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Kadkhodaee M, Khastar H, Seifi B, Najafi A, Delavari F,
Volume 70, Issue 2 (5-2012)
Abstract

Background: In a recent study, we were able to demonstrate a role for leukocyte transfer in the induction of liver damage in recipient mice after induction of IR (60 min of bilateral renal artery occlusion and 3 hrs reperfusion) injury in donors. The present study investigates the role of leukocyte transfer in the induction of kidney damage in recipient mice after induction of renal IR injury in donors.

Methods: Mice were divided into two sham and renal IR groups. After anesthesia, leukocytes were isolated from blood and were transferred to the two recipient groups: the intact recipient mice received leukocytes from the sham donor group (Sham recipient) and the intact recipient mice that received leukocytes from IR donor group (IR recipient). After 24 hrs, the recipient mice were anesthetized and blood samples and renal tissues were collected.

Results: Renal malondialdehyde (MDA) increased and glutathione and superoxide dismutase (SOD) decreased significantly in IR recipient group in comparison to sham recipient group. Although renal function tests, including BUN and plasma creatinine were significantly different between IR donor and sham donor groups, but they were not significantly different in two recipient groups. Renal tissues in IR donor group showed extensive damage compared to sham group, but in IR recipients' kidneys, they were different from IR donor tissues despite being different from their respective sham group.

Conclusion: These findings are suggestive of implication of leukocytes in renal tissue damage and oxidative stress after renal IR injury.


Fateme Azizi , Behjat Seifi , Mehri Kadkhodaee ,
Volume 75, Issue 9 (12-2017)
Abstract

Background: Renal ischemia reperfusion (RIR) injury is a common clinical syndrome that affects renal function and significantly increases morbidity and mortality. Hydrogen sulfide (H2S) is an endogenously gaseous mediator that exhibits many cytoprotective effects. Recently, studies have shown that H2S have opposite effects in different doses. Therefore, in the current study we investigated the effects of H2S at different doses on renal function after induced renal ischemia reperfusion injury model.
Methods: The present study is an experimental study in animals and was conducted in Tehran University of Medical Sciences in April 2014. Male Wistar rats were assigned to five main groups (n= 6): 1) Sham, 2) Ischemia reperfusion (IR), 3) Administration of 50 µmol/kg Sodium hydrosulfide (NaHS)+IR, 4) Administration of 75 µmol/kg NaHS+IR and 5) Administration of 125 µmol/kg NaHS+IR. Sham group underwent laparotomy without cross-clamping of renal pedicles. Renal ischemia (IR) was induced in rats by both renal arteries occlusion for 55 min followed by reperfusion. Rats in the NaHS groups received intraperitoneal injections of 50, 75, or 125 µmol/kg of NaHS 10 minutes before the onset of ischemia and immediately after the onset of reperfusion. After reperfusion, plasma was collected for functional evaluation.
Results: Compared to the sham, IR animals demonstrated a significant rise in plasma creatinine and BUN levels. Rats in the low-dose NaHS treated groups (H50, H75) had improved renal function by significantly decrease of creatinine and BUN levels. However, treatment with a high-dose of NaHS increased the levels of plasma creatinine and BUN levels as compared with these indices in the IR group.
Conclusion: Our study demonstrates that different doses of Sodium hydrosulfide (NaHS) can play diverse role in renal ischemia reperfusion injury. However, NaHS in the low-doses could protect the kidney from the RIR injury, in a higher dose NaHS exaggerated the renal function by increases plasma creatinine and BUN. Therefore, determining of the therapeutic doses of NaHS may be important in the protection of kidney from the RIR injury.


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