After 12 days, biometric data, collagen content, hepatocyte regeneration (proliferation cell nuclear antigen immunochemistry), and profibrotic gene expression (Collagen-a1, matrix metalloproteinase 2, tissue inhibitor of metalloproteinase 1, and transforming growth factor beta 1) were assessed. The results indicated that the rats treated with NHF after PH had an increased liver size, a reduced amount of collagen, and a higher hepatocyte proliferation index compared with the rats that underwent PH alone. In addition, collagen-a1 gene expression was decreased in the NHF-treated rats. Thus, postoperative improvement in the liver morphology following NHF treatment may cause a significant decrease in the risk of liver failure and mortality after hepatic resection.

show abstract

Section: Discussionsupporting

confidence: 64%

Section: Introductionmentioning

confidence: 99%

Parenteral Solution of Nutritional Hepatotrophic Factors Improves Regeneration in Thioacetamide-induced Cirrhotic Livers after Partial Hepatectomy

et al. 2013

View full text Add to dashboard Cite

show abstract

“…A via intraperitoneal representa um acesso rápido à circulação portal (Parra et al, 1995b; . De fato, a administração in vivo destes fatores demonstra a sua forte capacidade de acelerar e aumentar a proliferação celular e o crescimento de fígados normais (Parra et al, 1995a;Parra et al, 1995b;Cogliati, 2005;Aloia et al, 2010), fibróticos e cirróticos (Guerra et al, 2009), o que aumenta a proporção de parênquima em relação ao estroma. Além disso, em fígados com fibrose ou cirrose, os FHN também resultam em uma redução na quantidade tecidual de colágeno, facilitando o acesso das células à nutrição e oxigenação sanguínea, acompanhada por uma melhoria morfológica e funcional (Parra et al, 1982;Guerra et al,2009;Cogliati et al, 2010 …”

Section: Descriptorsunclassified

“…De fato, a administração in vivo destes fatores mostrou uma forte capacidade de acelerar e aumentar a proliferação celular e o crescimento de fígados normais (Parra et al, 1994;Parra et al, 1995b;Cogliati, 2005;Aloia et al, 2010), fibróticos e cirróticos (Guerra et al, 2009 (Parra, 1982;Guerra et al, 2009;Cogliati et al,2010). O uso de FHN promove um estímulo no fígado comparável ao da HP de 70% (Parra et al, 1996).…”

Section: Revisão De Literaturaunclassified

See 1 more Smart Citation

Efeito da hepatectomia parcial associada à administração de fatores nutricionais hepatotróficos sobre a morfologia, função e expressão de genes pró-fibróticos na cirrose hepática em ratos Wistar induzida por tiocetamida

Trotta¹

View full text Add to dashboard Cite

Nuclear Fructose‐1,6‐Bisphosphate Inhibits Tumor Growth and Sensitizes Chemotherapy by Targeting HMGB1

Zhang

et al. 2023

Advanced Science

View full text Add to dashboard Cite

Metabolites are important for cell fate determination. Fructose‐1,6‐bisphosphate (F1,6P) is the rate‐limiting product in glycolysis and the rate‐limiting substrate in gluconeogenesis. Here, it is discovered that the nuclear‐accumulated F1,6P impairs cancer cell viability by directly binding to high mobility group box 1 (HMGB1), the most abundant non‐histone chromosome structural protein with paradoxical roles in tumor development. F1,6P disrupts the association between the HMGB1 A‐box and C‐tail by targeting K43/K44 residues, inhibits HMGB1 oligomerization, and stabilizes P53 protein by increasing P53–HMGB1 interaction. Moreover, F1,6P lowers the affinity of HMGB1 for DNA and DNA adducts, which sensitizes cancer cells to chemotherapeutic drug(s)‐induced DNA replication stress and DNA damage. Concordantly, F1,6P resensitizes cancer cells with chemotherapy resistance, impairs tumor growth and enhances chemosensitivity in mice, and impedes the growth of human tumor organoids. These findings reveal a novel role for nuclear‐accumulated F1,6P and underscore the potential utility of F1,6P as a drug for cancer therapy.

show abstract

Modulation of extracellular matrix by nutritional hepatotrophic factors in thioacetamide-induced liver cirrhosis in the rat

Cited by 22 publications

References 36 publications

Parenteral Solution of Nutritional Hepatotrophic Factors Improves Regeneration in Thioacetamide-induced Cirrhotic Livers after Partial Hepatectomy

Parenteral Solution of Nutritional Hepatotrophic Factors Improves Regeneration in Thioacetamide-induced Cirrhotic Livers after Partial Hepatectomy

Efeito da hepatectomia parcial associada à administração de fatores nutricionais hepatotróficos sobre a morfologia, função e expressão de genes pró-fibróticos na cirrose hepática em ratos Wistar induzida por tiocetamida

Nuclear Fructose‐1,6‐Bisphosphate Inhibits Tumor Growth and Sensitizes Chemotherapy by Targeting HMGB1

Contact Info

Product

Resources

About