الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Liver diseases are one of the most common causes of death worldwide. Liver fibrosis is the first step toward death in those cases as it leads eventually, if not treated, to carcinoma or hepatic failure.
There are many causes of liver fibrosis for example alcohol abuse, non-alcoholic fatty liver diseases, chronic hepatitis C virus, autoimmune liver diseases and cholestatic liver diseases. Liver fibrosis is characterized by increased extracellular matrix production and collagen deposition as a result of chronic inflammation and activation of cells responsible for fibrosis, mainly hepatic stellate cells.
Thioacetamide (TAA) is a hepatotoxic drug that is widely used nowadays for the experimental induction of liver fibrosis. Hepatic fibrosis induced by TAA resembles to a great extent that of human fibrosis and is established in a relatively short time as compared to other hepatotoxic drugs.
Platelet-rich plasma (PRP) research is currently an area of intense scientific interest as an emerging method used for treatment of many diseases. Being rich in platelets, growth factors and secretory proteins contributes to the healing process in case of liver fibrosis. The concept of PRP preparation is simple and non-invasive, which makes it a relatively safe method of treatment.
The aim of our study was to assess the potential effect of PRP on TAA induced hepatic fibrosis in adult male albino rat model.
The study was carried out on fifty-four adult male albino rats, each of average weight 150-200 gm and age of 6-8 weeks. Thirty rats were used for PRP preparation. PRP was prepared by centrifugation of the whole blood from all rats under sterile conditions.
Twenty- four rats were randomly divided into 4 groups: (6 rats each)
• group I (control): received intraperitoneal (i.p) saline twice weekly for 7 weeks.
• group II (PRP): received PRP (0.5 mL/kg 1:1 in Phosphate buffer saline (PBS) i.p injection) twice weekly for 7 weeks.
• group III (TAA): received i.p injection of TAA drug (200 mg/kg) twice weekly for 7 weeks.
• group IV (TAA+PRP): received i.p injection of TAA drug (200 mg/kg) twice weekly for 7 weeks and PRP twice weekly starting from the 4th week of TAA drug administration to the end of the experiment.
After 24 hours of the last injection of the TAA and PRP doses, animals were sacrificed after ether anesthesia. Retro-orbital plexus blood samples of all animals were collected for biochemical analysis of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Liver was excised and specimens were prepared for light microscopic and electron microscopic studies. Morphometric analysis to determine area percentage of collagen for detection of the amount of fibrosis, the surface area of bile canaliculi, and the width of blood sinusoids were done.
Hematoxylin and Eosin (H&E) stained sections revealed normal structure of the liver in both group I (control) and group II (PRP). While H&E sections of group III (TAA) revealed disorganized hepatic architecture with the formation of fibrous tissue septa and complete lobules. Hepatocytes showed marked inflammatory degenerative changes involving both the cytoplasm and the nuclei. There was extensive perivascular cellular infiltration around portal areas and even in between hepatic cords. Blood sinusoids showed a significant dilatation that was confirmed by a morphometric study of the width of sinusoids. Whereas group IV (TAA+ PRP) H&E sections showed a marked improvement of liver architecture, with a decrease in the fibrous tissue deposition. Only a mild affection of the hepatocytes and most hepatocytes appeared more or less like the control group.
The examination of trichrome stained sections of group III (TAA) revealed a considerable amount of collagen fibers deposition with thickened complete connective tissue septa and formation of hepatic lobules. While examination of liver sections of group IV (TAA + PRP) revealed markedly reduced collagen fibers deposition. These findings were confirmed by a morphometric study which showed a significant increase in the area percent (%) of collagen in group III (TAA) in comparison to group I (control). On the other hand, group IV (TAA + PRP) showed a significant decrease in the area percent of collagen as compared to group III (TAA).
Electron microscopic examination of hepatocytes of group III (TAA) confirmed the light microscopic results. The cytoplasm of most cells showed marked rarefaction. It revealed mitochondria with dense matrix and loss of cristae. Many of the hepatocytes’ nuclei were irregular and electron-dense. In addition, some marginated nucleoli were revealed. Myofibroblasts were noticed where lipids droplets disappeared. Proliferation and dilatation of bile canaliculi were noticed, this was confirmed by a morphometric study that revealed a significant increase of the surface area of bile canaliculi in group III (TAA) in comparison to group I (control).
While electron microscopic examination of hepatocytes of group IV (TAA + PRP) revealed mostly a normal histological pattern of most of the hepatocytes. Few cells showed mild affection, where their cytoplasm revealed some rarefaction. Hepatic stellate cells were also seen.
Hepatocellular damage was confirmed biochemically by the significant elevations of liver enzymes ALT and AST in group III (TAA). While a significant decrease of levels of ALT and AST was recorded in group IV which was more or less similar to control group.
from the current study, it can be concluded that PRP might be an effective measure to stop the progression and even decrease the hepatic fibrosis induced by TAA.