Liver Fibrosis and Protection Mechanisms Action of Medicinal Plants Targeting Apoptosis of Hepatocytes and Hepatic Stellate Cells

Duval, Florent; Moreno-Cuevas, Jorge E.; González‐Garza, María Teresa; Rodríguez-Montalvo, Carlos; Cruz-Vega, Delia Elva

doi:10.1155/2014/373295

Cited by 37 publications

(33 citation statements)

References 90 publications

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“…Therefore, modulating above‐mentioned pathways in injured hepatocytes is one of critical therapeutic strategies to treat acute or chronic liver injury. Currently, there is no successful or standard treatment for acute or chronic liver injury concerning apoptosis, although numerous studies have shown that pharmaceutical drugs and medicinal plants can inhibit apoptosis in pathologic condition of liver (Duval, Moreno‐Cuevas, Gonzalez‐Garza, Rodriguez‐Montalvo, & Cruz‐Vega, ). Although pharmaceutical drugs are one of the widely used options for treating several diseases including cancer, these drugs have critical side effects as well as high cost of treatment.…”

Section: Discussionmentioning

confidence: 99%

Dietary zerumbone, a sesquiterpene, ameliorates hepatotoxin‐mediated acute and chronic liver injury in mice

Kim

Yang

Jeong

et al. 2019

Phytotherapy Research

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Acute liver injury (ALI) is a life‐threatening clinical syndrome. Long‐lasting liver injury can lead to chronic hepatic inflammation and fibrogenic responses. Zerumbone (ZER), the main constituent of rhizomes of Zingiber zerumbet Smith, has a variety of functions including anticancer activity. We investigated the role of ZER on the progression of hepatotoxin‐induced liver injury. Single or repeated injection of CCl4 was used to induce acute or chronic liver injury, respectively. Mice were orally administered with ZER (10, 50 mg/kg) during the experimental period. Histopathologic analysis and serum biochemical levels revealed that ZER had hepatoprotective activities against ALI. Similar effects of ZER on injured livers were confirmed by analyses of inflammation and apoptosis‐related genes. Western blot analysis showed that protein levels of apoptotic molecules were decreased, whereas antiapoptotic protein levels were conversely increased in injured livers treated with ZER. Furthermore, chronic liver injury and its associated fibrogenesis in mice were reduced by ZER treatment. These findings from our in vivo experiments further indicate that ZER could alleviate hepatocellular toxicity and inhibit activation of primary hepatic stellate cells. Our results suggest that ZER might have potential as a safe and prophylactic alternative to prevent acute and chronic liver injury.

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Section: Discussionmentioning

confidence: 99%

Dietary zerumbone, a sesquiterpene, ameliorates hepatotoxin‐mediated acute and chronic liver injury in mice

Kim

Yang

Jeong

et al. 2019

Phytotherapy Research

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“…The inflammatory cellular infiltration observed in Group III “KBrO 3 rats” in this study was associated with the presence of huge amount of collagen fibers around the portal zone and extended between cords of hepatocytes. This may be due to the damage and dysfunction of mitochondria caused by the reactive oxygen species with lipid peroxidation products leading to cell apoptosis and necrosis and stimulation of a cascade leading to fibrosis and collagen deposition (Duval et al, ). The deposition of collagen fibers in KBrO 3 rats’ livers was concomitant with the significant increase in the immunoexpression of HSC markers “GFAP.” HSCs play an important role in liver fibrosis due to the deposition of collagen type I and III and matrix proteins.…”

Section: Discussionmentioning

confidence: 99%

Effect of Potassium Bromate on the Liver of Adult Male Albino Rat and A Possible Protective Role of Vitamin C: Histological, Immunohistochemical, and Biochemical Study

Bayomy

Soliman

Abdelaziz

2016

The Anatomical Record

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Potassium bromate (KBrO 3 ) is a food additive which is used primarily as a maturing agent for flour. It is proved as a toxic agent with significant reduction in the activities of antioxidant capacity. The therapeutic efficacy of vitamin C as antioxidant may provide a possible solution to KBrO 3 mediated oxidative damage. Twenty four adult male albino rats were used to evaluate the protective role of vitamin C against KBrO 3 induced hepatotoxicity and divided into four groups; Group 1 (control), Group 2: received 30 mg/Kg/day vitamin C orally for 4 weeks, Group 3: received 20 mg/Kg/dose KBrO 3 orally twice weekly for 4 weeks and Group 4: received both KBrO 3 and vitamin C. Liver specimens were processed for histological study by light and electron microscopes and stained immunohistochemically to detect glial fibriller acidic protein (GFAP). Serum levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were estimated as well as the levels of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activities in all dissected tissues were determined. KBrO 3 induced histological alterations in the form of degeneration, cellular infiltration and significant increase in collagen deposition in portal tracts with a significant increase in immunoexpression of GFAP. Significant rise in serum levels of AST, ALT, and MDA in liver tissues were recorded. However, levels of GSH and SOD were significantly decreased. Most of these changes were improved by vitamin C treatment. In conclusion, vitamin C ameliorates the histological and biochemical alterations of the liver induced by KBrO 3 .

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“…Studies have shown that the process of hepatic stellate cells (HSCs) turning from quiescent state to activation state plays a central role in the development of hepatic fibrosis . Activated HSCs activate into myofibroblasts, resulting in deposition and unbalanced degradation of extracellular matrix (ECM) . Previous studies have shown that soluble egg antigens (SEA) from Schistosoma japonicum ( S. japonicum ) and Schistosoma mansoni ( S. mansoni ) can inhibit HSC proliferation and activation .…”

Section: Introductionmentioning

confidence: 99%

rSjP40 suppresses hepatic stellate cell activation by promoting microRNA‐155 expression and inhibiting STAT5 and FOXO3a expression

Zhu

Yang

Shen

et al. 2018

J Cellular Molecular Medi

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Activation of hepatic stellate cells (HSCs) is the central event of the evolution of hepatic fibrosis. Schistosomiasis is one of the pathogenic factors which could induce hepatic fibrosis. Previous studies have shown that recombinant Schistosoma japonicum egg antigen P40 (rSjP40) can inhibit the activation and proliferation of HSCs. MicroRNA‐155 is one of the multifunctional noncoding RNA, which is involved in a series of important biological processes including cell development, proliferation, differentiation and apoptosis. Here, we try to observe the role of microRNA‐155 in rSjP40‐inhibited HSC activation and explore its potential mechanisms. We found that microRNA‐155 was raised in rSjP40‐treated HSCs, and further studies have shown that rSjP40 enhanced microRNA‐155 expression by inhibiting STAT5 transcription. Up‐regulated microRNA‐155 can down‐regulate the expression of FOXO3a and then participate in rSjP40‐inhibited expression of α‐smooth muscle actin (α‐SMA) and collagen I. Furthermore, we observed microRNA‐155 inhibitor could partially restore the down‐regulation of FOXO3a, α‐SMA and collagen I expression in LX‐2 cells induced by rSjP40. Therefore, our research provides further insight into the mechanism by which rSjP40 could inhibit HSC activation via miR‐155.

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Liver Fibrosis and Protection Mechanisms Action of Medicinal Plants Targeting Apoptosis of Hepatocytes and Hepatic Stellate Cells

Cited by 37 publications

References 90 publications

Dietary zerumbone, a sesquiterpene, ameliorates hepatotoxin‐mediated acute and chronic liver injury in mice

Dietary zerumbone, a sesquiterpene, ameliorates hepatotoxin‐mediated acute and chronic liver injury in mice

Effect of Potassium Bromate on the Liver of Adult Male Albino Rat and A Possible Protective Role of Vitamin C: Histological, Immunohistochemical, and Biochemical Study

rSjP40 suppresses hepatic stellate cell activation by promoting microRNA‐155 expression and inhibiting STAT5 and FOXO3a expression

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