Regular ArticleProtection against TNF-Induced Liver Parenchymal Cell Apoptosis during Endotoxemia by a Novel Caspase Inhibitor in Mice
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The role of apoptosis in acetaminophen hepatotoxicity
2018, Food and Chemical ToxicologyCitation Excerpt :If this fact is overlooked and proper solvent controls are not included, then protective effects of caspase inhibitors against APAP toxicity can be observed (El-Hassan et al., 2003; Hu and Colletti, 2010), even in the verified absence of caspase activation (El-Hassan et al., 2003). However, as has been shown repeatedly, caspase inhibitors are readily absorbed and are highly effective within less than an hour during TNF- or Fas receptor-induced apoptosis (Bajt et al., 2000, 2001; Jaeschke et al., 1998, 2000) and therefore can be given right before the onset of the injury. Thus, in order to avoid the effect of DMSO on the oxidative metabolism of APAP, we generally treat animals 2–3 h after APAP (Gujral et al., 2002; Lawson et al., 1999; Jaeschke et al., 2006).
Diterpenoid trigonoreidon B isolated from Trigonostemon reidioides alleviates inflammation in models of LPS-stimulated murine macrophages and inflammatory liver injury in mice
2018, Biomedicine and PharmacotherapyCitation Excerpt :The liver is the most affected organ during sepsis [4]. Proinflammatory cytokines especially tumor necrosis factor-alpha (TNF-α) produced by activated macrophages have been shown to contribute to liver destruction through apoptosis cell death [5]. TNF-α mediates hepatocyte injury via apoptosis induction by binding with its death TNF-α receptor, which leads to caspase activation [6].
Caspase Inhibition Prevents Tumor Necrosis Factor-α–Induced Apoptosis and Promotes Necrotic Cell Death in Mouse Hepatocytes in Vivo and in Vitro
2016, American Journal of PathologyCitation Excerpt :However, in addition to hepatocytes, there are many nonparenchymal cells in the liver that also play important roles in hepatocyte injury. In the context of LPS/GalN-induced hepatocyte death, it is well established that LPS activates Kupffer cells to trigger the production and release of TNF-α, whereas GalN deletes UTP in hepatocytes to cause a transient block in transcription and protein synthesis resulting in NF-κb inhibition.26,41 Moreover, neutrophils are also known to be recruited to the liver sinusoids after LPS/GalN administration to aggravate liver injury.26,42
Lithocholic acid feeding results in direct hepato-toxicity independent of neutrophil function in mice
2014, Toxicology LettersCitation Excerpt :While there was an abundant amount of procaspase-3 in the liver at every time point, there was no cleavage into the active caspase-3 fragment in any of the samples from LCA-treated animals. In contrast, high levels of caspase-3 activities (Fig. 3A) correlated with the presence of active caspase-3 fragments in galactosamine/endotoxin-treated mice used as a positive control (Jaeschke et al., 2000). We also examined TUNEL-positive cells during LCA feeding.
Current issues with acetaminophen hepatotoxicity - A clinically relevant model to test the efficacy of natural products
2011, Life SciencesCitation Excerpt :In these models, apoptotic cell death of 20–30% of hepatocytes correlates with > 100-fold increase of caspase-3 activity (Bajt et al., 2000; Gujral et al., 2004; Jaeschke et al., 2000). Furthermore, pan caspase inhibitors completely prevent TNF- and Fas receptor-induced apoptosis (Bajt et al., 2000; Jaeschke et al., 2000) but have absolutely no effect on APAP toxicity (Jaeschke et al., 2006; Lawson et al., 1999; Williams et al., 2010b). The two manuscripts claiming protection with caspase inhibitors in vivo used a pretreatment regimen (El-Hassan et al., 2003; Hu and Colletti, 2010).
Role of caspase-1 and interleukin-1β in acetaminophen-induced hepatic inflammation and liver injury
2010, Toxicology and Applied Pharmacology