الفهرس 
Therapeutic role of platelet-rich plasma (prp) on cyclosporine a-induced nephrotoxicity in adult male albino rat Histological, Immunohistochemical, Biochemical and Gene Expression Study
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Abstract
ARenal function impairment and morphological damage are both
signs of CsA nephrotoxicity. Renal vasoconstriction, tubular epithelial cell
alterations, tubulointerstitial fibrosis, and glomerular abnormalities all contribute
to irreversible renal failure secondary to long term CsA treartment (Korolczuk et
al., 2010).
The stimulation of the renin-angiotensin-aldosterone system, upregulation of the transforming growth factor-beta (TGF-β), direct activation of
apoptosis genes and enhanced apoptosis in tubular and interstitial cells, and
oxidative stress are thought to be the underlying mechanisms of toxicity (AbuFarsakh et al., 2017).
Marx et al., (1998) were the first to describe platelet-rich plasma (PRP). Itis an autologous
growth factor-rich product made from a blood sample centrifuged to separate the platelet-rich
supernatant. Many growth factors, such as epidermal growth factor (EGF), hepatocyte growth
factor (HGF), platelet derived growth factor (PDGF), and vascular endothelial growth factor
(VEGF), are released locally by PRP up to three weeks following administration