LPS induced liver injury

Further study demonstrated that THS significantly inhibited hepatic DNA fragmentation, the emergence of apoptotic bodies and chromatin condensation in D-GalN/LPS-induced liver injury in mice. The extent of the inhibitory effect of THS on hepatocyte apoptosis at 5 hr paralleled that on serum ALT elevation at 8 hr [87]. As mentioned above, in this model, a large number of hepatocytes undergoing apoptotic cell death can... 

There is much interest in the pharmacological role of dietary nutrients in human health. Some nutrients have been recognized to have a hepatoprotective effect through interaction with TNF-a. For instance, dietary supplementation (5%, at the exp ense of casein) with glycine (30), a non-essential amino acid, attenuated LPS-induced liver injury and... 

To set up and validate the in vitro systems we initiated a study with rat Uver slices. Stimulation by Upopolysaccharide (LPS) in liver slices was used to evoke a pro-inflammatory response in the Uver. Lipopolysaccharide (LPS), a component of Gram-negative bacterial ceU walls (also called endotoxin), has been associated with tissue injury and sepsis. In the Uver LPS activates the resident macrophages, the Kupffer ceUs, which results in cytokine release [96]. Furthermore, LPS is cleared by the Uver, mainly by Kupffer ceUs [97]. One of the major features of endotoxic shock is the induction of nitric oxide S5mthase in the Uver [98]. Inducible nitric oxide synthase (iNOS), the expression of which is induced by LPS and cytokines, produces nitric oxide (NO) in large quantities [99]. 

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