Abstract
Curcumin exerted hepatoprotective influences on various animal models of liver injury such as carbon tetrachloride, endotoxin and thioacetamide. This Study aimed to investigate the protective effects of curcumin as compared to N-acetylcysteine in the rat model of acetaminophen induced hepatotoxicity. 55 albino rats were divided into four groups: group )control group(. Group II received acetaminophen. Group III received both acetaminophen and N-acetylcysteine and Group IV received both acetaminophen and curcumin. At the end of the experiment, liver specimens were processed for histological study by light microscope and stained immunohistochemically for detection of apoptosis in hepatic cells by using anti p53 and the oxidative damage by anti-inducible nitric oxide synthase (anti iNOS). Serum levels of liver injury markers were assessed as well as the levels of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) activity were determined in all dissected tissues. Histological examination of liver sections of acetaminophen treated group revealed degeneration, cytoplasmic vacuolation and hydropic necrosis of hepatocytes. The central and the portal veins were dilated and congested and invading infiltrative inflammatory cells were appeared in association with significant increase in p53 and iNOS positive cells. Significant rise in serum levels of liver injury markers and MDA in liver tissues were recorded. However, levels of GSH and SOD were significantly decreased. Both curcumin and N-acetylcysteine resolved most of these morphological, immunohistochemical and biochemical alterations. Curcumin has protective effect similar to N-acetylcysteine against liver damage induced by acetaminophen in rats by reducing oxidative stress and apoptosis.
Highlights
Acetaminophen popularly known as paracetamol, is randomly and widely used everywhere in the world as a common analgesic and antipyretic drug
The hepatocytes were arranged in anastomosing cords of cuboidal hepatocytes separated from each other by blood sinusoids lined with endothelial and phagocytic Kupffer cells
In the present study the ability of curcumin to protect the liver against the oxidative stress and the hepatocellular injury that follows an overdose of acetaminophen were studied and compared with N-acetylcysteine
Summary
Acetaminophen (paracetamol, N-acetyl p-aminophenol; APAP) popularly known as paracetamol, is randomly and widely used everywhere in the world as a common analgesic and antipyretic drug. It is the most commonly reported cause of acute liver failure in the western world [1]. The main safety concern with using paracetamol is to avoid over dosage; the intake of an overdose of acetaminophen frequently causes severe acute liver injury [2]. Previous studies showed that APAP binds to cellular proteins including mitochondrial membrane directly and causes mitochondrial dysfunction, induction of ROS and necrotic cell death [4]. Some studies revealed that acetaminophen produced DNA fragmentation, which suppose apoptotic cell death, in hepatocytes [5]. Mutations accumulation of P53 gives rise to modified proteins that can be detected by immunohistochemistry [6]
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