Advances in Nanonutraceuticals: Indian Scenario
Harishkumar Madhyastha, Durgesh Nandini Chauhan in Nanopharmaceuticals in Regenerative Medicine, 2022
Persistent inflammation, following liver damage, often results in the formation of fibrous tissue. Therefore, often, any medication which is given to reduce the inflammation ideally has an anti-fibrotic effect. The sequence of steps, which lead to fibrosis are outlined as oxidative stress caused by the generation of ROS followed by scar formation, leading to a reduced inflammatory response. This inflammation causes the crippling of hepatic stellate cell (HSC) activation causing fibrogenesis as seen in cirrhosis of the liver. In this context, it can be said, that certain natural compounds or Unani preparations which are identified as antioxidants, can be given as a therapy to reduce the ROS and in a way to prevent fibrosis of hepatic tissue. The effectiveness of this treatment depends upon the agility of the antioxidant reaching the target site i.e., liver (Kawada et al. 1998).
Anti-Hepatofibrotic Effect of Xiao-Chaihu-Tang (Sho-Saiko-To)
Sheng-Li Pan in Bupleurum Species, 2006
Hepatic fibrosis is often associated with inflammation and cell death, which accompanies the repair processes, and is a consequence of severe liver damage that occurs in many patients with chronic liver disease, including chronic HCV infection. The main origin of the abnormal ECM proteins is a cell known as the hepatic stellate cell (HSC) (also known as the fat-storing cell, lipocyte, or the Ito cell). HSCs are located in the space of Disse in close contact with hepatocytes and sinusoidal endothelial cells. Their three-dimensional structure consists of the cell body and several long and branching cytoplasmic processes (Wake, 1999) (Figure 14.2). It is now evident that HSCs undergo proliferation and transformation under inflammatory and peroxidative stimuli into myofibroblast-like cells, which serve as the origin of much of the collagen hypersecretion and nodule formation that occurs during hepatic fibrosis and cirrhosis (Shimizu, 2001).
Fatty Liver Disease
David Heber, Zhaoping Li in Primary Care Nutrition, 2017
In hepatitis and cirrhosis, abnormal hepatic gene expression of methyl donor metabolism, specifically in methionine and glutathione metabolism, occurs and often contributes to decreased hepatic S-adenosylmethionine (SAM), cysteine, and glutathione levels (Lee et al. 2004). Rodent and primate studies demonstrate that SAM depletion occurs in the early stages of fatty liver infiltration, and decreased SAM concentration, liver injury, and mitochondrial damage can be reversed with SAM supplementation (Lieber 2002). SAM appears to attenuate oxidative stress and hepatic stellate cell activation in an ethanol-LPS-induced fibrotic rat model (Karaa et al. 2008). Clinical trial evidence is lacking.
Relevance of vitamin D on NAFLD and liver fibrosis detected by vibration controlled transient elastography in US adults: a cross-sectional analysis of NHANES 2017–2018
Published in Annals of Medicine, 2023
Yuan Ji, Chang-Bao Wei, Wei Gu, Lin-Lin Hou
Currently, why vitamin D could effectively suppress the LF in NAFLD patients remains unclear. During the development of LF, hepatic stellate cell activation plays important effect. Activated hepatic stellate cells can effectively induce cell growth and transformation from a quiescent vitamin A-storing cell into an activated myofibroblast-like cell, increasing the production of extracellular matrix and tissue inhibitors of metalloproteinases [33]. Through inhibiting the activation of TGF-β/Smad signalling pathway in hepatic stellate cells, vitamin D can effectively impair the fibrosis of liver [34]. A recent study further indicated that vitamin D reduced hepatic stellate cells and TGF-β/Smad signalling activation through negative regulation of histidine-rich calcium binding protein [35].
Evening primrose oil attenuates oxidative stress, inflammation, fibrosis, apoptosis, and ultrastructural alterations induced by metanil yellow in the liver of rat: a histological, immunohistochemical, and biochemical study
Published in Ultrastructural Pathology, 2023
Amany Mohamed Shalaby, Rania H. Shalaby, Mohamed Ali Alabiad, Doaa I. Abdelrahman, Mohammed Alorini, Fatima A. Jaber, Shaimaa Mohamed Abdelfattah Hassan
The current work depicted a considerable rise in collagen fibers in the livers of rats given Myl. Electron microscopy revealed the existence of collagen fiber bundles between hepatocytes, confirming this observation. This might be attributed to the rise in the activity of Kupffer cells, which in turn increases the synthesis of fibrosis-promoting components, including reactive oxygen species (ROS), Transforming growth factor beta 1, TNF- α, IL-1 β, and NF-kB, which all cause liver fibrosis.31 The observed rise in liver fibrosis might be explained by an increase in hepatic stellate cell activity and population. In liver tissue, this is the most common kind of fibrogenic cell. Damaged hepatocytes trigger hepatic stellate cells to take on a phenotype resembling myofibroblasts and increase collagen synthesis and secretion when the liver is harmed.32 All of these findings corresponded to the significant rise in the mean area percentage of GFAP-positive stellate cells as well as the mRNA expression of GFAP, which our research revealed.
Polystyrene microplastic particles induced hepatotoxic injury via pyroptosis, oxidative stress, and fibrotic changes in adult male albino rats; the therapeutic role of silymarin
Published in Toxicology Mechanisms and Methods, 2023
Arwa A. Elsheikh, Sulaiman Mohammed Alnasser, Amany Mohamed Shalaby, Mohamed Ali Alabiad, Noha Ali Abd-Almotaleb, Mohammed Alorini, Fatima A. Jaber, Eman El-Sayed Khayal
Hepatic fibrotic changes were attributed to hepatic stellate cell (HSC) activation by oxidative stress or lipid accumulation. Activated liver stellate cells developed into myofibroblasts that deposit collagen fibers. Another recent suggestion attributed to MPs that induce liver fibrosis by activating the cGAS/STING pathway is cell stress and tissue damage are key mediators that induce inflammation. A study carried out in rats proved the role of iNOS in developing liver fibrosis by inducing the expression of hypoxia-inducible factor 1 and matrix metalloproteinase-9. It improved liver DNA damage, which is the pathway of the fibrosis process (Li et al. 2019). Another suggestion reported the role of the NLRP3 inflammasome and inflammatory mediators induced fibrotic changes in the liver of mice by activating HSC. Finally, it was suggested that changes in liver lipid metabolism that regulate the synthesis and metabolism of the extracellular matrix of cellular energy led to the activation of HSCs producing fibrosis (Haas et al. 2016).
Related Knowledge Centers
- Cytoglobin
- Cytoplasm
- Fibrosis
- Hepatocyte
- Pericyte
- Liver
- Perisinusoidal Space
- Liver Sinusoid
- Scar
- Chloroauric Acid