Efficacy of platelet rich plasma on pancreatic injury induced by renal ischemia reperfusion in adult male rats

ABSTRACT

Renal ischemia-reperfusion (I-R) injury is the main cause of acute renal failure. Acute pancreatitis is one of the fatal remote lesions that occurs in patients with renal I-R injury. Platelet-rich plasma (PRP) is a hopeful aiding therapy for tissue injuries. Forty adult rats were utilized in this study, ten for PRP preparation and thirty were divided into three groups; Control: subdivided into three equal subgroups, I-R group: exposed to bilateral renal pedicles clamping and I-R+ PRP group: were experienced identical procedures as I-R group then subcutaneously (S.C) injected with 0.5 ml PRP two times weekly for three weeks. Blood samples were taken for detection of serum urea and creatinine, blood glucose level and serum amylase. The pancreas was dissected and prepared for histopathological examination by light and electron microscope. Statistical analysis of all collected results was performed. Our biochemical results revealed deleterious effects of renal I-R on the pancreas as evidenced by a highly significant increase in serum amylase and blood glucose level. In I-R group, histopathological examination revealed wide septa and congested blood vessels, acinar cells showed disrupted rough endoplasmic reticulum and few secretory granules. Some islet cells showed pyknotic nuclei and vacuolated cytoplasm. PRP treated group showed nearly normal structure in the form of numerous acinar cells’ granules, extensive rough endoplasmic reticulum and mitochondria. Most of Beta cells had euchromatic nuclei and numerous secretory granules. Accordingly, PRP treatment reduced the pancreatic biochemical and histopathological alterations caused by renal I-R injury and so considered a promising therapy for pancreatic damage.

KEYWORDS:

• PRP
• pancreas
• renal ischemia reperfusion

Abbreviations

AKI: Acute Kidney Injury; ABC: avidin biotin complex; ANOVA: Analysis of Variance; AP: Acute pancreatitis; ASK-1: Apoptosis signal-regulating kinase-1;ATP:Adenosine Tri Phosphate; BUN: Blood urea nitrogen; Ca2: Calcium; DAB: 3-3 Diaminobenzidine; DNA: Deoxy ribonucleic acid; RNA: Ribo nucleic acid; EGF: Epidermal growth factor; ER: Endoplasmic reticulum; Fig: Figure; GFs:Growth Factors; GLUT2: Glucose Transporter2; gm: Gram; H&E: Hematoxylin and Eosin; HGF:Hepatocyte Growth Factor; IGF: insulin-like growth factor; IL: Interleukin; I-R: Ischemia-Reperfusion; IU: International unit; MAPK: Mitogen-activated protein kinase; MPT: mitochondrial permeability transition; NF-κB: Nuclear factor kappa-B; NO: Nitric oxide; NOS: Nitric oxide synthase; PBS: Phosphate Buffer Saline; PDGF: Platelet derived growth factor; PMNs: Polymorph nuclear leucocytes; PSCs: Pancreatic Stellate Cells; PPP: Platelet Poor Plasma; PRP: Platelet Rich Plasma; RER: Rough Endoplasmic Reticulum; ROS: Reactive Oxygen Species; rpm: revolutions per minute; SC: Subcutaneous; SD: Standard deviation; SPSS: Statistical Package for Social Science; TGF-β: Transforming Growth Factor- β; TNF-α: Tumor necrosis Factor- α; UPR: unfolded protein response; VEGF: vascular endothelial growth factor, IGF-1: Insulin Growth Factor-1; bFGF:b-Fibroblast Growth Factor.

Author contributions

A.S.S: Conceptualization, Supervision. R.A.Z.: Methodology, Visualization. S.M.H.E: investigating, Writing—Original Draft, data curation. S.A.A.: Formal analysis, Writing—Review& Editing. All authors contributed to editing and critical review of the manuscript.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

The author(s) reported there is no funding associated with the work featured in this article