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Advances in Nanonutraceuticals: Indian Scenario
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
Amthul Azeez, Mubeen Sultana, Lucky, Noorjahan
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).
Pathological Manifestations and Mechanisms of Metal Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Iron (Fe) hepatic overload in adults can have multiple etiologies, including hereditary hemochromatosis (when there is abnormal Fe absorption in the intestinal tract), excessive Iron intake, and repeated blood transfusions. Increased accumulation of Fe in any parenchymal organs is called hemosiderosis. When it becomes excessive and causes parenchymal lesions, such as increase fibrous connective tissue, it is called hemochromatosis. Hepatic hemochromatosis has been associated with increased risk of hepatocellular carcinoma (Anderson & Frazer, 2017; Curtis, 2013). However, hepatic Iron overload is also frequently observed with chronic liver disease regardless of its etiology. The {Rubino, 2015 #256} major route of Iron entry into the hepatocyte is via receptor-mediated endocytosis of transferrin by transferrin receptor-1 (TFR1). After internalization, the Iron is released into the lysosomal compartment and can be delivered into other organelles. Iron can cycle between two stable oxidation states, ferrous Iron (iron(II) or Fe2+) and ferric Iron (Iron(III) or Fe3+) (Sangkhae & Nemeth, 2017). When in excess, Fe is oxidized into the ferric form and can be sequestered within the ferritin (Bloomer & Brown, 2019). Increased levels of Fe can accelerate the Fenton reaction in which the ferrous form of Iron interacts with H2O2 and generates highly reactive hydroxyl radical (Fe2+ + H2O2 → Fe3+ + •OH + OH− & Fe3+ + H2O2 → Fe2+ + •OOH + H+). These ROS can lead to hepatocellular injury by disruptively reacting with biological structures such as unsaturated lipids in cellular membranes, DNA and RNA components, and other essential chemical groups in catalytic and signaling proteins (Rubino, 2015). Prolonged injury causes chronic stimulation of hepatic stellate cells (HSC) that become sources of transforming growth factor-beta (TGF-β) that, in turn, stimulates further proliferation of HSC and their differentiation into myofibroblasts producers of extracellular matrix that can lead to a fibrotic state. This state can progress into cirrhosis and ultimately cancer (Mehta, Farnaud, & Sharp, 2019). Iron has also been implicated with inflammatory pathways such as NF-ƙB in liver Kupffer cells that can increase inflammatory cytokines like, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) (Bloomer & Brown, 2019). Increased Fe associated with increased intestinal absorption has also been reported as a possible factor in the etiology of nonalcoholic fatty liver disease (NAFLD) (Malik, Wilting, Ramadori, & Naz, 2017). A key hepatic hormone that regulates Iron systemic levels is hepcidin (HAMP or HEPC). Disturbances in HEPC are associated with many Iron overload disorders including chronic inflammatory diseases and cancer (Sangkhae & Nemeth, 2017).
Intermittent fasting and probiotics in non-alcoholic fatty liver in rats: interplay between FGF19 and FGF21
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Yomna M yehya, Zeinab H. El-Said, Mohamed Adel, Basma H Othman, Atef A Mansour, Sabry M Gad
Insulin resistance plays a critical role in the pathophysiology of NAFLD via augmenting fatty acids flow to hepatocytes and increasing hepatic lipogenesis, resulting in mitochondrial damage, endoplasmic reticulum stress, autophagy, the release of pro-inflammatory cytokines and a rise in peroxidation processes [8]. These effects cause hepatic stellate cell activation, which contributes to fibrosis and hepatocellular ballooning. These histopathological changes can lead to fibrosis, cirrhosis, hepatocellular carcinoma, and an increase in mortality from liver-related causes [47]. IF was stated to improve the accumulation of hepatic TG and liver steatosis independent of the diet [14,26], which may be due to improved oral glucose tolerance, restoring peripheral insulin sensitivity and glucose homeostasis, normalizing adipokine and cytokine secretion from adipose tissue, altering the frequency and amount of fatty acid delivery to the liver, and changing the composition of the gut microbiota in a beneficial way, which can reduce inflammatory immune responses [48]. Interestingly, there was no extra benefit from probiotics in addition to fasting; Mohamad Nor et al., 2021, revealed that supplementation with probiotics did not elicit any improvement in the NAS [28]. The underlying NAFLD mechanisms that our study investigated and the effect of PR and IF on them are summarized in Figure 4.
Histological and immunohistochemical study of the effect of liraglutide in experimental model of non-alcoholic fatty liver disease
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Mai Salah Nour, Zeinab Abd El-Hay Sakara, Nawal Awad Hasanin, Shereen Mohamed Hamed
The present study showed mononuclear inflammatory cells infiltration in the FLD group. Chemo attractive cytokines released by activated hepatic stellate cells (HSCs) provided more explanation of this phenomenon. Response to the paracrine action of hepatocytes, sinusoidal endothelium and KCs is one of the first indicators of HSC activation [41].