scholarly journals Protective Effects of Methane-Rich Saline on Renal Ischemic-Reperfusion Injury in a Mouse Model

2018 ◽  
Vol 24 ◽  
pp. 7794-7801 ◽  
Author(s):  
Yan Meng ◽  
Zhengyu Jiang ◽  
Na Li ◽  
Zhenzhen Zhao ◽  
Tingting Cheng ◽  
...  
Keyword(s):  
Mouse Model ◽  
Reperfusion Injury ◽  
Protective Effects ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

620 COMPARISON OF PROTECTIVE EFFECTS OF N-ACETYLCYSTEINE AND MANNITOL ON RENAL ISCHEMIC/REPERFUSION INJURY

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Michael Degen ◽  
Andrew Fishman ◽  
Bobby Alexander ◽  
Muhammad Choudhury ◽  
Majid Eshghi ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Protective Effects ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

scholarly journals Klotho Reduces Necroptosis by Targeting Oxidative Stress Involved in Renal Ischemic-Reperfusion Injury

2018 ◽  
Vol 45 (6) ◽  
pp. 2268-2282 ◽  
Author(s):  
Yingying Qian ◽  
Xiangjiang Guo ◽  
Lin Che ◽  
Xuejing Guan ◽  
Bei Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Tunel Staining ◽  
Protective Effects ◽  
Oxidative Stress Biomarkers ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Renal Ischemic Reperfusion Injury

Background/Aims: Klotho is a multifunctional protein expressed predominantly in kidney tubular epithelium. Here, we investigated the protective effects of Klotho on necroptosis in renal ischemic-reperfusion injury (IRI) and the role of oxidative stress in this process. Methods: Mice were subjected to bilateral renal pedicle clamping. Mouse renal tubular epithelial (TCMK-1) cells were exposed to hypoxia/reoxygenation (H/R) or H2O2. Kidney samples from acute kidney injury (AKI) patients and controls were examined by immunofluorescence. Klotho protein and N-acetyl-L-cysteine (NAC) were used to define their roles in mediating necroptosis. Necroptosis was assessed by TUNEL staining, immunoblotting, and real-time PCR. Oxidative stress was studied via ELISA, immunoblotting, colorimetric, and thiobarbituric acid reactive substances assays. Results: Renal IRI induced Klotho deficiency in the serum and kidney, but an increase in the urine. The levels of the necroptotic markers receptor-interacting protein kinase (RIP) 1, RIP3, IL-1β, and TUNEL-positive cells increased after IRI; all increases were ameliorated by Klotho. In TCMK-1 cells, Klotho and NAC attenuated the elevation in RIP1, RIP3, and LDH release induced by H/R or H2O2. Moreover, Klotho decreased the levels of oxidative stress biomarkers and elevated superoxide dismutase 2 expression in both in vivo and in vitro experiments. Studies in human samples further confirmed the Klotho deficiency and increased formation of RIP3 puncta in AKI kidneys. Conclusion: Klotho protects tubular epithelial cells from IRI and its anti-necroptotic role may be associated with oxidative stress inhibition.

scholarly journals The Nephroprotective Effect of Lycopene on Renal Ischemic Reperfusion Injury: A Mouse Model

2019 ◽  
Vol 35 (4) ◽  
pp. 474-481
Author(s):  
Yasmeen A. Hussien ◽  
Hussien Abdalkadim ◽  
Waddah Mahbuba ◽  
Najah R. Hadi ◽  
Dina A. Jamil ◽  
...  
Keyword(s):  
Mouse Model ◽  
Reperfusion Injury ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Nephroprotective Effect ◽  
Renal Ischemic Reperfusion Injury

scholarly journals Role of IL-1 in renal ischemic reperfusion injury.

1998 ◽  
Vol 9 (4) ◽  
pp. 614-619 ◽  
Author(s):  
M Haq ◽  
J Norman ◽  
S R Saba ◽  
G Ramirez ◽  
H Rabb
Keyword(s):  
Renal Function ◽  
Reperfusion Injury ◽  
Interleukin 1 ◽  
Organ Injury ◽  
Central Component ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
And Control ◽  
Renal Ischemic Reperfusion Injury

Interleukin-1 (IL-1) is a central component of many acute inflammatory processes. Blocking IL-1 receptor (IL-1R) with IL-1R antagonist (IL-1Ra) has attenuated ischemic reperfusion injury in brain, heart, and liver models. However, the role of IL-1 in renal ischemic reperfusion injury (IRI) is not known. Therefore, the role of IL-1 in renal IRI was evaluated using the complementary approaches of IL-1R blockade in wild-type mice in addition to the study of renal IRI in IL-1R knockout (KO) mice. Ischemia was induced by bilateral renal pedicle clamping for 30 min. IL-1Ra was administered at 10 mg/kg every 4 h, high doses that have been protective in previous organ injury models in mice. IL-1R KO animals, previously characterized as insensitive to IL-1, had the absence of IL-1R1 confirmed by DNA blots. IL-1Ra, IL-1R KO, and control groups had similar elevations of blood urea nitrogen (114 +/- 13, 133 +/- 11, and 120 +/- 11 mg/dl) and serum creatinine (1.7 +/- 0.3, 2.1 +/- 0.2, and 1.6 +/- 0.3 mg/dl) 24 h after ischemia. Furthermore, acute tubular necrosis scores were also similar in IL-1Ra-treated mice (3.0 +/- 0.3), IL-1R KO mice (2.7 +/- 0.3), and control mice (3.1 +/- 0.2). However, both IL-1Ra and IL-1R KO groups, compared with control animals, developed significantly less infiltration of polymorphonuclear leukocytes per 10 high-power fields in postischemic renal tissue (1111 +/- 228 and 967 +/- 198 versus 1820 +/- 190, P < 0.05). In contrast to the comparable renal functions at 24 h, recovery of renal function was significantly accelerated in the IL-1R KO group compared with control at both 48 (P < 0.05) and 72 (P < 0.05) h. Recovery in the IL-1Ra group was similar to that in the control animals. These data demonstrate that IL-1 is unlikely to be beneficial in the recovery of renal function after ischemia and may play a deleterious role.

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