ArticleHistochemistry and cell biology2005
Immunohistochemical distribution of activated nuclear factor kappaB and peroxisome proliferator-activated receptors in carbon tetrachloride-induced chronic liver injury in rats.
Article in Histochemistry and cell biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 40 citations in OpenAlex.
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- Potent hepatoprotective activity of common rattan (Calamus rotang L.) leaf extract and its molecular mechanism.BMC complementary medicine and therapies · 2023Article
- An Integrated Mutually Oriented "Chemical Profiling-Pharmaceutical Effect" Strategy for Screening Discriminating Markers of Underlying Hepatoprotective Effects to Distinguish Garden-Cultivated from Mountain-CultivatedMolecules (Basel, Switzerland) · 2021Article
- Antifibrotic effects of crocin on thioacetamide-induced liver fibrosis in mice.Saudi journal of biological sciences · 2018Article
- Article
- Forskolin, a hedgehog signalling inhibitor, attenuates carbon tetrachloride-induced liver fibrosis in rats.British journal of pharmacology · 2016Article
- Antifibrotic effect of meloxicam in rat liver: role of nuclear factor kappa B, proinflammatory cytokines, and oxidative stress.Naunyn-Schmiedeberg's archives of pharmacology · 2016Article
- Protective effects of the nuclear factor kappa B inhibitor pyrrolidine dithiocarbamate on experimental testicular torsion and detorsion injury.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2014Article
- Ethanol extract of Portulaca Oleracea L. reduced the carbon tetrachloride induced liver injury in mice involving enhancement of NF-κB activity.American journal of translational research · 2014Article
- Propofol Attenuates Toxic Oxidative Stress by CCl4 in Liver Mitochondria and Blood in Rat.Iranian journal of pharmaceutical research : IJPR · 2014Article
- Butein inhibits ethanol-induced activation of liver stellate cells through TGF-β, NFκB, p38, and JNK signaling pathways and inhibition of oxidative stress.Journal of gastroenterology · 2013Article
- CCl4-induced hepatic injury in mice fed a Western diet is associated with blunted healing.Journal of gastroenterology and hepatology · 2010Article
- The antioxidant activity of chondroitin-4-sulphate, in carbon tetrachloride-induced acute hepatitis in mice, involves NF-kappaB and caspase activation.British journal of pharmacology · 2008Article
- Effect of ribavirin alone or combined with silymarin on carbon tetrachloride induced hepatic damage in rats.Drug target insights · 2007Article
- The histochemistry and cell biology vade mecum: a review of 2005-2006.Histochemistry and cell biology · 2006Review
- Recent progress in histochemistry and cell biology: the state of the art 2005.Histochemistry and cell biology · 2005Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated the immunohistochemical distribution of active NF-kappaB p65 and peroxisome proliferator-activated receptor (PPAR) subtypes alpha and gamma in the different phases of liver steatonecrosis and cirrhosis induced in rats after 3 and 9 weeks of carbon tetrachloride (CCl4) intoxication. CCl4 treatment can induce changes in the expression of NF-kappaB and PPARs. Immunohistochemical analysis of liver tissue sections from rats with steatonecrosis or cirrhosis demonstrated a significant increase in the number of NF-kappaB-positive and TNF-alpha-positive hepatocytes and Kupffer cells. In healthy controls, no expression of active NF-kappaB was detected. In previous studies, we have demonstrated that Kupffer cells isolated from rats with CCl4-induced steatonecrosis produced more reactive oxygen intermediates than cells isolated from normal rats. These oxidants could activate NF-kappaB and lead to an overexpression of TNF-alpha, observed in liver tissue sections. After CCl4 ingestion, the rat livers demonstrated a significantly decreased number of hepatocytes expressing PPARalpha and PPARgamma and a significantly increased number of ED2-positive Kupffer cells expressing these transcription factors, compared to normal. The activation of the p65 isoform of NF-kappaB correlates negatively with transcription of the alpha and gamma isoforms of PPAR in hepatocytes, and positively in Kupffer cells. These results suggest that the regulation and the role of these two transcription factors differ in the two cell types studied.
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