Gambaran Histopatologi Pankreas Tikus Putih (Rattus norvegicus) Pasca Perlakuan Iskemia-Reperfusi Ginjal

Elva Rosiana, Wiwit Ade Fidiawati, Darmawi Darmawi

Abstract

Ischemic-reperfusion injury is defined by a condition of hypoperfusion in the spesific organ followed by reperfusion (reoxygenation) inducing tissue damage. Tissue damage produces reactive oxygen species (ROS) leading to oxidative stress condition. Oxidative stress mediate the lipid peroxidation reactions, harm the cell and finally facilitate the cell death. The aim of this study was to evaluate the histopathologic feature of white rat’s pancreas post renal ischemiareperfusion. This study was an experimental laboratory research with post-test-only control group design including 20 male white rats. Rats were divided into 5 groups, control, treatment 1 (45 minutes ischemia), treatment 2 (45 minutes ischemia followed by 1 hour reperfusion), treatment 3 (45 minutes ischemia followed by 2 hours reperfusion) and treatment 4 (45 minutes ischemia followed by24 hours reperfusion). We found the change of the histopathological characteristics of white rat’s pancreas in term of edema, leukocyte infiltration and vacuolization.

Keywords

renal ischemia-reperfusion, pancreas, histopathology, reactive oxygen species (ROS).

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References

Granger DN, Kvietys PR. Reperfusion injury and reactive oxygen species: The evolution of a concept. Redox Biology 6 (2015) 524-51.

Zarbock A, Eroglu A, Erturk E, Ince C, Westphal M. Ischemia-reperfusion injury and anesthesia. Biomed research international. 2014 Jun 19;2014.

Malek M, Nematbakhsh M. Renal ischemia/reperfusion injury; from pathophysiology to treatment. J Ren Inj Prev. 2015;4(2):20.

Hussein AM, Abd-Elkhabir A, Abozahra A, Baiomy A, Ashamallah SA, Sheashaa HA, et.al. Pancreatic injury secondary to renal ischemia/reperfusion (I/R) injury: Possible role of oxidative stress. Physiol Res. 63: 47-55. 2014.

Collard CD, Gelman S. Pathophysiology, clinical manifestasion, and prevention of ischemia-reperfusion injury. Anesthesiology. 2001;94(6):1133-8.

Salvadori M, Rosso G, Bertoni E. Update on Ischemia-Reperfusion Injury in Kidney Transplantation: Pathogenesis and Treatment. World J Transplantation. 2015 June 24;5(2): 52-67.

Kalogeris T, Baines CP, Krenz M, Korthuis RJ. Cell Biology of Ischemia/Reperfusion Injury. Int Rev Cell Biol. 2012; 298: 229-317.

Galindo MF, Jordan J, Garcia CG, Cena V. Reactive oxygen species induce swelling and cytochrome c release but not transmembrane depolarization in isolated rat brain mitochondria. British Journal of Pharmacology (2003) 139, 797-804.

Chrysikos DT, Sergentanis TN, Zagouri F, Psaltopaulou T, Theodoropoulos G, Flessas I, et.al. Lazaroid U-74389G administration in pancreatic ischemia-reperfusion injury: A swine model encompassing ischemic precondition. JOP. J Pancreas (Online) 2015 Mar 20; 16(2):176-84.

Warzecha Z, Dembinski A, Ceranowicz P, Dembinski M, Kownacki P, Konturek SJ, et.al. Immunohistochemical exprression of FGF-2, PDGF-A, VEGF dan TGFβ RII in the pancreas in the course of ischemia/reperfusion-induced acute pancreatitis. Journal of Physiology and Pharmacology 2004, 55, 4, 791-810.

Amiralevi SH, Trianto HF, Novianry V, Zakiah M. Efek paparan formaldehid oral akut pada histologi hati tikus wistar jantan. Jurnal Cerebellum. Vol 3. No 3. Agustus 2017.

Warzecha Z, Dembinski A, Ceranowicz P, Cieszkowski J, Konturek SJ, Dembinski M, et.al. Ischemic preconditioning of the hindlimb or kidney does not attenuate the severity of acute ischemia/reperfusion-induced pancreatitis in rats. Journal of Physiology and Pharmacology 2008, 59,2, 337-52.

DOI: https://doi.org/10.26891/JIK.v13i1.2019.58-66

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